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Sex and human's sexual urge.
Why is it necessary for humans to feel pleasure while having sex? Why is it that other animals don't need to experience it? Is it evolutionary ? Why do we mate for pleasure when it's so energy wasting/ time consuming?

How do you know other animals don't like sex?

@user137 I know animals like to have sex as well but they do it only for reproduction and not for pleasure. Only certain species do it for pleasure. I know this kinda sound taboo but I'm curious about this

How do you reconcile your two assertions "animals like to have sex" and "they do it ... not for pleasure"? Seems contradictory to me. How well do you think, say, a dog understands its own reproductive biology? Is the dog thinking "I must propagate my species" while copulating?

http://biology.stackexchange.com/users/29114/solanacea I mean that's their instincts to reproduce

@TheoneandonlygreatK Wouldn't enjoyment of something be a great way for an evolutionary process to "enforce" an instinct? What other options are there? Withdrawal/relief from a negative stimulus can also be somewhat pleasurable/enjoyable: i.e., drinking or eating when you are thirsty/hungry.

Plenty of animals have sex for pleasure, dolphins and porcupine are known masturbators. your assumptions are just wrong.

This is logical question and somehow related to evolution.
See mating is pleasurable to most of animals
Second thing during course of evolution mating became pleasurable not because humans can take pleasure but to attract them towards mating therby increasing population of a species helping it to survive.


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Ugly people and genome
Why haven't ugly and dumb people been eliminated be evolution ? Why do they still exist despite Charles Darwin theory of natural selection.

This is essentially a duplicate of Why do some bad traits evolve, and good ones don't?

Perhaps alcohol?

As long as there is variation on the traits you mention, there will be one person to call those at the low extreme of the spectrum dumb or ugly. This would be true even if the average IQ was around 200. So the question really does not make much sense!
One will note that directional selection reduces genetic variance but this is quite clearly not what the OP had in mind so let's not go down this path.
On top of that you are assuming that these traits are under selection. Typically, you are assuming that higher intelligence is necessarily beneficial which might very much turn out to be wrong. As a start you can have a look at the wikipedia article on the Flynn effect or this Skeptics.SE post.
You talk about "Charles Darwin theory of natural selection" please note that our understanding of evolutionary processes is much more advanced today than Darwin's understanding. We call our theory of evolution the modern evolutionary synthesis. If you are curious to know a thing or two about what this theory says, you can have a look at Understanding Evolution for example, a free and short online introductory course to evolutionary biology from UC Berkeley.

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Why are there still useless traits/mutations in our body
Why is it that through decades of evolution , some seemingly useless body traits such as earlobes and pubic/chest hair still remains while other traits are generally replaced through evolution?

Natural selection "selects" the trait that is less advantageous and removes/ reduces its frequency. It is like a filter paper. All solids are filtered out of mixture while clear liquid is collected. So if there is a difference in fitness of organisms by variations in traits, then only they are SELECTIVELY removed. Now, if a person without an earlobe would have had an increase in fitness, it would have had eliminated over time. And it might (I said might) be that there IS some pressure but it might be so slow that we can not realise it. But in case of earlobes, evolution will be evident in the case of elephants and Jackrabbits.

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Bacteriophages and their role in genetic editing?
I know how plasmids and restriction enzymes work to change the dna of a bacteria cell, but I do not really understand how a bacteriophage works to edit the genome of a cell. Is it related to crispr since its a virus which inserted genetics in bacteria? Also, is it during the lysogenic or lytic stage that the bacteriophage alters the DNA?

Putting CRISPR to one side (since that is the bacterium editing its own DNA) where have you got idea that phage do have an effect on their host's genome? Do you have any sources that you could cite?

Yes, I think its called transduction.

https://en.wikipedia.org/wiki/Transduction_(genetics)

That Wikipedia page looks quite comprehensive and answers your question about lytic or lysogenic cycle. What specifically is puzzling you? Bear in mind that transduction isn't really something that phages do 'purposefully', it is rather an example of the old adage in E coli genetics: 'anything that can happen will happen'. The trick is to find a way to detect the event by selection or, as a last resort, by screening.

Why do you think a bacteriophage "edits" the genome of a cell?

Why do you think a bacteriophage "edits" the genome of a cell?

I mean I read someone it is manipulated in genetic editing. It obviously doesn't just edit the genes willingly for humans' benefit ...

As explained in the Wikipedia page that you have linked to, transduction is the name given to a particular phenomenon whereby phage can be used to move bacterial DNA between cells.
Depending upon the phage, some aberrant or infrequent process can result in the packaging of host cell DNA into a phage particle during a lytic cycle. The resulting defective phage particle is still infective however, and when it infects a new host cell it injects the bacterial DNA that it is carrying. This DNA can then recombine with the host DNA.
So, for example, if the second host was a lacZ mutant but the parent host was lacZ⁺, then it would be possible to select lacZ⁺ in the second host.
Transduction was an important tool in E. coli genetics. Phage P1 can be used for general transduction, which means that any piece of DNA can be moved. As I said in my comment: anything that can happen will happen.


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Placebo effect and why they work
I'm just wondering how the placebo effect works on people. If a patient is given fake drugs , how does that make him better? So what if they feel more "assured", how would that help the body immunity (t cells, phagocytes, etc) fight the infection better? How does phycological emotions affect the physical aspects of our immunity? Also I've read an interesting article online showing us that placebo effect works even when you know you are given fake drugs? This really complicates my understanding. How would such a approach even work?
http://www.health.harvard.edu/blog/placebo-can-work-even-know-placebo-201607079926

well for a start it helps if your remember emotions are chemical reactions occurring in the body, psychological and physical are not separate.

The paper isn't about immunity, and the answer is in the paper you cite: Kaptchuk says placebos... can work for conditions that are defined by “self-observation” symptoms like pain, nausea, or fatigue. “People can still get a placebo response, even though they know they are on a placebo,” he adds. “You don’t need deception or concealment for many conditions to get a significant and meaningful placebo effect. Placebos don't work on serious illnesses (they don't fight infections or cancer); they work on perception of illness and on the mind-body connection in illness, which is too broad.


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Why will happen if plant phloem does not contain sieve plates?
What are the primary functions of the sieve plates that make them so crucial? I've done a bit of reading online and found
"Sieve plates are perforated end walls separating the component cells (sieve elements) that make up the phloem sieve tubes in vascular plants. The perforations permit the flow of water and dissolved organic solutes along the tube and are lined with callose."
However, wouldn't the flow of water or organic diluted be faster without the extra sieve plates obstructing the flow? Or is there some other functions of the sieve tubes?

First of all, phloem sieve cells (opposing to xylem vessels) are live cells. In the phloem, a transport occurs not like in water pipes (with free movement of liquids) but through cells transport structures, particularly through plasmodesmata. As live cells, sieve elements need all standard structures, including cell wall, to sustain functionality.
Moreover, the phloem transport is (at least partially) an active process. I.e. to transport something you have to spend some energy. Today the most supported hypothesis of phloem transport is Pressure Flow Hypothesis . According to Wikipedia:

While movement of water and minerals through the xylem is driven by
  negative pressures (tension) most of the time, movement through the
  phloem is driven by positive hydrostatic pressure. This process is
  termed translocation, and is accomplished by a process called phloem
  loading and unloading. Cells in a sugar source "load" a sieve-tube
  element by actively transporting solute molecules into it. This causes
  water to move into the sieve-tube element by osmosis, creating
  pressure that pushes the sap down the tube. In sugar sinks, cells
  actively transport solutes out of the sieve-tube elements, producing
  the exactly opposite effect. The gradient of sugar from source to sink
  causes pressure flow through the sieve tube toward the sink.

So, a plant needs live cells to support such mechanism.
Here we come to sieve plates. In plants, live cells interacts by means of plasmodesmata. In simple words, they are extensions of endoplasmatic reticulum which connect the cytoplasm of two cells and act as transport channels. And sive plates are simply places of highly hypertrophied plasmodesmata region.
So in conclusion:

Phloem transport is a partially active transport which occurs with
an involvement of cells transport structures like plasmodesmata.
The region of hyper-developed plasmodesmata on sieve elements wall
appears as sieve plate.
That is why an absence of such structure will not provide any gains in conductivity.

UPD. In response to Jim Young comment.
Damage protection is not a major role of sieve plates. Again, sieve plates are areas where plasmodesmata penetrate cell wall. Plasmodesmata act as the main vector of intercellular transport. So, the transport is the main purpose (or a reason) of sieve plates.  The damage protection is an additional property and not an aim of these structures. As to tyloses, yes it is a common mechanism of vertical transport prevention in xylem. But xylem vessels consist of dead cells. They are literally pipes. Therefore it is possible to cork up xylem vessels by simply inserting packs of fibre. BTW, that is why cavitation in vessels can cause embolization.  In contrast, phloem cells are live cells (with cytoplasm and EPR). They conduct water and sugars not by free flaw but with an involvement of intercellular mechanisms. That is why mechanical embolization is not a case for phloem cells.


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Is the heart more relaxed when stretched or contracted, and how does it affect cross-bridge interactions?
In the heart, are stretched muscles during the diastole more relaxed or are the contracted muscles more relaxed? Depending on the answer, are there then more cross-bridge interactions in cardiac muscle cells when the heart is stretched or contracted?

Can you clarify your question? What do you mean by "more relaxed". There are a few things to consider here: the contracted or relaxed state of cardiac muscle, as well as the baseline stretch in that muscle. But your use of "relaxed" in your question isn't standard.

Well that is the question itself. When the heart is contracted, is that when it is more relaxed? Or, is it more relaxed when it is expanded? Which state is the resting state of a heart?

Relaxed is the opposite of contracted, so when it is contracted it is exactly not relaxed, by definition. Are you referring to the pathological state of stretching that occurs in some forms of heart failure, e.g., dilated cardiomyopathy?

It's completely possible I have terminology mixed up, I'm not biology expert and different sources gave conflicting descriptions. I'm not referring to any kind of disease, what I want to know is which state, expanded or "smaller", is the heart's resting state when it is not exerting energy to pump blood, and thus, which other state must then be the one that takes more energy to allow more cross-bridge interactions to maintain. Is the heart more relaxed when it is expanded? Or when it is...I guess I can only say "smaller" since contracted could be for either direction.

Contracted literally means to shrink in size: "contracted" cannot mean "either direction"

@BryanKrause I used to think that too before Dan commented. But, for instance, when muscles in your biceps contract, part of them becomes shorter, but then another part of them bulges up and becomes larger. So muscle "contracting" could cause surround tissue to expand.

Nothing in Dan's comment suggests that contracted could mean anything but shrunken in size.

@BryanKrause They said relaxed is the opposite of contracted, but there is nothing in biology that says a larger or smaller structure has to be either in general. Just hold out your fingers, they are moderately suspended from your hand, not completely dropping to a 90 degree angle, but not completely risen up either. When the muscles in your fingers contract, your finger can either rise, Or Also curl. Either way, a muscle "contraction" occurs.

I should correct to say length instead of size: length is the important dimension of size in the context of muscle action. When your fingers extend that is not because the muscles that bend your fingers are lengthening in some way, it's because another muscle pulls the back of your finger taut.

@BryanKrause You mean the length of the sacromere. Yes, I imagine that always decreases during muscle contraction which is what allows the ratcheting to occur in the first place based on what I had found.

@BryanKrause But your finger description is exactly my point. Even though muscles always contract to exert force, they can affect surrounding tissue in different ways. So, I can't simply say that the heart shrinks just because I read cardiac muscles contract since as you pointed out, contraction can lead to different kinds of movement, more information is needed.

I mean the length of the whole muscle. More information is not needed to answer your question "Is the heart more relaxed when stretched or contracted": you are asking "Is the heart longer when it is longer or shorter?"

@BryanKrause We just agreed that just because one muscle contracts, it doesn't mean all the surrounding tissue shrinks. In the finger example, some of the tissue shrinks, but also the opposite part of it expands. So, simply stating cardiac muscles contract isn't enough to be 100% sure that that is what causes the heart to shrink in size, especially when we're dealing with all kinds of different contractions in different 3D directions.

The muscular portion of the heart is comprised of cardiac myocytes, elongated cells filled with bundles of actin and myosin called sarcomeres. These cells are similar in many respects to skeletal muscles, but are shorter, have only one nucleus, and slightly different isoforms (versions) of the proteins involved. The purpose of this cell, like the skeletal muscle cell, is contraction, or shortening on activation.
This image of cardiac muscle cells shows how full they are with long bands of proteins (proteins stain pink).

Because the heart is a muscular chamber, instead of simply a band of muscle (like the bicep), the relevant dimension for the organ is volume instead of length. Where your bicep gets shorter when it contracts (and pulls your forearm toward your upper arm, bending at the elbow joint), when your heart muscle contracts, it twists and squeezes against the fibrous part of the organ, decreasing the volume of the chamber.
Since there is no air in a healthy live heart, when the heart contracts, reducing the volume of the container, the blood is forced out of the heart (ejection) through whatever opening is available. This is called systole. When the heart relaxes, the volume of the container increases, and blood enters the container through whatever opening is available. this is called diastole.

Now, how is this related to cross-bridge interactions?
The mechanism for contraction itself, in both skeletal and cardiac muscle, is cross-bridge cycling. Those pink bundles of actin, myosin, and associated proteins in the picture above form bonds, change conformation, break bonds, change conformation, and form new bonds:

This cross-bridge cycling occurs during contraction when $Ca^{++}$ enters the cell as part of the cardiac action potential. Relaxation occurs when $Ca^{++}$ concentrations decrease, through the action of the $Ca^{++}$-ATPase, causing cross bridge interactions to decrease.

Okay, so just to make it clear before I select it as the answer, when the heart is expanded, that is it's natural resting state, and when the cardiac muscles exert force through contraction, it is only to shrink the size of the heart? I just want to make sure on whether it is the expanding or the shrinking that requires the cardiac muscle to contract, and so far it seems like it's the shrinking action.

You are correct. Contraction causes the volume inside the heart to decrease (the volume inside the chamber shrinks).

You're putting a lot of work into the question and I appreciate that, but I don't want you to over-invest when I am focused so much on a singular question. I can infer the cross-bridge interactions depending on what the answer is and I am familiar with the theory behind it.

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What are the max angles of human eyeball rotation?
How much can our eyeballs rotate towards the nose, away from it, towards the top and bottom?

There shall be slight differences due to physiology. Nevertheless, the average vertical ascending angle is 25 degrees and descending angle, 30 degrees.
Within the x-y plane of which we assume to be coplanar with the central line of vision, the maximal angle of rotation is 35 degrees in the left and right directions respectively.

I attempted to construct an image which depicts these angles - simply a Cartesian diagram.
You can find further clarification of details from this link by Nelson & Associates
Finally, it is important to note that although the eye may be capable of these rotations, the eye may not be able focus on all objects in this field acutely, namely, focusing light on the fovea.
Happy muscular experiments.

"Finally, it is important to note that although the eye may be capable of these rotations, the eye may not be able focus on all objects in this field acutely, namely, focusing light on the fovea."  Any ideas wht that happens? Also, how reliable are Nelson & Associates as a scientific source?

@MarkLegault  To answer your first question, I can consider two primary reasons: at the farthest rotation of one of the two eyes respectively, there is no binocular vision. Therefore, the depth-perception is limited in these areas. Moreover, for an object to be acutely focused on by the eye, the reflected light waves must hit a certain area of the retina: the fovea. Full eyeball rotation may allow for increased peripheral vision - around 95 degrees total vision. Regrettably, perhaps due to the difficulty in measuring rotation as opposed to field of vision, data are limited.

These angles roughly correspond to the angle which would achieve the maximum peripheral vision, available from: www.vision-and-eye-health.com/visual-field.html


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Can I execute/model a genome?
Hi I am wondering if we can execute a genome on the sub-cellular level by running it on the computer. What I mean is using the genome as data to examine by having the cells reproduce and see what happens as they grow.

Given that Nicolai has adequately answered the question, I vote to close this question.

Welcome to Biology.SE! Please take the [tour] and then go through the help pages starting with [Ask] questions effectively on this site. In particular, note that "speculative" questions are off-topic. ——— You might also want to make sure you have a good grounding in the basics of biology — that will help you understand why the answer is "No". I have found that when learning about a new area starting with a relatively accessible and reliable source like Khan Academy is very helpful.  Thanks!

A simple genome can be modeled, however imperfectly, on a computer, where some have taken experimental genomics data and built simulations from it.
For instance, from the paper A Whole-Cell Computational Model Predicts Phenotype from Genotype:

Understanding how complex phenotypes arise from individual molecules and their interactions is a primary challenge in biology that computational approaches are poised to tackle. We report a whole-cell computational model of the life cycle of the human pathogen Mycoplasma genitalium that includes all of its molecular components and their interactions. An integrative approach to modeling that combines diverse mathematics enabled the simultaneous inclusion of fundamentally different cellular processes and experimental measurements. Our whole-cell model accounts for all annotated gene functions and was validated against a broad range of data. The model provides insights into many previously unobserved cellular behaviors, including in vivo rates of protein-DNA association and an inverse relationship between the durations of DNA replication initiation and replication. In addition, experimental analysis directed by model predictions identified previously undetected kinetic parameters and biological functions. We conclude that comprehensive whole-cell models can be used to facilitate biological discovery...
We have developed a comprehensive whole-cell model that accounts for all of the annotated gene functions identified in M. genitalium and explains a variety of emergent behaviors in terms of molecular interactions. Our model accurately recapitulates a broad set of experimental data, provides insight into several biological processes for which experimental assessment is not readily feasible, and enables the rapid identification of gene functions as well as specific cellular parameters.

(cite)
Also:

Given the vast behavioral repertoire and biological complexity of even the simplest organisms, accurately predicting phenotypes in novel environments and unveiling their biological organization is a challenging endeavor. Here, we present an integrative modeling methodology that unifies under a common framework the various biological processes and their interactions across multiple layers. We trained this methodology on an extensive normalized compendium for the gram-negative bacterium Escherichia coli, which incorporates gene expression data for genetic and environmental perturbations, transcriptional regulation, signal transduction, and metabolic pathways, as well as growth measurements. Comparison with measured growth and high-throughput data demonstrates the enhanced ability of the integrative model to predict phenotypic outcomes in various environmental and genetic conditions, even in cases where their underlying functions are under-represented in the training set. This work paves the way toward integrative techniques that extract knowledge from a variety of biological data to achieve more than the sum of their parts in the context of prediction, analysis, and redesign of biological systems.

(cite)
Gentle advice: Avoid answers from cartoonists, whose domain of knowledge does not include biology.

I think it's a bit of a stretch calling these sorts of models "executing a genome". They are using a whole lot more data than DNA.

I can't speak to semantics but the question directly asks if it possible to model the genome on a computer. Researchers have done this using sequencing data, as the cited articles show.

Shrug Whatever.

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What is allosteric regulation?
I've found multiple definitions for allosteric regulation and struggling to understand which one is correct. My text book says:
'Another way of regulating enzyme activity is through allosteric regulation. This is where an
inhibitor binds to a different part of the enzyme, called an effector site, which changes the
shape of the enzyme. This binding can occur at any time. Product can only be formed (and
released) if the inhibitor, I is not bound to the enzyme, E. Assume that binding of the enzyme
to the substrate or the inhibitor is independent of one another so that the inhibitor, I, can bind
to both the free enzyme, E and the enzyme-substrate complex, C1, and the substrate, S, can
bind to both the free enzyme and the enzyme-inhibitor'
What I'm struggling with is if the inhibitor changes shape of the enzyme then how can the substrate still bind to the enzyme-inhibitor complex? Or does it just change the enzyme so that no reaction can occur and the substrate can still bind to it?
Thanks

The topic of allosteric regulation is well covered in reputable text and articles available on line. Berg et al. has a summary at the start of Ch 10 and a more detailed section 10.1 on aspartate transcarbamoylase.

This question really boils down to semantics, and the definition can be clarified by discussing enzyme regulation in general.  The 3 main ways that enzymes can be inhibited are through the following mechanisms: competitive inhibition, non-competitive inhibition, and uncompetitive inhibition.  In competitive inhibition, the inhibitor binds directly to the active site and blocks the substrate from binding (so they are "competing" for the active site, hence "competitive inhibition").  Non-competitive and uncompetitive both involve the inhibitor binding to a separate regulatory site on the enzyme that is different from the active site (the second sentence of your book's definition of allosteric regulation).  However, we have to differentiate between the two, and a nice, concise delineation can be found here.  This page states:

While uncompetitive inhibition requires that an enzyme-substrate complex must be formed, non-competitive inhibition can occur with or without the substrate present.

Therefore, your book's definition is more in-line with non-competitive inhibition.  I'd encourage you to look at this page for a more thorough read, and because they have a nice simple illustration that might help put it in perspective.
Here's a more abbreviated answer:
Inhibitors may change the active site to prevent substrate binding, but that's not the only mechanism of inhibition. Specifically, non-competitive inhibitors may limit the ability of the enzyme to carry out its action without changing the shape of the substrate binding site (see this figure).
Final thought
If you actually look at the etymology of the word "allosteric," its word roots come from the Greek allos that means "other or another" and from the Greek stereos that just means "solid or object."  So in actual etymological terms, it's a more general term that should apply to both uncompetitive and non-competitive inhibitors because both bind at some other or allosteric site on the enzyme.  However, the way your book defines it is more like the definition of a non-competitive inhibitor.

I downvoted this answer because it does not refute the poster's book's definition of allosteric regulation being exclusively to do with inhibition and focuses purely on different types of inhibition. Hence it does not answer the question in the title, which, in any case, is well answered online. I would also add that the etymology cited in terms of "solid or object" is unhelpful as the actual usage of stereos in English and especially chemistry is to do with shape or structure: "…two, stereospecifically different, non-overlapping receptor sites…" (Monod et al.  J.Mol.Biol. (1963) 6, 306--329)


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Can hair follicle miniaturisation affect hair color?
We all know that follicle miniaturisation affects hair texture, making it look thinner(the hair shaft/root itself will be thinner), but does it affect hair color as well? So if an individual has thick mid brown hair in his/her 20s, hair follicle miniaturisation kicks in in the 40s. Does this person's hair look light brownish due to hair follicles being thinner, fewer, and they reflect light better? Is my hypothesis right? A thinner hair shaft/follicle reflects light better, ie becomes more transparent? Is this broscience on my part, or am I right? I have a hard time believing that a person's hair color doesn't look lighter/more frail if you will, after miniaturisation kicks in.


text:
Why does the rain increase our chances of catching a cold?
Why do I catch cold after getting drenched in the rain? I don't catch cold after taking shower.
What special quality does rain water have which increases the chance of getting a cold?

Because the rain is colder than your shower. Plus the wind cool you down even more. Have a look at Why do we get runny noses in the cold? for more information.

I suspect you don't take a shower with your clothes on, then walk around in the wet clothes for a while.


text:
How does the human ear guess the direction of the source?
Suppose a sound is produced behind you. You can easily tell that the sound came from behind.
Our ear lobes face towards the front and hence traps the sound waves which come from the front. Yet, we can detect   that the sound came from behind.
How does the ear/brain manage to identify the sources of sound accurately?

The ear doesn't actually find the source, it's how the sound is perceived across both ears.
A sound coming from the side is the most obvious case where you get blasted on 1 ear and a relative muffled identical sound on the other ear.
A sound coming from the front is balanced across both ears. Same as behind, except that the forward-biased shape of the ears will distort the acoustics, leaving a distinct distortion signature that tells you the sound is coming from behind you. (For reference, modern 3D video game engines mimic this distortion so you can tell when something is happening behind your character or the camera if you are wearing headphones).
Sound from above or below you will have slightly different distortion signatures due to how the shape of the ears is different from above versus below.


text:
advantages of shivering in cold environments
When we feel cold, our the muscle tries to generate heat by shivering and the brown adipose tissue tries to generate heat by non-shivering methods. The muscle generates heat but also spends energy on movement whereas the adipose tissue produces heat directly. This feels like muscle is not as efficient as BAT in generating heat.
What makes the muscle cause shivering? Isn't it sort of unnecessary movement which wastes energy which could otherwise have been used to directly produce heat?

Firstly, movement by shuddering or shivering, in simplicity, effects the conversion of potential energy into kinetic energy. This is achieved by expending ATP in muscular tissue, causing rapid bursts of contraction.
Brown adipose tissue, although located within most mammals ranging from infants to elderly, is predominantly found in infants differing from white adipocytes insofar as brown adipose tissue has a greater capillary network. Due to the higher surface area to volume ratio of the infant comparative to adults, the rate of heat loss is appreciably greater than a human adult. Thus a more efficient means of thermogenesis is required, namely, when the BAT detects body temperature below the homeostatic norm, the hormone norepinephrine is released, reacting with lipases to form triglyceride. This may subsequently decomposed further, to be converted into heat energy around the body (there are of course various intermediate stages).
Additionally, located primarily in brown adipose tissue is a protein named UCP-1. This allows the cells respectively to undergo 'non-shivering thermogenesis', heat generation without shivering by uncoupling the respiratory cycle in the mitochondria to oxidise more rapidly the substrate. As a consequence, fewer molecules of ATP are produced but heat production is increased.
Therefore, the differences may be rested on 1) the required efficiency of heat generation between infants and adults; 2) the act of shivering per unit of muscle area generates more heat.
You can find further information regarding the UCP-1 uncoupling mechanism in BAT from, https://www.ncbi.nlm.nih.gov/gene?Db=gene&Cmd=ShowDetailView&TermToSearch=7350


text:
human body in an environment where temperature is above body temperature
What would happen if humans were to live in an environment where the temperature is above the body temperature?
Does the human body have a mechanism to cool the body?
When the surrounding temperature is below the body temperature, the body has a mechanism to heat up. When the surrounding temperature is above the body temperature, the body would require some mechanism to cool down since there will be a net heat transfer into the body.

Temperatures greater than ~37C occur commonly on Earth where people live. Have you thought about possible ways that people keep cool that you already know about? Please [edit] your question and tell us where you've looked for answers, what you do know about the topic, and where exactly you still have questions. Unresearched questions may be subject to down-voting and closure.

My bad. I wasn't clear enough. I was looking for specific active metabolic processes for cooling. I'll edit it in a few hours.


text:
Why is heparin contraindicated in patients with severe uncontrolled hypertension?
Heparin is a parenteral anti coagulant- prevents clot formation by inhibiting factors 2 a and 10 a mainly. Now, patients with severe uncontrolled hypertension- have persistent bp of more than 140/90. Here we are considering the force exerted by the blood on the wall of the arteries. Increased pressure of blood means, blood is trying to flow through a smaller diameter of the vessel, hence you can say that blood flow is decreased in such patients. Shouldn't heparin be useful in patients of hypertension because it will prevent clots from blocking the blood flow ? Why is it contraindicated ?

I would suggest that your question is more appropriate for SE Medical Sciences, where you are more likely to receive an authoritative answer.

Thank you for the suggestion.


text:
Why do some insects constantly move their abdomens?
Why do some insects, such as wasps, constantly move their abdomens?

Insect respiration is passive, with sclerotized tracheal tubes taking oxygen directly to the tissues, and moving carbon dioxide out. By pulsating the abdomen, the movement of gases through this system is accelerated. Wasps, as in your example, are relatively active metabolically, so it is not a surprise that they tend to use this strategy.


text:
Any evidence that getting a covid booster works for omicron?
I've been hearing colloquially that the booster helps for immunity to Omicron, but haven't actually found any evidence supporting this. Does anyone know of any studies that look at the efficacy of the vaccine for Omicron cases?

Does this answer your question? Why are scientists saying that the Omicron COVID-19 variant is a reason to get a booster?

The Omicron variant of SARS-Cov-2 is still so new, that until the last few days there has been no statistical raw material on clinical experiences and patient-data to show what protective effect is given against it by the original covid-19 vaccines.
In default, therefore, of patient data, laboratory tests have been made on antibody serum samples from boosted vaccinees, and these have indicated the likelihood of much better protection against Omicron by boosted doses (i.e. a 3-dose schedule) of the original vaccines rather than the original two, which have shown themselves effective against the original form of this coronavirus and its kown previous variants before Omicron.
Naturally of great interest is actual clinical patient data, and within the last week, the original laboratory data have been supplemented by publication of a (preprint) report of a UK-based case-control study surveying actual patients.
The report itself can be found at (https://khub.net/documents/135939561/430986542/Effectiveness+of+COVID-19+vaccines+against+Omicron+variant+of+concern.pdf/f423c9f4-91cb-0274-c8c5-70e8fad50074),
and its results are described and excerpted in this answer:
(Why are scientists saying that the Omicron COVID-19 variant is a reason to get a booster?) .
(The link here is to a 'second/supplementary answer' at tab /105626#105626 .)
In brief, these are early patient data, the identifiable Omicron cases are predominantly of milder infection, and the patient statistics in the case-control study, so far as they go, confirm the laboratory test data in showing a markedly enhanced vaccine effect against Omicron when a booster dose of the Pfizer/Biontech vaccine is used.
The report's conclusions include that

"our findings support maximising coverage with third doses of vaccine
in highly vaccinated populations".

For more, see the earlier answer.


text:
Any reasonable avenues toward extending telomere length for humans?
Is there any biological research progress toward extending the length of telomeres for humans?
It seems as though this has seen some moderate success in extending the length of life of mice -- is it possible that current living humans could have some way of extending or preserving the length of their telomeres (given some realistic advancement in biological science)?


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Does the zeta potential of a nanoparticle generally take into account ligand charge?
For example, if I had a quantum dot nanoparticle with conjugated linker peptides capped with polyarginine tracts.
Would the localization of negative charge from arginine change the zeta potential of the overall np-peptide complex?
Or does the polyarginine tract have its own stationary layer and its own zeta potential separate from that of the QD? Especially if it extends outside the slipping plane of the QD?

Welcome to Biology.SE! Please take the [tour] and then go through the help pages starting with [Ask] questions effectively on this site. In particular, this question doesn't seem to have a biological component — is there some reason you think this question belongs in Biology.SE? Thanks!

I'm voting to close this question as off-topic because it doesn't seem to have anything to do with biology.

Sorry I'm new and this is my first ever post.  How related to biology the question has to be? I suppose the question is more of a literal chemistry or physics question.  However, I posit that zeta potential is critical to how effectively nanoparticles and drug delivery systems interact with any biological model?

The links put in my first comment contain the official guidelines. I agree that chemistry or physics would seem more appropriate, but lack the background to suggest which would be more appropriate — I suggest searching for terms like "zeta potential" on both of those sites and see whether anything remotely similar to this turns up. If they do then try there. Good luck!


text:
Can you be infected by two coronaviruses at once?
E.g. could you be infected by COVID-19 as well as a different strand of coronaviruses (e.g. those that circulate in the population every flu season)?

SE Biology is a question and answer site — not a discussion site or a site for floating ideas. It is concerned with the mechanisms of biological processes, not medical or social aspects of biology. For one of these reasons I think  that your question on the coronavirus outbreak is off-topic here. Question of a medical nature might be on-topic at SE Medical Sciences. Otherwise you are advised to consult more appropriate reputable sources for such information, some of which are listed here.

I honestly don't think this is a bad question... though I think you'll need to be a bit more detailed and probably have to do more research and [edit] to show exactly what research you've done and what is confusing you.

Yes:

Coinfections involving multiple HCoVs were also detected (Table 2).
...

Human Coronaviruses HCoV-NL63 and HCoV-HKU1 in Hospitalized Children with Acute Respiratory Infections in Beijing, China, Advances in Virology (2011)


text:
What is the definition of a polybasic cleavage site?
I keep coming across the term "polybasic cleavage site" which is implicated in increasing the virulence of many viruses, but I'm struggling to find a definition. Is it just a sequence of amino acids where more than one has a basic side chain? I'd also love to know why it is so important to the function of a virus.

I would define a “polybasic cleavage site” as:

A region on a protein consisting of several basic amino acids (generally arginine (R) and lysine (K), rather than histidine) that determines the substrate specificity of certain classes of proteases for that protein.

It can also be regarded as a recognition site for the enzyme.
The relevance of this to the virulence of some viruses is as follows. Many RNA viruses are translated into one or more polyproteins that are subsequently cleaved proteolytically at specific sites to generate further proteins. In certain instances these sites are ‘polybasic’, and the products generated by the cleavage of such sites play a role in the virulence of viruses.
This is nicely illustrated by a paper by Nao et al. in mBio on the mutation of haemagglutinin (HA) cleavage site of Avian Influenza Virus, where increasing the number of basic amino acids increased the virulence. I included an illustrative figure from that publication.

HA cleavage site sequences of the ShimH5 virus strain and its variants passaged in chickens
The current (2021) interest in polybasic cleavage sites no doubt relates to the presence of such a site (PRRAR) at the S1/S2 junction in the spike protein of SARS-CoV-2 — see, for example, this paper by Peacock et al. in Nature Microbiology.

A polybasic cleavage site is a cleavage site consisting of polybasic amino acids. An acid is polybasic when it is able to donate more than one proton in aqueous solution. In a titration curve, polybasic acids show as many equivalence points as they are poly.
https://www.w3spoint.com/ionization-of-a-polybasic-acid

Unfortunately, your logical analysis of the word  —  a site with a single acidic amino acid residue with multiple ionizations — is incorrect because no such amino acids exist in proteins, and, as I indicated in my comment on the question, the usage is for a site with many basic amino acid residues.

You are right thank you for pointing this out


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Can virus and bacteria move on the surface?
Do viruses/bacteria have some motive mechanism? I mean if the virus/bacteria reach some surface by touching, can it move on that surface?
Life example: suppose the cooler is not so clean and has some viruses on his surface. My cup came into contact with the cooler in some little area, so virus migrated to that little area of my cup. Can the virus eventually move to another area of my cup's surface? Or can I be sure that it remained at the point of contact? If yes, is this also true for bacteria?
P.S. obviously parasites can move, but I can't figure out are the viruses and bacteria can..

What's a silent downvote? Please explain.

Viruses and bacteria are very very different from one another; asking about them both in one question is asking too many questions. I've marked a duplicate for the virus half of your question.

I didn't downvote but I can guess the reason. You did not do a simple search for this question yourself. It is elementary microbiology (also physics). And as @BryanKrause pointed out bacteria and viruses are very different.

@WYSIWYG Also easily found here. I located the duplicate by searching this site for the two words "virus move". The ask-a-question dialogue pretty clearly suggests askers search the site before asking.

@BryanKrause Indeed. There is a similar question. Sorry, it is because of my bad English..


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Factors of infection rate
I refer to J.H. Jones' Notes on R0.

Preliminaries
The standard SIR model consists of a system of three differential equations
$$ds/dt = -\beta  s  i$$
$$di/dt = \beta s  i - \nu i$$
$$dr/dt = \nu   i$$
for the fractions $s, i, r$ of susceptible, infected, and recovered (removed) individuals, $dt$ = 1 day.
$\beta$ is the infection rate, i.e. the number of individuals an infected indiviual infects per day, $\nu$ is the removal rate, being defined as the reciprocal of the duration of infectiousness $d_i$ (measured in days), i.e. $\nu = 1/d_i$. The reproduction number $R$ is the product of infection rate and duration of infectiousness, i.e.
$$R = \beta \cdot d_i$$
To reduce the growth of spreading of a disease, mitigation measures typically target at the infection rate, at least when a reduction of the duration of infectiousness is not at sight.
To estimate the impact of a mitigation measure on the infection rate, it is worth to consider it as the product of several factors, which may be influenced separately and more specifically.
One common approach is to consider the infection rate as the procuct of

transmissibility per contact $\tau_c$, i.e. the probability of getting infected when being in one contact with an infected person and

mean rate of contact $c$, i.e. the number of single contacts an average individual has per day, i.e.

$$\beta = \tau_c \cdot c$$
Let alone that it is not so easy to define what a contact is, other factorizations are conceivable when considering these candidates:

transmissibility per hour $\tau_h$, i.e. the probability of getting infected when being in contact with an infected person for one hour

mean duration of contact $h_c$ (measured in hours)

Let "being in contact" specifically mean "closer than 1.5 m in the average".
We then have
$$\beta = \tau_h \cdot h_c \cdot c$$
We can group factors:
$$\beta = \tau_c \cdot c$$
with $\tau_c = \tau_h \cdot h_c$, and
$$\beta = \tau_h \cdot h_d$$
with $h_d = h_c \cdot c$ the number of hours per day an individual is in contact with other persons.
Question
I am looking for references where such factorizations of the infection rate are considered, especially in the context of Covid 19.

I have not found texts relevant to your question and related to the spread of SARS-CoV-2.  However, here is a publication that discusses the utility of contact duration data when constructing infection models, in the general case --
Simulation of an SEIR infectious disease model on the dynamic contact network of conference attendees
Methods
At a conference, 405 attendees volunteered to wear RFID tags. Over two days, the time and duration of 28,540 face-to-face interactions between these individuals were recorded, with a temporal resolution of 20 seconds. Note the spatial limits of the RFID data:

RFID devices engage in bidirectional radio communication at multiple power levels, exchanging packets that contain a device-specific identifier. At low power level, packets can only be exchanged between tags within a radius of 1 to 2 meters.

From these data, three networks were constructed:

dynamic network (DYN) -- this network preserves the sequence and duration of contacts between individuals.  Using the language of graph theory, this is a directed network with weighted edges.
So, if individual A comes into contact with individuals B and C, and individual B is infectious, individual A must contact individual B before individual C in order to have a chance of A → C transmission.  Causality constrains the chain of transmission.
heterogenous network (HET) -- this network preserves the duration of contacts between individuals but disregards the sequence of contacts. The graph of this network is weighted but undirected. Adopting the previous example, B can infect C via A regardless of the relative order of the A ↔ B and A ↔ C interactions.  Causality is suspended, and the probability of transmission depends on the number and duration of contacts.
homogenous network (HOM) -- this network inherits the topology of HET, but ignores the duration of contacts.  The graph of this network is unweighted and undirected. Each contact event carries an equal probability of resulting in transmission, so the probability of transmission depends solely on the number of contacts.

To simulate the spread of an infectious disease over realistic time-scales, each network was longitudinally extended using three procedures:

repetition (REP) -- the recorded contacts are repeated with the same duration and order.
random shuffling (RAND-SH) -- the structure of the network is preserved, but the IDs associated with the nodes in the network are shuffled between iterations.
constrained shuffling (CONSTR-SH) -- same as RAND-SH, but the reordering of IDs is constrained to preserve individual social activity (i.e. IDs with many contacts are not assigned to a low-contact node in the network) and repeated contacts.  This procedure rectifies the oversimplifications of REP and RAND-SH by acknowledging that people tend to interact with the same people day-to-day, with occasional contacts with strangers.

The authors applied a SEIR epidemic model (Susceptible, Exposed, Infectious, or Recovered).  For each network-procedure pair, they considered two disease scenarios with different assumed values of mean latency period (σ -1), mean infectious period (ν -1), and transmission rate (β):

very short incubation and infectious periods

σ -1 = 1 day
ν -1 = 2 days
β = 3.10 -4/s

short incubation and infectious periods

σ -1 = 2 days
ν -1 = 4 days
β = 15.10 -5/s

A note from the authors on why these values were chosen:

These sets of parameter values were chosen to maintain the same value of β/ν, which is the biologic factor responsible for the rate of increase of cases during the epidemic outbreak, while changing the global timescales of incubation and infectious periods, and assessing the role played by the social factors embedded in the contact patterns.

Results
Epidemic outbreaks in the three networks across the three data-extension procedures were compared by computing the mean R0, defined by the authors as the mean, over all iterations, of the number of secondary cases from the single initial randomly chosen infectious individual.
Considering the simplified REP procedure, higher values of R0 were observed in the HOM network compared to the HET and DYN networks, for all scenarios.  The authors explain this observation by noting that the probability of rapid extinction of the pathogen was smallest for the HOM network; indeed, this held true independent of procedure.
In terms of the final number of cases (R∞) and the rate of spread, the HET and DYN networks were similar for both disease scenarios.  The peak of the epidemic was reached first in the HOM network, on average, consistent with the reduced probability of extinction.
In the RAND-SH procedure, spread was slower but lasted longer, leading to a larger R∞ for all networks.  In general, greater shuffling of ID tags led to more efficient disease spread, such that R∞(RAND-SH) > R∞(CONSTR-SH) > R∞(REP) for all networks and scenarios.  The interaction of more efficient disease spread in the RAND-SH procedure with increased values of σ -1 and ν -1 in the "short" scenario seems to produce consistently higher R0 values across networks (see Figure 3), though high variance in R0 means the effect of this interaction is not significant.
Conclusions
By comparing the different network types across all procedures and scenarios, it was shown that ignoring the direction and duration of contacts overestimates both the rate at which a disease spreads and the total number of individuals infected.  Additionally, shuffling individual positions in contact networks while preserving network topology increases disease spread when compared to a static model, though this effect is buffered by the "realistic" inclusion of preserved sub-networks of repeated contacts.
While this publication does not directly integrate factors for the duration and rate of contacts into the SEIR model, as suggested by Hans-Peter Stricker, the authors are able to show that mapping such a model to networks in which the direction and duration of contacts are encoded as edge weights leads to different measured outcomes (R0, R∞, time to peak) when compared to topologically identical networks lacking these encodings.

Thanks for this great answer which will give me a lot of reading. It - and the study you point to - seems to be related to this question I asked at Mathematics SE: https://math.stackexchange.com/questions/3682077/how-does-the-reproduction-number-depend-on-characteristics-of-the-physical-conta

@Hans-PeterStricker, if you do really believe mine is a "great answer", I'd appreciate if you accepted it.  Given the bounty is now a week old and no other answers have popped up, I think it's appropriate.

I usually wait until the bounty would expire - which will be tomorrow - but thanks for the hint.


text:
What plant is this? Edible, tastes like cress
My girlfriend got this at a Turkish supermarket in Berlin. It tastes like garden cress or a bit like radish. I looked up cress varieties but couldn't find this particular leaf shape.

you might get a faster response from the cooking exchange called Seasoned Advice

I think this resembles some sort of radish (german 'Radieschen') ... Different cultivars have quite some variety in terms of leave shape, so it is difficult to tell.

@John that was a very good idea, people there suggested a variant of watercress which it most probably is. https://cooking.stackexchange.com/q/81309/7718


text:
Does X-inactivation lead to expression of sex-linked recessive disorders in half of carrier females' cells?
If one of the two X chromosomes in female mammals is randomly inactivated (i.e. becomes a Barr body) in each cell, shouldn't half of all cells in a female who is a carrier for an X-linked recessive disorder (say, Duchenne muscular dystrophy) express the disorder?

Similar question to: http://biology.stackexchange.com/questions/31635/in-human-females-one-x-chromosome-is-inactivated-forming-barr-body-then-how-exa

Yes and No... You are correct that X-Chromosome Inactivation will randomly inactivate the good X-chromosome (i.e. the one NOT carrying the mutation/disease) half of the time. However, this doesn't always seem to be associated with a disease phenotype. It likely depends on the gene and other factors, like the gene allele's function, to determine whether there is a disease phenotype that manifests with inactivation. Check out this paper that looked at Duchenne muscular dystrophy in females that is available freely on PubMed.


text:
Edible macroalgae?
I know that kelp is edible because the concept of eating kelp is all over the interwebs.  However, there is incredibly little information available online about what species of "seaweed" is edible.  I specifically am currently staying on Lake Geneva, and would be especially interested in edibility information about plants living in the lake, such as starry stonewort.  However, given the seeming general lack of information about the subject online, I would love to know about any common species of easily-accessible (e.g. by skin-diving) seaweeds that are edible and have any manner of nutritional value.
What species of seaweeds are edible?

this paper has a nice list of species found in Lake Geneva.  Most prominent are the Chara, Nitellopsis and Potamogeton genera.  Apparently Chara and Nitellopsis are common invasive species all over the place.  Information specifically regarding the edibility of these would be most valuable.

Edible (marine) seaweeds with nutrition facts:

Kelp: Kombu, Arame, Wakame
Red alge: Nori, Dulse, Irish moss, Laver
Hijiki

Other types of edible marine seaweed:

Red algae: Carrageen moss
Green algae: Sea lettuce
More edible seaweeds with pictures on Wikipedia on Food and Agriculture Organization

Freshwater macro algae are often toxic (Wikipedia, Biology Libre Texts). Starry stonewort does not appear to be edible, either.


text:
Tiny black mushrooms growing from veggies?

I've found these tiny black mushrooms sprouting from my scallions.  I'm in Salt Lake, UT, but the scallions are store-bought, so I'm not sure where they're from or where they've been. Anyone know what these are?  Are they dangerous?

Related: What are the white eggs growing from a black stem on the Napa cabbage plant?

@theforestecologist that looks spot on.  I flagged my question as a duplicate


text:
What causes the cardiac ventricular pressure change during the isovolumetric part of the cardiac cycle ?
Why does the cardiac ventricular pressure change during isovolumetric contraction and relaxation. The volume ( both valves are closed)  is constant, Does Boyle's Law not apply?  P1V1= P2V2 at constant temperature.

Remember - during isovolumetric contraction and isovolumetric relaxation that the wall tension and thus pressure within the ventricle is changing, despite no changes in volume. Can you add some more to your question to show that you've given more of a research effort? Like add an illustration or graph of what you're thinking? It would definitely improve the quality of your question.

Boyle's law doesn't apply to all fluids: only gasses, not liquids. Liquids like blood are (mostly) incompressible, so their volume does not change substantially when you add pressure.
During isovolumetric contraction, the ventricular walls are pushing in on the blood contained in the ventricle, causing the increase in pressure, but there is not yet sufficient pressure to force the blood out the pulmonary/aortic valve.
Source:
Hillegass, E. (2016). Essentials of cardiopulmonary physical therapy. Elsevier Health Sciences.

The pressure increase in Ventricle is due to the depolarization of Ventricle myocardial cells I.e. the continued action potential through the ventricle noted as QRS wave in ECG.
This makes the ventricles contract and hence the pressure increases without changing the volume of the blood as all the valves during isovolumetric contraction are closed.


text:
Amount of animals to use for animal trials
I am working on an independent research project involving animal models. I am unsure how to deterine how many animals (rats) to use for the project. The rats will be injected with different solutions to examine the effect on a target. There is nothing in the literature about trying any of the solutions in rats. How do I determine the amount of rats to use?

I might be wrong, but I don't believe we consider general stats questions to be on-topic here even though we allow questions on technique. What you are asking about is called a "power analysis" in statistics; to do a power analysis you do need to have some prior expectation or knowledge of the estimated magnitude of the effect and variability or at least what magnitude of effect would be 'interesting' to you.

I'm voting to close this question as off-topic because it is about statistics and not biology. As Bryan said, you are interested in power analysis, the type of analysis for which you will need to estimate (eventually just a gut feeling estimate) the effect size that you're expecting.

The topic pertains to biostatistics which is a valid tag.

This paper should help https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3826013/

@Remi.b this is a completely valid question for here many factors for this have little to do with statistics and a lot to do with the animals physiology.


text:
How are monocytes larger than capillaries?
I have read that the average size of a capillary is about 8 micrometers. How is it possible that the 15 micrometer or so monocytes in blood do not block these vessels?
https://en.m.wikipedia.org/wiki/Blood_vessel#Vessel_size
https://www.britannica.com/science/monocyte

They aren't completely rigid and can change shape to squeeze through (see Downey et al).
If they are activated, monocytes can get stuck in capillaries and block them, which contributes to poor circulation following reperfusion after an ischemic blockage (see Engler et al).

Downey, G. P., Doherty, D. E., Schwab 3rd, B., Elson, E. L., Henson, P. M., & Worthen, G. S. (1990). Retention of leukocytes in capillaries: role of cell size and deformability. Journal of applied physiology, 69(5), 1767-1778.
Engler, R. L., Schmid-Schönbein, G. W., & Pavelec, R. S. (1983). Leukocyte capillary plugging in myocardial ischemia and reperfusion in the dog. The American journal of pathology, 111(1), 98.


text:
How to get ants/termites to attack
I am working on ant resistant coatings that are meant to make a material resistant to ants or chewing through them. The question is - how do I get ants to attack the material?
I have considered leaving a plastic bag full of water that is coated in the material outside of an ant hill. Does anyone have any suggestions?

Sugar and grease are strong ant attractors.

It is possible that a sugar solution could work. I would not have expected grease. Is there a specific type of grease that is the most effective?


text:
Does the use of UV light beam lead to poorer contrast in optical microscopy of cells than the higher wavelengths visible light?
I am reading about "diffraction-limited system" on Wikipedia, which mentioned

"To increase the resolution, shorter wavelengths can be used, such as UV and X-ray microscopes. These techniques offer better resolution but are expensive, suffer from lack of contrast in biological samples and may damage the sample."

without giving a more detailed explanation for why the higher energy EM waves might lead to poor contrast. I have tried to search on Google, but still can't find a satisfying answer. Can anyone here kindly refer me to more detailed discussion on this question? Thank you.

This source says UV microscopy offers better contrast. I think it all depends on what method you use to visualize the sample after magnification. UV is not visible, so I guess it has to be converted digitally?

Most biological samples are not electron-dense enough and need to be treated with heavy metals for EM. See wikipedia article for a brief introduction.

"EM" in the question referred to "electromagnetic".  Heavy metals are used to increase contrast for "electron microscopy".  Not the same meaning for "EM".

UV microscopy is not a form of electron microscopy, it seems to be a technique in its own right.

Contrast in optical microscopy typically depends on different substances having different absorption spectra. Practically everything absorbs UV light, so there tends to be less contrast in that range than in the visible spectrum where there is a bit more selectivity.  All of this changes when there are contrast-enhancing substances added.  For example, molecules that absorb in one wavelength and emit at a different wavelength via fluorescence, attached to antibodies that bind selectively to specific cell components, can provide very high contrast.  E.g., see [https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2156041/].
An alternative optical microscopy technique is phase-contrast microscopy which does not use absorption at all.  Instead, it measures the effective optical path length through the sample, which depends on local refractive index of the sample.
Yet another alternative is x-ray fluorescence microscopy, which can identify specific elements in the composition of a sample.  See, for example,[https://www.americanlaboratory.com/913-Technical-Articles/18833-Three-Dimensional-Elemental-Imaging-Using-a-Confocal-X-Ray-Fluorescence-Microscope/].

I suppose I am looking for a more detailed explanation for why "practically everything (in cells) absorb UV light ... (while) there is a bit more selectivity (for the visible spectrum)". But thanks for pointing out to us the alternative optical microscopy, in relation to the fluorescence microscopy. I have found a useful post on chemistry.stackexchange: link, which has nicely given me a chemistry perspective on my problem.

@Fan Fan, if you do a search for "UV absorption spectrum" and proteins, DNA, or lipids, you'll see that a huge number of biomolecules absorb in the UV range (~200nm to ~400 nm).  The chemistry of it relates to the energy levels in the types of bonds in the biomolecules, but you'll need a biochemist to explain to a greater depth.


text:
Pictures of trigger point muscle fascia
Are there any pictures of an actual trigger point looks like? All I am able to find online are animations.

I found plenty of pictures of therapists conducting trigger point therapy on their patients. Are you looking for a picture of the actual trigger point picture underneath the skin?

Yes, exactly...

You can use @TheLastWord in your comment such that your comment will be seen in the inbox of the tagged user.

@TheLastWord Yes, exactly.

You could have easily find these using a simple google search, however I will point several out:

See figure 1 of this article for an ultrasound image of a trigger point. Really interesting!
See figure 1 of this article for a schematic representation, and figure 2 for a real image. Although you did not ask for a deeper understanding of this topic, if you want to read more about it I would recommend reading this paper as it covers a lot of aspects (such as pain signals to the brain).
This article covers different imaging techniques and facilitates interpretation by using arrows to point out the trigger points.

If this is not what you are looking for please specify what you mean with "pictures"? (vibration sonoelastography, schematic, ultrasound, etc.) I cannot point you in a direction for real life images (if these even exist).

This is so insightful. Thanks for aggregating all of the info in this answer.


text:
Why and how does falsifying sensory information work?
Some context, before the question:
Whenever I have a craving to binge on something sugary, I just prepare a cup of extremely bitter green tea (with 3 bags of tea) and I imagine myself binging on something sugary, but at the same time I take a gulp of this bitter stuff and let that sit in my mouth for a few seconds.
The very next moment, I immediately notice that the craving comes down and after a few more sips the craving completely goes away. I feel nauseous if I think about something sugary for another day.
Actual question:
Why and how does this work? Even though I consciously know that I am fooling myself, with a false sensory perception, why does my brain associate sugary treat to be revolting and poisonous(cause of nausea)?

I'm voting to close this question as off-topic because, IMO, the question belongs to psychology.SE

@Remi.b I don't understand why does it belong in psychology. I am seeking to know why is sensory perception ignored for evolutionary knowledge on bitterness.

I might be misunderstanding your post then. I don't see the word "evolution" in your post (excluding the tag) and the only answer for the moment does not talk about evolutionary biology but about psychology and cognitive science. I am not sure what you would mean by "evolutionary knowledge". Maybe, you could try to clarify your post but it might be problematic as it already received an answer.

These are learning phenomena you describe. I'll try to explain a simple way to think about this.
By default, sweet foods are appetitive and, for instance, strongly bitter foods are aversive. However, it is possible to condition yourself to associate a stimulus, no matter how it presents originally, with a different valence (appetitive or aversive).
There are several well understood forms conditioning can take. I list a few here, and some subtypes. They are described well on Wikipedia:

Classical conditioning
-- Serial application of classical conditioning can be called second-order conditioning.
-- You can also condition yourself through self-evaluation, called evaluative conditioning
Covert conditioning is a technique more than a type of conditioning, it may directly apply to your question. It involves the use of imagery.
Operant conditioning

Operant and classical conditioning are the two major paradigms to know. Classical or Pavlovian conditioning involves pairing an "unconditioned" stimulus with a neutral "conditioned" stimulus. Operant conditioning involves providing a feedback, usually a reward or punishment, to reinforce learning.
You can self-learn or condition yourself. This does not mean necessarily it is intentional or conscious on your part, often things can be subconscious or unconscious. For instance, if you associate eating crisps with watching a movie, watching movies without crisps can become uneasy, in spite of the fact that watching a movie was originally a pleasurable activity. In a neuroscience seminar involving conditioning in fruit flies, I once recorded a saying which captured the spirit of the experiment quite well: An expected reward, not experienced, can feel like a punishment, and vice versa. Rewarding yourself after doing chores can also be a easy and practicable way to build good habits with doing chores.


text:
Do plant cells recycle carbon dioxide from their respiration during photosynthesis?
It seems one of my colleague's biology textbook claims that plant cells, with presence of light, feed back 100% of carbon dioxide molecules from their respiration into photosynthesis. Can you say that carbon dioxide molecules, gas or dissolved, get transferred from the mitochondria to the chloroplast?

Please provide a source for your colleague's text book and quote verbatim what it says. That way we can help clarify questions that may arise from misunderstanding what the author intends.

Will do that tomorrow, but it's in Korean so it has to undergo translation. Thank you anyway.

@tyersome It does I think! Gaseous carbon dioxide must be no exception from random diffusion.

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2884119/
This paper found mitochondria move to be next to chloroplasts when exposed to light. So carbon dioxide is  more likely to be recycled in lighted conditions.

Wow, it's a whole new perspective!


text:
Is there a chemical that can be used to subdue ants only temporarily without permanent harm?
I would like to know as I want to contribute to a biodiversity project that wants to create a database with ant feature measurements. I'm not sure if I like the idea of killing ants however (even though it's just a single ant with limited ability to suffer, I know) so I'm looking for a way to immobilize ants long enough to take some detailed measurements but without having to kill them or harm them permanently.
Related question: how could I clean the ant so that it's not marked with the chemical used in the perception of other ants?
I know that for the database they may require keeping the specimen (and therefore killing it) in the name of science so that it can be checked by others but I'm more concerned with the question whether in principle these measurements could be taken without permanently harming the ant and how this could be done in practice.
Thank you for your help!

You can try insect anaesthetics: https://peerj.com/preprints/2571.pdf scientists like to take ants home for the microscope and collecting.

Thanks, that article is pretty solid. Wish it were published so there would be more people looking into it.

CO2 is often used for temporary knockouts of insects. I've used it myself for fruit flies (Drosophila melanogaster), and it's quite straightforward and very effective to hit them with it until they're asleep. However, this was in a rather expensive lab that had CO2 on tap - not a particularly accessible method to the average person.
What I'd recommend instead is to chill the ants. Simply capture them and put them in the fridge for a while. Read this wiki article and go to the part about "quiesence" for more. Quote: "quiescence acts like an anesthetic". It's short term, non-harmful and fully reversible. Also much more accessible to someone who isn't working in a big expensive lab. I assume that the ants will stay still long enough for your measurements - if not: put them back in the fridge for a bit. And better yet, there's no chemicals used, so no need to clean the ant and there's no cost to you.

Thanks! I will try quiescence first I think and if that doesn't work well enough I'll see how hard it is to get an affordable and portable CO2 applier. Found this tip so far: http://www.instructables.com/id/Rapid-Insect-Anesthesia/


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Limit on the Number of Facial Phenotype
Individuals of each species all have unique facial structure variations (shape of nose, position of chin etc) from humans to birds and fish etc. We humans don't seem to be reaching mathematical limit of uniqueness easily (maybe till the end of the world) considering huge variation and all possible combinations that define our facial structure/traits. However some animal populations are way more larger than humans and each year they reproduce in large amounts.  Considering their huge populations, is it possible for some species to reach their mathematical limit of having unique facial structure variations therefore start repeating the same facial structures?  For example can individuals of some fish species (sardines, sea breams etc) be already sharing exact same facial structure/geometry as a result of reaching all posible facial structure  variation limit?

Why do you think this facial uniqueness is the case?  It would seem to be easily disproved by observing a population, say blonde Hollywood starlets, and noticing that most of them are pretty much indistinguishable.

Are you talking about uniqueness to the exact atom? Or maybe this is too extreme. If it is, then you need to clearly define how similar two faces need to be to be considered the same. The question for the moment is unclear.

Okay, theoretically possible, but only in theory.  Practically, it's totally impossible.  Let's start by defining why it would theoretically be possible.
Theoretically, there are only so many possible arrangements of proteins in the face, which would represent a limited number of possible facial appearances.  However, as you probably guessed, there are zillions of proteins being expressed in each body organ, such as an eye.  So just from the perspective of the number of different possibilities, it would be impossible.
One might think that since the facial features are controlled by genetic variation, eventually these features will begin to repeat themselves, but such is not the case, for two reasons:

There are way to many genes - and alleles - that control facial features.  We're talking thousands if not millions.  When you raise that number of alleles to each others' powers, you start to see the impossibility of repeating the exact same combination, especially since every new generation is introducing new alleles from a new blood line.

Genetic code is not the only thing that changes how you look.  A whole branch of genetics, epigenetics, is devoted to the changes of gene expression unrelated to DNA sequence.  The expression can be changed by environmental factors, even as early as when the embryo is forming the placenta.  This is why identical twins (who have identical DNA) do not actually look exactly the same, or even have identical fingerprints.

Bottom line, totally impossible.

Sources:

Face shape is in the genes, PLOS, 2016
Epigenetics, Wikapedia, 2017
Why do identical twins have physical differences?, Anonymous, 2005
Introduction to epigenetics, University of Leicester, 2013
How many Proteins exist in human body?, Innovateus, 2013

You seem to assume that all of the facial variation is due to genetics. The only environmental variance you accept is via epigenetics and use twin fingerprints as example. Most traits do not have a heritability greater than 0.3. See this post if you don't know much about quantitative genetics and the definition of heritability.

I am downvoting because the post invites the reader to think that only genetics matter and that the question can be boiled down to genetic diversity.

Thank you @Remi.b, I appreciate your frankness.  I will definitely give that post a read.


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Why was the evolution of large, slowly reproducing organisms preferred?
One of the very basic facts that Darwin pointed out was about the life span of organisms. Organisms with smaller lifespan reproduce quickly and hence variations are produced faster. This helps in faster evolution.
One of the main goals of living organisms is to reproduce, this fact being the backbone of neo-Darwinism.
For organisms with longer life span, say humans, the amount of time required for new generations to come up, as well as the energy requirement is high, much higher if compared to bacteria. Then why did evolution of complexity arise if bacterial life forms could survive in harsh conditions and reproduce and mutate faster?

Successful lineages survive. That doesn't mean they are restricted to minimally long generation times. All that is required is that they compete sufficiently in the struggle for life. Sure, they may adapt slower, show lesser variation, require more energy for sustenance, etc. But it works as an evolutionary strategy, and large animals not being extinct are a testament to this. I don't see the difficulty of the question, sorry! Additionally, there are advantages that come with size.

This is a good, but very broad (and complex^^) question. Bacteria and humans are worlds apart (and both complex in their own way). If you mainly meant complexity of a single organism, the link S Pr gave should give a good overview, this wiki article mentions a couple of mechansims that can affect complexity. I'd recommend you to focus on complexity in a specific trait (like size), since otherwise a proper answer might not even fit in a textbook.

Related: If evolution is not about increased complexity, why does so much complexity evolve?

The simple answer is that the evolution of large, slowly reproducing organisms is not preferred: it is simply not selected against.
The key mistake in your thinking is this statement:

One of the main goals of living organisms is to reproduce

Most living organisms have no such goal, they simply take actions that have, historically, led to the continuation of their lineage.
In a complex world, there are many different strategies that can lead to survival and propagation of an organism, and cooperation between cells is one of them.  Even simple bacteria often form large multicellular aggregates, which can provide physical advantages for their members over dissociated individuals, such as resistance to physical damage and formation of protected microclimates. The inside of your body is another such protected microclimate. So multicellularity can be quite advantageous.
As for limiting reproduction: remember that the closest competitors every new organism has are its own relatives, who occupy the same space and compete for the same resources.  Even bacteria will often limit their reproduction when resources are limited. Reproduction also takes significant resources. A faster reproduction then, is also not necessarily advantageous for long-term survival.
Bottom line: neither large nor small, fast nor slow is preferred.  Instead, the study of evolution predicts that we will see what we do see: a multiplicity of forms and strategies adapted for different niches in the ecosystem formed by their interactions with other species and the external environment.

Also, we could easily argue that the large & slowly reproducing life forms are not PREFERRED, they just manage to survive.  There are many more rabbits & mice than elephants & whales, they're outnumbered by insects, which are vastly outnumbered by microorganisms.


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Have some humans evolved to be less attractive to mosquitoes?
https://www.youtube.com/watch?v=38gVZgE39K8 at 10:10 minutes in the video.
It has been found out that single letter differences in people's genomes at specific locations have affected their attractiveness towards mosquitoes. This means there might be a possibility that some humans might have evolved to be less attractive to mosquitoes. Does any proof exist regarding that?

We now know based on a twin study that attractiveness to mosquitos is heritable (with a fairly high heritability of 0.62). Based on a genome-wide association study (GWAS) [which is probably the study referenced in the youtube video] we have found some of the genetic loci that control attractiveness; in particular, 15 single-nucleotide polymorphisms (SNPs) relating to (self-reported) attractiveness, were discovered in the latter study. These SNPs were in regions of the genome related to the immune system (which isn't surprising since immune system genes are closely linked to human odor profiles).
However, figuring out (a) whether these genes have been under selection (by looking for signs of genetic hitchhiking or unusual ratios of synonymous to non-synonymous substitutions) and (b) whether that selection is due to mosquito avoidance will probably a great deal more work - and may be very difficult given that the immune system is under selection for many different characteristics simultaneously ... the GWAS study says its results

illustrate the complex genetic and immunological landscapes underpinning human interactions with mosquitoes ...


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Why did we evolve to be able to see this specific set of wavelengths only?
It is understandable that life didn't evolve the capability to sense all wavelengths of light, it simply didn't need it. My question is, why did it evolve the set of wavelengths it has, for example, the human visible range is 390-700nm, so why couldn't it be a different set of wavelengths, like, (say) 300-620nm? Is there a reason for it?

I also think this is a duplicate of above linked question

Well humans actually have a reduced spectrum compared to non-mammals. Reptiles and birds have 4 color sensitive cell types (cones), mammals lost two of these as modern mammals are descended from early mammals who were nocturnal. Primates evolved a third cone, (a mutant variant of one of the two they had before) Primates did this because many a frugivores and color is excellent for determining when fruit is ripe.

Can you add your sources?


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Myoglobin in meat
When looking at the reason why some meat is white and the rest is red, I found out it is down to the levels of myoglobin as higher levels of myoglobin are found in "slow twitch" muscles.
I have also seen that myoglobin is not the same as haemoglobin, so what is the source of myoglobin?  Does it come from the blood?

Myoglobin is a protein made in muscle cells. It is similar to hemoglobin, a protein made by blood cells. The answer you linked helps explain the difference, which it sounds like you understand. The source is simply the ribosomes in the respective cells that express that protein. The color in both blood and uncooked or rare meat is due to the heme group in hemoglobin and myoglobin respectively.


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In plant photosynthesis, in the light dependent reactions, why is 3 ATP produced per 2 H2O?
I've been looking at the light-dependent reactions on Wikipedia and Khan Academy.
This is the net reaction:
$$2H_2O + 2NADP^+ + 3ADP + 3P_i \to O_2 + 2NADPH + 3ATP$$
So for every $2H_2O$ I expect $2NADPH$ and $3ATP$. I tried to count:

These are my assumptions:

Cytochrome b6 complex pumps $1H^+$ for each $1e^-$.
FNR makes $1NADPH$ for each $2e^-$.
ATP synthase makes $1ATP$ for each $1H^+$.

If we want to end up with $3ATP$, then $3H^+$ need to diffuse through. The thing is, there's too many $H^+$. $4H^+$ is contributed by the cytochrome b6 complex pumping alone, and another potential $4H^+$ is contributed by the water splitting.
Clearly I'm missing something here that would lead to the correct count.

I remember being confused by the numbers when I first studies it primarily because most sources seem to differ on the stoichiometry. I have tried to explain why is it difficult to comment upon such large equations, hope it helps!
Short Answer
There are two faults in your assumptions.

The plastoquinone-cytochrome cycle actually pumps $2H^+$ per electron (terms and conditions apply)
ATP-synthase requires $\approx 4$ protons per ATP produced

So, 12 protons per 2 water molecules is what is pumped, which makes 3 ATP.
Full Answer
As you might notice, the above scheme does not account for many things. For starters, since the 4$H^+$ from water splitting are produced and not pumped, only 2 of those need to be pumped back via ATP-Synthase to restore equilibrium. So even if you account for the $2H^+$ consumed by $2NADP^+$, there is still something that doesn't quite fit. Furthermore, some sources also try to account for the acidity of the inorganic $Pi$ in the ATP-synthesis which will further allow for changes in the $H^+/e^-$ ratio.
Why the confusion?
Most of what we know of the stoichiometry is based on a conglomerate of experiments, beginning with experiments on isolated chloroplasts. As a result, some experiments give us some parts of the stoichiometry (we know that the $NADPH/ATP$ ratio is around $2/3$) and others give us the reactions. Often times, many possible reactions are proposed, from which, the ones which can best be integrated with results from different experiments are thought to represent the actual truth. But this process is often mangled with complications, unexplained patches in the theory and the like. Furthermore, biological processes often are stochastic and do not have perfect stoichiometries. This is all overlooking the actual disagreements between experiments (the $H^+/ATP$ ratio for the synthase had significant variations in different experiments).
Okay, so now what?
Don't loose hope. We do know quite a bit about photosynthesis. What we currently understand about photosynthesis (light reactions) is thus:

There are three distinct processes that can produce a chemiosmotic gradient of $H^+$.
a. Non-cyclic Photophosphorylation is the main method. This constitutes the popular Z-scheme involving a linear electron transport from water to the final acceptor $NADPH$, and this process pumps about $12H^+$ per $2H_2O$
b. Pseudo-cyclic Photophosphorylation which is basically the same as above, but the final acceptor is an $O_2$ molecule, with similar ratios.
c. Cyclic Photophosphorylation which allows for recycling an electron, that is, proton pumping without there being a final acceptor of electron solely by internal shuffling of the electron between different states (primarily involved Plastoquinone (Q) cycle. This can pump $2H^+$ extra for 1 electron.
The ATP-synthase is slightly different from that found in animal mitochondria. The number of protons per ATP depends on the rotational symmetry of the synthase. (details in the references below). Basically, initially, it was thought to have 12-fold symmetry (needing $12H^+$ per rotation, in which $3ATP$ is produced, hence $4H^+$ per $ATP$) but was later found to have 14-fold symmetry actually needing $14H^+$ for the observed $3/2$ ratio of $ATP/NADPH$.
The number of Photosystem 1 units(where the cyclic version operates) is more than that of Photosystem 2 units. This means, that cyclic photophosphorylation goes on simultaneously at these centres, and will account for the extra $2H^+$ required to meet the experimentally observed ratio (1 in every 5 electron is "recycled").

References

A good overall paper addressing all the main issues. Photosynthesis of ATP—Electrons, Proton Pumps, Rotors, and Poise; John F.Alle; Cell Volume 110, Issue 3, 9 August 2002, Pages 273-276
General resources on these reactions. Here, here and here.
Studies on the $H^+/ATP$ ratio.
a. Petersen, Jan et al. “Comparison of the H+/ATP ratios of the H+-ATP synthases from yeast and from chloroplast” Proceedings of the National Academy of Sciences of the United States of America vol. 109,28 (2012): 11150-5.
b. Watt IN, Montgomery MG, Runswick MJ, Leslie AG, Walker JE. Bioenergetic cost of making an adenosine triphosphate molecule in animal mitochondria. Proc Natl Acad Sci U S A. 2010;107(39):16823-7.
Old studies to illustrate the difficulty of explaining the results of many studies:
a. Function of the Two Cytochrome Components in Chloroplasts: A Working Hypothesis; R. HILL & FAY BENDALL; Nature - volume 186, pages136–137 (1960)
b. Photosynthesis by Isolated Chloroplasts; DANIEL I. ARNON, M. B. ALLEN & F. R. WHATLEY; Nature - volume 174, pages394–396 (1954)


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How badly will warmer air affect birds' ability to migrate long distances?
I recently read about how warmer air decreases lift for airplanes.
I wondered whether birds would also experience reduced lift, and whether that might make it harder for them to migrate long distances. And might that endanger some bird species that take long, arduous migration routes?

I suppose it is (sometimes) exactly the same for birds as for planes.
[same]
Newton's second law tells us that Force = mass times acceleration, and Newton's 3rd law tells us that for every force there is an equal and opposite reaction. Because both airline and bird wings are fixed size, they interact with a fixed volume of air, meaning if the air is less dense, they will get less force against their wings as they push the air down.  Thus they generate less lift.
[not same]
However, unlike planes, birds don't use jet engines to suck in air (which will be less dense) to generate their forward velocity at takeoff.  Instead they usually run on the ground or jump.  Their ability to run on the ground or jump should not be affected by air density.  I believe for most birds, taking off is the limiting factor, not sustaining flight once airborne.  Thus, birds should be able to continue flying.
But, once airborne, will hotter temperatures affect their migration? Probably not too much as the CNN article you link to says for planes the effect is 1% for 3 degrees celcius, meaning if the earth warms 3 degrees, birds will only have to expend 1% more energy.  Now it could get worse in some areas, but birds can also move, and if a wind pattern changes, they can just fly to a different area where the wind pattern still exists, so hopefully they'll be alright.
But I don't know enough about bird behavior to say for certain.  But from a physics perspective, there's no reason to suspect birds have it worse than planes in terms of what their wings can do with the air, so if planes lose 1% energy for every 3 degrees warming, birds should lose even less than 1% energy.  Hopefully the planet won't warm much more than 3 degrees. :)
As a final note, once the bird is flying high in the sky, the air temperature should no longer be scorching like it is at ground level, so even though the ground might be 20 degrees hotter, the higher up air probably won't be that much hotter, and remember that near the ground at takeoff, birds get their power from their legs, not wings.


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are dead ants returned to colony?
Do foraging ants carry dead ants back to colony for disposal or leave them where they died?  I would think they would leave them behind just based on the energy expended that would be needed to transport them.  If they brought the dead back to the nest that might indicate 'feeling' or 'emotion' which everybody seems to say is impossible.

Social insects can respond in different ways to nest mates corpses. They can bury them (sometimes "entombing" is used in the literature, especially in honeybees because they can seal cells or use propolis to build tombs), eat them ("cannibalism"), but most often a specialized group of workers takes care of carrying them outside of the nest, far from the colony. Usually the older workers specialize in undertaking behaviors, it has been hypothesized that this allows to reduce the risks of contamination because older workers are already more likely to die or have fewer social interactions than younger members of the colony.

Sun, Q., & Zhou, X. (2013). Corpse management in social insects. International journal of biological sciences, 9(3), 313.

What social insects do with the corpses wouldn't be a good indicator of emotions, simply because they may bring them back to eat them, or take them away to avoid contamination. Whether insects do experience emotions is a complex topic, the most advanced piece of work on the subject has been done on bumble bees:

Perry, C. J., Baciadonna, L., & Chittka, L. (2016). Unexpected rewards
  induce dopamine-dependent positive emotion–like state changes in
  bumblebees. Science, 353(6307), 1529-1531.


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What is the botanical definition of a tree?
I recently saw a shared post on Facebook which states

Trees - even a young child knows what a Tree is, however there is surprisingly no universally recognised precise definition of what a tree is, either botanically or in common language. In its broadest sense, a tree is any plant with the general form of an elongated stem, or trunk.

Wikipedia points out (without citations)

In botany, a tree is a perennial plant with an elongated stem, or trunk, supporting branches and leaves in most species. In some usages, the definition of a tree may be narrower, including only wood plants with secondary growth, plants that are usable as lumber or plants above a specified height. In wider definitions, the taller palms, tree ferns, bananas, and bamboos are also trees. Trees are not a taxonomic group but include a variety of plant species that have independently evolved a trunk and branches as a way to tower above other plants to compete for sunlight.

I always considered palm trees and banana trees to be trees. Is it true that botanically, they are not trees? What is the true botanical definition of a tree?

Here is a reference that might suffice to convince you that there is no "true botanical definition of a tree": https://silvafennica.fi/article/463 And since I like to nitpick occasionally: A definition is not something that can be true or untrue. At most, a definition can be common and accepted, possibly even endorsed by a scientific society or codified in regulations or laws.

You will find for many biological concepts they don't bother trying to use or recreate vague lay concepts. You will also find biological definiens are often not hard and fast because life exists in a continuum.

According to "Plant Identification Terminology: An Illustrated Glossary" (Harris & Harris, 2001):

Tree: a large woody plant, usually with a single main stem or trunk.

An emphasis here should be on the woody characteristic. I'm not sure many botanists (if any) would define 'trees' without woodiness being part of the definition. As such, botanically speaking, the growth habit of neither bananas nor bamboo would be considered a tree.
The variation between tree and shrub is much less well-defined, and no "standard" definition exists. Often times, the number of stems coming from the base is used to differentiate trees (one or few stems) from bushes (many stems), but this is not universally applied or useful.
Emphasis here is "usefulness". Differentiating shrubs from trees is honestly arbitrary and typically dictated by the application to which the definitions are being applied. In many cases, simply differentiating by maximum or average growth size can serve as the differing characteristic as size is going to often be most relevant for landscaping (i.e., trying to achieve desired sizes) and ecological applications (i.e., which part of the community strata the tree reaches in terms of light availability). Often, botanical studies will explicitly indicate their definitions of tree vs shrub by indicating a cutoff or transition height tat they use to differentiate the two. However, in many studies, both would be considered relevant and a "cutoff" would be unnecessary.

In other words, number of stems and maximum growth can and are often used to differentiate trees from shrubs, but no standard number of stems or specific growth size are universally used to differentiate both woody growth habits.


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Can box jellyfish see with their eyes?
While normal jellyfish don't have any eyes, box jellyfish have 24 eyes.
Looking into my question on the internet, in one answer on Quora to the question Do jellyfish have eyes?, it is said that:

While box jellyfish have eyes, they cannot process images at all because they simply don't have the central nervous system to process images [Source: GRE Biology question I got right].

I heard somewhere though that box jellyfish do have a nervous system and they can see with their eyes.
I have found answers on Quora to be a bit hit and miss with their accuracy and wondered what the facts are.

This article from Live Science provides some insight (no pun intended) into box jellyfish eyes.
“Whereas we have one set of multi-purpose eyes that sense color, size, shape and light intensity, box jellyfish have four different types of special-purpose eyes. The most primitive set detects only light levels, but one set of eyes is more sophisticated and can detect the color and size of objects.”
This article from Science Daily may also help.
“The researchers examined the function of one of two types of "upper lens eyes," already known to form images, to work out just what those eyes can see and how well. It turns out that those four eyes cover precisely the visual field needed to see through the water's surface up into the world above.”