text:
Is there a physiological reason why direct lightning strikes are not lethal for everyone or does it all come down to dumb luck?
Some people who get directly struck by lightning and some more than once (starts at 00:25) survive while others die instantly or later on due to complications/injuries.
Looking at a wiki page for Lightning injuries

Lightning injuries are injuries caused by lightning strikes.
They result from three factors:

electrical damage.
intense heat.
the mechanical energy which these generate.

While sudden death is common because of the huge voltage of a lightning strike, survivors often fare better than victims of other electrical injuries caused by a more prolonged application of lesser voltage.

Lightning can strike or injure humans in four different ways but I'm going to focus on direct strikes.

Reported mortality rates range from 10–30 percent, depending on the source of data. Most people who are struck by lightning live to tell the story, but many suffer from long term injury or disability.
  Airforce medicine site

Is there a physiological reason why direct lightning strikes are not lethal for everyone or does it all come down to dumb luck?

There is a very wide range of energy in lightening strikes.

To expand on @blacksmith37 comment: being "struck" by lightening doesn't necessarily mean  a direct hit on your person. Even if lightening strikes several yards away you may suffer from electrical shock and be stunned from concussion. In general the further you are from ground zero the less likely you are to be injured, but even then the nature of the local terrain may strongly affect the resulting ground currents, which can be lethal.

Yeah "struck by lighting" covers a fairly wide range of occurrences, including different type of lighting and different types of strikes including direct and indirect. This is like asking why all burn victims do not die as if a first degree burn on the hand and a third degree burn across the entire body was the same thing.

Specified question to direct strikes only.

That youtube video looks like a hoax, though. The camera should have picked way more light based on the distance from the lens to the strikes. Different google search results suggest it may be fake too.

Is there a physiological reason why direct lightning strikes are not lethal for everyone or does it all come down to dumb luck?

To be lethal a lighting strike has to do enough damage to a critical organ that the injury is not survivable.  Since electricity can take highly variable paths through a body, the amount of damage inflicted is also highly variable.
For example, current entering on the head and exiting on the foot stands a good chance of passing through both the brain and heart.  This is likely to be a very severe injury.  Conversely, current entering on the left hand and exiting on the left foot does not cross the body and may leave superficial burns but limited internal injuries.

Lightning strikes the ground which then conducts to you.
By keeping minimal contact with the ground, you give the electricity less of a chance to conduct to you. And if your heels touch, this gives the electricity a shorter path to travel.
It is also important to avoid conductors, such as metal items.


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What is a false crocodile?
On the wikipedia page about crocodiles crocodiles are called true crocodiles. Does this mean there are (or where) false crocodiles as well?

Crocodiles (subfamily Crocodylinae) or true crocodiles are large semiaquatic reptiles that live throughout the tropics in Africa, Asia, the Americas and Australia. Crocodylinae, all of whose members are considered true crocodiles, is classified as a biological subfamily.https://en.wikipedia.org/wiki/Crocodile

The only "false crocodile" I found was the False gharial.
What is a false crocodile? if it exists at all. If not what is the reasoning behind the naming of a true crocodile?

If you keep reading the next sentence it makes clear what is meant (emphasis mine):

Crocodiles (subfamily Crocodylinae) or true crocodiles are large semiaquatic reptiles that live throughout the tropics in Africa, Asia, the Americas and Australia. Crocodylinae, all of whose members are considered true crocodiles, is classified as a biological subfamily. A broader sense of the term crocodile, Crocodylidae that includes Tomistoma, is not used in this article

So, the Crocodylidae family refers to crocodiles, the Crocodylinae subfamily are the true crocodiles which includes almost everything known as a crocodile, and indeed, you found the one that gets left out:

The crocodylian family Crocodylidae includes the true crocodiles, which are the members of the subfamily Crocodylinae, as well as potentially the false gharial, the only extant member of the subfamily Tomistominae. The latter is a subject of controversy as to whether it is a crocodile or actually belongs in the family Gavialidae.

(via Wikipedia)
Wikipedia further states:

Gavialidae have conventionally consisted of only one surviving species, the gharial (Gavialis gangeticus), which is native to India and Nepal. Many extinct species are also known

and also

Tomistominae is a subfamily of crocodylians that includes one living species, the false gharial. Many more extinct species are known, extending the range of the subfamily back to the Eocene epoch. In contrast to the false gharial, which is a freshwater species that lives only in southeast Asia, extinct tomistomines had a global distribution and lived in estuaries and along coastlines.

So there are many other extinct relatives of crocodiles in these groups; the question is to which the extant false gharial belongs. In either case, the other Tomistominae would be non-true crocodiles, according to a definition that subfamily Crocodylinae are the true crocodiles.
The words "true" and "false" are not necessarily used in their boolean meaning here, but rather, "true" in taxonomy fits better with other definitions, for example from Merriam-Webster: "typical" (Merriam-Webster explicitly references the "true cats" as a use for this meaning). A synonym would be more like "archetypal" or refer to a clade or other more robust grouping, rather than a linguistic/non-scientific grouping.

source: Stack Exchange

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

sort: votes


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Chickpeas as feed for house sparrows , ringneck parrots?
I've put up a bird feeder outside my house, and so far I have been feeding uncooked
 white rice , and the birds seem to enjoy them.
However, since I read somewhere  that a variety should be maintained in the diet, lest the birds start suffering malnutrition, I want to know whether I can use chickpeas as a substitute for a while. Is it safe for house sparrows, ringneck parrots ? These are the only type of birds that have been visiting my feeders for a while now.
Thanks !

I have read that raw rice can be dangerous for birds to the extent that it should not be thrown at wedding., It absorbs water and swells to a dangerous level. From personal experience I can say that can happen in a dog. Why not use bird seed ?

Sorry, but uncooked rice is not harmful for birds. For the time it takes for rice to expand in presence of water, it already gets digested and broken down in the bird's system. So the question of swelling doesn't arise. I have seen parrots break the seeds into smaller pieces before swallowing, so no question of trouble there too.

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


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Can foraging worker ants become queens?
The TL;DR is in the subject line.
The back story is as follows:
I am combating ants in my high-rise apartment unit.  One piece of online advice was to vacuum regularly, and pay attention to edges of the floor.  I'm considering taping up the vacuum bag opening so that I'm not tossing out a nearly empty bag every day (almost $10 each, and terrible for the environment).
I had initial concern that an ant might get out, so I also double bagged the vacuum bag.  This is making it inconvenient to use, meaning that I'll vacuum less.  Exactly the opposite of the online advice.
I think that the chances of an ant getting out is low, and even if escape was possible, it probably wouldn't be more than one or two.  I can accept that, if they don't go start generating more ants.
I haven't found anything online about workers being able to transform into queens once they are foraging.  What I have read is that it has to do with genetics and extra nutrition during the formative stages.
Is it safe to assume that foraging workers will not be able to turn into queens?
After note: It just occurred to me, if ants can chew through wood, then there's nothing to prevent them from chewing through a vacuum bag over the course of a day or more.  They can even chew through the plastic bag in which the vacuum bag is sealed.  Is this a valid concern, or is their ability to chew limited to wood?

It depends on the species. Apparently there are species where workers can mate and lay fertilized eggs. However, it's unlikely to be a relevant issue for you because without the colony the few escapees won't be able to care for the eggs and larvae. Your issue is the colony and that your apartment attracts foraging ants.

Thanks, Roland.  Did you want to post that as the answer?

Workers cannot become "queens" because the development of a larvae into a worker or a queen happens during the larval stage, depending mainly on the food that the larvae is given. That being said, once the queen is removed from a colony, in many ant and other social hymenopteran species, workers are no longer inhibited by the pheromones produced by the queens that prevent the growth of the worker's ovaries. So in some species, removing the queen can lead to workers laying eggs but these will most often be parthenogenetic and lead to the production of males only. In a very few species, workers can produce female eggs by parthenogenesis or mate with males after the removal of the queen. Such traits are usually associated with large body size and small colony size, so they are unlikely to be the ones you have in buildings.

Bourke, A. F. (1988). Worker reproduction in the higher eusocial
  Hymenoptera. The Quarterly Review of Biology, 63(3), 291-311.
Page, R. E., & Erickson, E. H. (1988). Reproduction by worker honey
  bees (Apis mellifera L.). Behavioral Ecology and Sociobiology, 23(2),
  117-126.
Wenseleers, T., Helanterä, H., Hart, A., & Ratnieks, F. L. (2004).
  Worker reproduction and policing in insect societies: an ESS analysis.
  Journal of evolutionary biology, 17(5), 1035-1047.


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Are there pre-synaptic alpha 2 receptors in the post-ganglionic synapses of the heart?
Are there pre-synaptic alpha 2 receptors in the post-ganglionic synapses of the heart?
I haven't found any sources that clearly state whether they do or not. I'm also not sure if they exist in most post-ganglionic synapses, or if they do in just specific ones. The reason I ask is wanting to understand the reflex tachycardia non-selective alpha blockers like phenoxybenzamine cause.
One of the side effects of phenoxybenzamine is reflex tachycardia, caused by, from my understanding, partly a reflex to the initially decreased blood pressure and due to the blocking of alpha 2 receptors, increasing nor-adrenaline release. Does this occur by :

Blocking alpha 2 receptors at other sites, causing increased blood levels of nor-adrenaline, which then cause increased heart rate.

OR

Blocking alpha 2 receptors in the heart, increasing local increase of nor-adrenaline?

The heart of course does have Alpha 2 pre synaptic receptors , the definition states that alpha 2 receptors are present on sympathetic postganglionic endings , so I don't see why heart should be an exception .
I will explain to you how reflex tachycardia occurs .
When you give non selective blockers , presynaptic Alpha 2 are blocked , therefore the pre synaptic neurons cannot sense NE amount in synaptic cleft , so they release large amounts of NE . BUT , post synaptic alpha1 is also blocked , so this large amount of NE cannot act BUT THE HEART DOES NOT HAVE alpha 1 it has BETA 1 receptors which are perfectly capable of being stimulated by this large amount of NE that is released , hence causing tachycardia.


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What advantage does lactose have as the main sugar in milk?
Most organisms have lactose as their main sugar in their milk.
What advantage does lactose give have over sucrose (Which is a common sugar in the plants, so it makes sense for it to be present in milk)
Is lactose synthesis easy? Or is the enzyme B-galactosidase easy to make?
Or is it more easily digestible, allowing mammalian infants to get energy faster?

Possible duplicate of What selective factors drove the evolution of lactose in lactation?

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It doesn't make sense to have sucrose in milk if mammals are unable to produce it.

As @anongoodnurse states elesewhere, the comparison with sucrose is arbitrary. The question is better stated in terms of lactose v. other disaccharides, but unfortunately has been asked before. I would mention that ideas like "synthesis being easy", "enzymes being easier to make" and "get energy faster" are biochemically naive. (And most organisms do not produce milk. Try "mammals".)

If you feel the existing question and answer do not answer your question please explain why or expect the question to be closed.

Yes it is thought to provide safer milk, less vulnerable to every bacteria that respires and multiplies on sucrose, and which lets the baby grow faster due to higher sugar content.
Milk has evolved from pouch mucus, antimicrobal secretions of the immune system, Lysozyme in mucus is a glycoside hydrolase which ruptures bacteria cell walls. So the origins of milk are very different than for plants.
Lactose is a larger molecule than sucrose, so it exerts less osmotic effect per unit mass, allowing more carbohydrate to be included in am isosmotic secretion such as milk.
for example:
marsupials have mostly longer oligosaccharides and their milk contains 11-14% sugar,
zebras and and horses with only lactose achieve 7%
humans and other primates achieve 8-9% using milk and polysaccharides.
Another advantage is that it's a molecule rarely produced in nature, and fewer bacteria have evolved the enzymes required to digest it, upgrading the lac-operon to produce galactose-permease, save for beneficial lactobacilli, e-coli, and other mostly mutualist species.
full text.
It is thought that milk evolved from secretory glands in the synapsid egg pouch which helped to protect parchment eggs, with moisture and antimicrobial secretions. In fact, lactose is thought to have come from mucus sugars, which are used to encapsulate and neutralize microbes in the body, "Because α-lactalbumin evolved from lysozyme before the division of amniotes into synapsids and sauropsids (see Figure Figure1),1), the capacity to produce lactose was an ancient trait that preceded its utility in milk synthesis"
Intro to synapsid and sauropsid precursors of lactose.

"and not many bacteria have evolved the enzymes required to digest it" There is clearly no problem for bacteria in evolving lactase/beta-galactosidase — the whole dairy industry depends on that — so this argument clearly does not hold. For the rest your answer does not explain why lactose is preferred to sucrose — the poster's primary concern. The complex argument proposed in the question that this is a duplicate of, implies that there is no obvious easy answer.

If you want to contradict what a professor of dairy chemistry states, the author of the stated arguements, it would be wise to have some fact to support your arguement. For the rest my answer explains that sucrose tends to osmotically travel through the membranes into teh cell walls and presumably to the capillaries, and lactose doesn't because it's too big thereby increasing the energy content of the milk, and also that botulin and every bacterial that respires and grows on petri dishes can process glucose and infect udders adn babies, but not lactose.

This answers a question, but not the OP's question. The OP is comparing mammals to grapefruit, then asking why.

The two factors convey a huge gargantuan advantage compared to a banana/fig. If common bacterial resistance is not an advantage, then what is it? A baby and udder without botulin issues sounds like a good idea to me. Ease of containment and transport of sugars due to lower osmotic pressure is also an advantage, because it allows for more energetic milk than with sucrose, and therefore allows the child to put on weight faster, and more safely.

The validity or not of arguments  depends on their logic, not on who makes them. The one at issue is rehearsed in an answer to an earlier version of the question. I have not commented on that answer, only on the defects in yours. In particular I criticized the original statement about the lack of bacteria that can metabolize lactose, which now seems to have morphed into an equally contentious argument about the bacteria with sucrase v. those with beta-galactosidase. To this I would query the statement that "lactose is a larger molecule". Lactose and sucrose have the same molecular weight.

The original version of your answer — to which my criticism was directed — contained no mention of the hypothesis of Urashima et al., quoted by Alan Boyd in his answer to a similar question. It did, and still does, contain the false assertion that “lactose is a larger molecule than sucrose” — an assertion Urashima et al. certainly did not make. In fact both lactose and sucrose have  molecular weights of 342.3! As you now seem to be leaning on the hypothesis of Urashima et al., would it not be better to vote to close this question as a duplicate, rather than rehashing Alan Boyd’s answer?

One of the advantages of lactose in breast milk is that it is digested slower than sucrose and its ingestion results in lower fluctuations of blood glucose levels thus being a stable source of energy.

Lactose, a disaccharide of glucose and galactose, is uniquely present
  in mammalian milk. Human milk provides the infant with about 40%
  energy as lactose and 50% from fat. With 6-7 g/dL lactose, the breast
  fed infant consumes high carbohydrate/kg body wgt, suggesting
  carbohydrate induced hepatic lipogenesis would be problematic with a
  high fat milk diet. However, galactose, unlike glucose is
  non-insulinogenic and shows high hepatic clearance. We propose
  lactose in human milk confers unique metabolic advantage to the infant
  by delivering non-insulinogenic carbohydrate which can be slowly
  metabolized in the liver to glucose or to support fatty acid
  oxidation. We determined insulin, glucose, triglyceride, free fatty
  acid and amino acid responses in 16 healthy adult men given in random
  order 650 mL carbohydrate-free infant formula reconstituted to contain
  50g lactose, glucose, sucrose or corn syrup solids. The milk formula
  was given 3 hr after a lactose and sucrose-free meal, then again after
  3 hr, to model the carbohydrate load and continuous feeding of
  breast-fed infants. Blood was drawn every 15 min, and total and
  incremental area-under-curve change in insulin and glucose determined.
  Lactose gave a significantly lower rise in plasma insulin and glucose, in the first and particularly second 3 hr following intake,
  compared to glucose or corn syrup solids (P <0.001). Individual
  variability in triglyceride responses was high, with no difference due
  to carbohydrate in this 6 hr study. We show lactose enables
  maintenance of glucose and insulin equilibrium, avoiding high
  postprandial peaks achieved with glucose or corn syrups in milk fed
  at 3 hr intervals. We propose an important metabolic homeostatic role
  for lactose as carbohydrate source in human milk.

The lower glycemic index of lactose (46) compared to sucrose (65) also reflects slower conversion of lactose to blood glucose (gisymbol.com)


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Water potiental

I think solution x should be present at Z as this solution has moved out of cell causing cell to be plasmolysed but the answer is Y. How?

It is not solution X what is going out of the cell, but the solvent (water) of solution X.
Also, you need to keep in mind that the cell wall permeability is by far less selective than the cell membrane. This is why solution Y can diffuse freely to Z.


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Why do tails of some lizards break so easily?
When I was younger once I have tried to catch a ground lizard by its tail but,
unfortunately the tail got broken and the lizard ran away.
Why did the lizard's tail get broken so easily while other animals have stronger tails?

It's a self-defense mechanism, the tail falls off during threatening situations, to which the reptile responds by excessively contracting the tail muscles. This process is known as "Autotomy", or "Self-Amputation". Other animals have got "stronger tails" simply because such self-defense mechanism hasn't been developed.
https://science.sciencemag.org/content/20/500/149.2
Check this link for more in depth information!


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Can anyone help me with these Biology evolutionary properties homework questions?
my teacher assigned these worksheet questions, they are ungraded, but he said something might come up on the test really similar to this so I really want to get all of them right. I am pretty confident with all of them except for two,
In the layer below a mass extinction that devastated the region, the paleontologist observed that shells of species A was present in small numbers over a widespread area whereas species B was abundant and found in a few restricted areas. Which of the following predictions about the fossil record in the layer above the mass extinction is the MOST likely to be supported by further excavations?
A.

Species A survived because of its widespread range including some areas that were not as affected by mass extinction.
B.

Species A survived because the low number of individuals meant that there was less competition for resources.
C.

Species B survived because it was the more abundant and more individuals survived.
D.

Species B survived because the population was concentrated in a few areas and had a higher chance of survival.
and
A scientist analyzes the vision receptor molecule in invertebrates and vertebrates. The results show that the genes for opsin, the protein part of the photoreceptor, share strong homology in the regions that code for domains involved in light response. Which of the following conclusions is the MOST likely?
A.

The receptor molecules will be structurally different but respond to the same light cues.
B.

The receptor molecule will be similar in invertebrates and vertebrates because of convergent evolution.
C.

The receptor molecules will be different because invertebrates and vertebrates perceive visual cues in different environments.
D.

The receptor molecules will be similar in invertebrates and vertebrates because they appeared early in evolution.
For the first one, I reasoned that it was most likely A, however, D caught my attention and now I am seriously doubting myself on it. This is due to the fact that the wide range of an organism might lend itself to higher survival, as some regions might better be protected or missed by harm, however, it could just as likely be D, in my opinion, as more animals might lend to quicker recuperation in any instance. For the second, I am pretty confident it is A, as homology means they come from the same source but may evolve to differ, but again, D is pretty tempting as it may be simply as it was an element that appeared early on and thus is present in both. I am only an undergrad premed, so not too savvy yet, but any help would be great.

Homework questions are off-topic on Biology unless you have shown your attempt at an answer. For more information see our homework policy. See also https://biology.meta.stackexchange.com/questions/3377/homework-questions Please edit your question to have an informative title, limit your question to a single specific question, and explain the reasoning behind your answer attempts rather than just your guesses and confidence. It would also be better to phrase your question as a conceptual question rather than multiple choice.

Thank you for the reply, I explained my reasoning further and updated my title. But I didn't see anything about asking one single question in your links, thank you very much for them by the way, I am not being rude! I will totally cut it down if necessary

We really don't answer homework questions, as @BryanKrause stated very politely. Our goal, ado, is not to simply be an answer site, but rather a site that promotes self-learning with some expert help along the way :)  I was about to close vote, but it's better after the edit.

Thanks for taking the time to reply :) I totally understand that, I can add more to my question, I really want to completely grasp the topic, or I can rewrite it completely if you guys think that would be best. I would ask my prof but I wont be able to until a little while.

Your two questions are unrelated (other than the fact that both of them are parts of your homework). Therefore I am voting to close your question as broad. Your edit is good enough to make the question on-topic. I recommend that you ask two separate questions and rephrase your question titles accordingly.

The first question is poorly designed the only things with a high chance of surviving mass extinctions are organisms that occur in large numbers over a wide range of environments, without more detail neither A nor B would have a strong preference for survival compared to the other. Mass extinctions are too unpredictable, neither by itself gives you a large advantage.
It really depends on how they define terms the only organisms that occur over a truly wide range of environments that is both marine and terrestrial ones are tiny and thus have huge population numbers. the more localized the measure of widespread the less being widespread matters. for instance Ammonites occured in every marine environment in large numbers (so a wide range of local environments) but were completely wiped out because the ocean PH changed which hits every portion of the ocean equally.
The best you might be able to say is A might have a slight advantage because it is more of a generalists as it occurs in more environments but that use of the term "within a region" means it does not help much.
The second question is easy, if the genes are sequentially similar it is due to a common ancestor. since the sequence is part of the functional component then the ancestor likely used it for the same function, so D would be your best answer.


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How could pharmaceutical metabolizing bacteria be used to synthesize them?
Lets say I have a pharmaceutical "P". It can be broken down by enzymes of one strain of bacteria into two molecules one of which can be further metabolized enzymatically by a different strain of bacteria. Both strains as a result can decompose "P" to the simplest metabolites.
Could one hope to reverse the reaction using the same enzymes and have the two bacteria produce "P" from basic nutrients and if so, how would the conditions have to be altered? Or perhaps would it be possible ex vivo?

Why are you complicating your question with two bacterial strains. As far as I can see, your question is whether a series of reactions that degrade a xenobiotic could be used to synthesize it, presumably on the premise that all reactions are reversible. Or do I misunderstand you?

You're quite right, however i will clarify that the core of the question is whether enzymes could too strongly affect the reversibility/equillibrium of the reactions, and if not, could this be done with living organisms or perhaps ex vivo? Also since i read about a pharmaceutical decomposed only by a certain two strain coculture i wonder if it would affect the answer in that case.

After posting I realized that you must have a particular situation in mind. My immediate reaction is that it won’t work because of the thermodynamics of synthesis and degradation pathways and the different enzyme specificity required. However I never answer questions in comments. If you need this explaining I’ll do so if nobody else does. But it may be a few days as I have other fish to fry at the moment.

In principle yes, because almost all reactions exist in an equilibrium and enzymes are catalysts (meaning they affect mainly the activation energy for a specific reaction).
The best approach is to purify the enzymes in question (probably not even from their original species, but from another transgenic bacterium), since this reduces your total systems from two different organisms and all their enzymes and metabolites to a very specific set of two enzymes and a handful of metabolites.
But ...

The natural equilibrium of the reaction might favor the more basic metabolites.
Even if you speed up the generation of "P", that won't help much if only a fraction is converted in the first place. Many biological systems deal with this problem by coupling unfavourable steps with hydrolysis of high energy molecules (like ATP), but linking to this to a given enzyme would be a very challenging process.
The enzyme(s) might not be overly specific for "P".
Many enzymes that remove or break down 'unwanted' products can act on multiple similar molecules. This make sense for cells, since its much more efficient to have one enzyme taking care of multiple 'bad things'. However, this makes reversing the process tricky since your reaction will yield multiple products of which only one is interesting. Optimising the enzyme to be more specific is relatively straight forward using in vitro evolution though.
'Basic metabolites' is not a clearly defined thing.
Many pharmaceuticals are pretty complex, and enzymes that break them down likely literally chop it into two pieces. Whether these pieces are actually easy to obtain chemicals that can be used as input for an enzymatic reaction is a different question. Depending on the complexity of 'P' you might have to use a pretty large number of enzymes (all of which may come with the above mentioned problems) to be able to start from reasonably basic molecules.


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What kind of spider is this? hoping its not poisonious

Found outdoors, after it was killed we found little tiny baby spiders on our ceilings throughout our house. really wanting to know if this spider is venomous or not as we have a baby of our own in the house..
Found in Bligh Park 2756, Sydney NSW Australia.
I would say it’s around 10cm.

Hi Emily. Please review the guidelines for writing a [tag:specied-identification] post. Specifically, we need your location and the size of the specimen. Ideally, if you can provide additional photos of the spider (especially of its abdomen and eyes) that could benefit getting a positive ID, too. Please [edit] your post with this additional information. Thanks. Please also consider taking our [tour] and checking out How do I ask a good question?


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Is it impossible to increase skeletal bone mass, as opposed to just bone density?
I've heard exercise and resistance/strength training increases the density, but doesn't increase mass. So basically, experimentally or theoretically possible at least, can modern science do this/is it feasible?
Density is just how "packed" the current bone is on the micro-level -- i.e., doesn't affect total mass potential. Filling or adding "density" is just like putting water in a fixed-size bucket until it fills. By "adding mass" I want the bone's bucket to be able to hold more density, i.e., a larger potential of density along with an overall greater weight to the bones themselves. I can't find any evidence that this is possible with long and flat bones alike, AKA the spine, leg and arm bones, clavicles and etc. -- or any bone.
I've heard facial bones are more malleable, but their bone mass cannot change with diet/training either.
So to make this as easy to understand as possible: Can bone mass in an adult be significantly changed somehow? Can I make my whole skeletal set heavier somehow, rather than just dense? Like for example, say I am considered "small framed." Rather than just density, could I make my frame bigger? Could I make my entire frame base more robust through some possible bio/drugs/etc. means?
And since I know someone will come along and claim this is a "medical/personal question," explain to me how this would be possible to ask in a non-medical/personal way then to enlighten me. Go ahead.

Bone mass probably does vary with bone density, and it's the volume of the space that the bone occupies that doesn't change much due to exercise and resistance/strength training, at least in the short run. But I could be wrong...

Density = mass/volume. If volume stays the same and density increases, mass would also increase.

@MelaGo My assumption would be that it's a limitation on volume in which density can take place. You can't "out-volume" the potential of the bone, which is my argument the whole "density vs. mass" simplification -- i.e., you can add as much density to the given volume/genetic/epigenetic/adult size/etc., but cannot really make the bones bigger in any significant way such as a smaller frame to a medium/large one.

@WasteOfTime, your entire question can be clear enough if you just ask if exercise can make someone's bones bigger in the sense of a bigger frame. There's a lot of unnecessary confusion by mentioning mass and density.

If you search for
 - bone growth training
 - bone hypertrophy athletics,
 - bone diameter increase,
 - bone strengh hunter gatherer,
on google, you will find more articles than I could possibly summarise:
stimulation of longitudinal bone growth and widening of the joint space (cartilage hypertrophy) occur. The possibility of bony hypertrophy as a result of athletic training, especially with regard to increases in of bone density and bone diameter, should lead to incorporation of sports medical considerations into the prophylaxis and therapy of osteoporosis.
https://www.ncbi.nlm.nih.gov/pubmed/7856798
https://www.ncbi.nlm.nih.gov/pubmed/7478507
I have slender bones and it was the gain of muscle which helped me to balance my physique.

Gaining muscle != making any significant difference of skeletal bone mass/shape/volume/etc. If anything, muscle can at best hide some smaller frame along with fat if you have the natural genetic potential for decent musculature (unlikely with a small skeletal frame).

When you are 15-18 your bones grow a lot faster than what your musculature can adapt for. I found myself with hands and arms which were 30 percent longer in the space of a few years, so they would basically flap about and I didn't know why they had lost their agility. In that sense, you get used to your physique as it adapts.

I've found the opposite -- good muscle strength, but frame not good enough (on my body/my experience). A smaller skeletal frame overall is a death sentence when it comes to your ability to play brutal contact sports, as you're more susceptible and injury prone, along with generally having less physical potential due to bone shape/etc. There is a reason why most pro athletes don't have very frail/narrow/small bones/etc.

I mean nobody will believe this guy plays in the NFL just by virtue of his body frame alone: https://discourse-cdn-sjc1.com/tnation/uploads/default/optimized/3X/f/8/f83761f1b6276c54d664c7e07eef63bdb2fdbb16_2_405x500.jpeg And no amount of muscle building will improve such a small body/skeleton shape/etc. that's always vulnerable. This is what I mean when I talk about skeletal mass, as it's the overall structure that can't be changed in any significant way vs. just merely adding some density/etc. that won't really do much if the guy in the photo above wanted to play organized contact sports.

In short, yes, you can increase your bone mass by increasing both the bone density and thickness, but the increase may not be as great as you expect.
The body frame consists of the length and thickness of your bones, and is mainly genetically determined. After age about 20, you cannot increase your bone length further, but you can increase the bone thickness by few millimeters by regular heavy exercise. In this study in tennis players, the bones in their main arms were thicker by 2 mm at most compared to the weaker arms.
The bone mass also increases with bone density, which means more collagen fiber in your bones or, as you compared, more water in a glass. Bone density is 95% determined at the age about 20, when your bones stop to grow. Your bone mass probably reaches the peak between age 25 and 30 (OrthoInfo).
Until your bones still grow, you can somewhat increase your bone density by consuming enough calcium and vitamin D and by being regularly physically active (PubMed, 2015). Please note, that consuming excessive amounts of calcium or vitamin D will note further increase your bone density.
After your bones stop to grow, you can maintain your bone density, again, by sufficient calcium intake and regular physical activity (PubMed, 2008).

Wouldn't the thickness be attributed to just the most density built possible? They use the arms a lot so it's obvious the bones would be a little more dense there in their dominant arm/etc. This doesn't really mean an overall change in bone mass, other than just the same bone structure becoming more ossified/calcified/etc. I mean the actual bone didn't really "grow" or change in any significant way. The same bone shape/size/etc. that was/were genetically determined for the most part just became more dense by a super-tiny bit (2mm isn't even noticeable without like a DEXA scan or etc. maybe).

I mean it's obvious sports and exercise make anyone's bones more dense, but this doesn't really make a real change in the overall bone mass/volume that is comparing, say, a small-framed man's skeleton to a large-framed man's. The bones may get stronger and as dense as possible, but do not really gain mass/noticeable thickness/size in any way that one could compare like an untrained individual's muscle mass to that of a multi-year weightlifter (on average). So no, this seems more like repeated use adds (very insignificant) density to bones, which is known -- but no real change in frame/size.

They DID observe an increased diameter (thickness) of the arm bones but this was relatively small, so I said you may be disappointed. This bone growth doesn't really change your look and it certainly doesn't make your frame larger. It's not even nearly comparable with muscle mass increase. Looking only at bones you would barely notice the increase. You asked for a scientific evidence and that's it.

I'm not discrediting your post or the source you gave -- both are valid/"okay" as far as info and sourcing/answering goes. What I am just adding on to is the fact that this doesn't and cannot make any significance in overall skeletal base/mass/frame by adding density itself. So it's meaningless in that regard, but still valid in general. Basically this confirms that it is indeed impossible to make any significant change to your overall skeletal frame from exercise at least, as evidence shows negligible results over long durations.


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How do apiarists cultivate homeycomb without nicotine or a smoker?
I don't see a better stack site for this so I'll just post it here. I remember an apiarist I met saying they cultivated honeycomb without a smoker or anything like that, but I never asked them how. Figured it would be interesting to ask if there is any consensus on how one could do that without bees swarming or anything like that.

for the rest of us, "Apiarist is a fancy word for a beekeeper." Phys.org: Nicotine enhances bees' activity CBSNews: Are bees getting addicted to nicotine? fyi the nicotine comes from neonicotinoid pesticides in places the bees visit, not from the bee-keepers' use of smokers.

Ok, well is there a consensus on how to do it without a smoker?

It'a a good question! If you would like to ask about beekeeping without a smoker, then it's better if you click "edit" and adjust the wording of your question along the lines of your comment. I don't think you want to ask about neonicotinoid pesticides, and the smokers can use various kinds of smoke. You might consider asking a second question also, as a new post, something like "How do beekeeper's smokers have a calming effect on Bees?"


text:
Is there anything that can tell me precisely how the cross sectional area/radius of a snake changes over length?
I am trying to 3D model a green anaconda which I thought would be simple, then I realized there is actually this very gradual change in thickness from a minimum around its neck to a maximum somewhere in the middle then to another minimum around its tail.
Is there some kind of specific terminology or archive I can look up to get precise measurements? Regular google searches aren't doing it and there is a high amount of variation in this thickness gradient between species.

Maybe just pick a function with such properties and adjust the parameters until the snake "looks right"?

@electronpusher that would work only if there is data. OP is asking for data, not modeling tips.

If there was a perfectly straight snake that had both top and side pictures of it next to a ruler, then I could take measurements until it "looked right", but unless I have at least that, there's no accurate way to approximate it other than shear guessing.


text:
What is this tree growing in my town?
Can anyone tell me what kind of tree this is? I took this picture today. It's in Iowa City, Iowa.

Have to see the bark to know, it looks like a fruit tree, perhaps an ornamental apple or cherry tree.

@com.prehensible I added a picture of the bark, as you requested. Also, thank you!

It looks like a white crab apple or an obscure cultivar of apples, of which there are many.
The best identifier will be the fruit. Because there are not millions of flowers, It looks like there may be less fruit and bigger than a crab apple, although it varies by year.
The fruit of crab apples are small apples which can be used to make jelly. Crab apple trees can grow to 10m, a lot bigger than table apples.
White flowering crab apple:

https://en.wikipedia.org/wiki/Malus
comparison images.


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What is the use of futile reaction cycling such as Fruc-P to Fruc-BP?
One rate-limiting step of glycolysis is the conversion of Fructose-6-Phosphate (Fruc-6-P) to Fructose-1,6-Bisphosphate (Fruc-1,6-BP), catalysed by Phosphofructokinase 1 (PFK 1). The reaction involves hydrolysing one ATP to ADP.
The reverse reaction of gluconeogenesis is catalysed by Fructose-Bisphosphatase (FBP). This reaction uses 1 H2O for hydrolysis and yields 1 phosphate (Pi).
One would expect the cell to be utilising only one of the two reactions at any one time, either to break down glucose or to generate it. However, the case is commonly that both reactions are taking place simultaneously in an equilibrium [ref 'Biochemistry', Voet & Voet, 4th ed., 628-629 (Section 17-4-F-f,g,h,(i))], cycling Fruc-1,6-BP to no apparent benefit, at the expense of valuable ATP.
What is the purpose of such futile cycles?

I'd like to note that I have known the reason before, and I'm almost certain I have it somewhere in my material from last year - I just realised that I couldn't explain it to someone right now and I believe this question would be a valuable addition to our site. I am currently busy, but will answer it myself once I am free (unless someone else does beforehand).

gluconeogenesis is not continuously happening and is tightly regulated at the step of FBP. Therefore there is no continuous futile cycle

This question, like many others on metabolism, is meaningless in referring to "the cell" without specifying what cell one is talking about because the poster does not understand that different animal tissues have different metabolism which is different again from bacteria. Unsupported as it is by any references it should have been clarified when it was asked. Let's just bury it now.

As evident below, the question is perfectly clear and answerable within reasonable scope without specifying which cell type in which species at which developmental time point performs (seemingly) futile metabolic cycling. If there is a meta discussion relevant to this close request, please point me there. "Unclear" is not a valid reason for a close here imo.

As far as I am aware there are various regulatory mechanisms (allosteric regulation, hormonal control) in place to minimise futile cycling by ensuring that phosphofructokinase (glycolysis) and fructose 1,6 bisphosphatase (gluconeogenesis) are not both active at the same time.
See this Wikipedia article for a starting point.

The precise regulation of PFK1 prevents glycolysis and gluconeogenesis from occurring simultaneously. However, there is substrate cycling between F6P and F-1,6-BP. Fructose-1,6-bisphosphatase (FBPase) catalyzes the hydrolysis of F-1,6-BP back to F6P, the reverse reaction catalyzed by PFK1. There is a small amount of FBPase activity during glycolysis and some PFK1 activity during gluconeogenesis. This cycle allows for the amplification of metabolic signals as well as the generation of heat by ATP hydrolysis.

The last two sentences of the quotation are probably what you remember reading about. There is a theory that having some cycling provides an element of regulatory responsiveness. See here for example. I'm not enough of a mathematician to explain this idea well.

all_licenses: Creative Commons - Attribution Share-Alike - https://creativecommons.org/licenses/by-sa/3.0/


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What is the minimum atmospheric pressure at which bees can live/thrive?
Bees are amazing little critters. (Gosh, they're cute.) But what if we colonize Mars and start terraforming it? At what point will bees (and other insects) be able to live/thrive in that environment?
Obviously, there need to reasonable conditions:

total atmospheric pressure
partial O2 pressure and general atmospheric composition
no toxins
flowers to pollinate and get nectar from
a wider ecosystem to thrive in

For now I'm just wondering: What atmospheric environment do bees need to live on Mars?

Perhaps we should give them little space suits?

Yeah they're cute alright. I'm not an expert on this topic. However maybe this article with too many ads for its own good (https://www.dailymail.co.uk/sciencetech/article-2552098/Bees-scale-MOUNT-EVEREST-Insects-fly-altitudes-air-kill-human.html) might help a bit in understanding how change in atmospheric pressure can affect bees and also show's how awesome they are!

Also, insects used to be much bigger in the past and scientists believe this is because of the higher concentration of oxygen in our atmosphere during prehistoric times (https://www.nationalgeographic.com/news/2011/8/110808-ancient-insects-bugs-giants-oxygen-animals-science/). Imagine what that would look like!

They need a temperature over 0°C for starters. Insects thrive in mild temperatures, and Mars I fear is pretty cold (-65°C and lower). If we were to colonize Mars it would requiere to build indoor habitats to replicate Earth conditions, not only pressure but temperature, oxygen and humidity).


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What causes the sound of climaxing bees?
I just saw the funniest video of bumblebees(?) having sex. (mirror) As they were getting it on, there seemed to be an almost audible 'moaning' coming from the pair. From what I presume it was a sexual climax we heard!
Bees have neither vocal chords nor lungs, so I wonder: what is that sound?

As the pair is mating on a newspaper, I'm almost certain we're hearing transduced vibrations from the bees made audible through the paper and not the bees themselves. (Nonetheless, what a beautifully humorous anthropomorphism! Moaning bees certainly give vivid color to the birds and the bees!)
I have multiple theories:

The ejaculation of sperm by the drone is known to be 'explosive', even rupturing the endophallus and making a 'popping' sound. I wouldn't call the sound in the video 'popping' by any means, though.
(Un)controlled movements of legs or wings by either of the pair. This seems very likely considering the subjective frequency of the sound, but that's just speculation on my part.
Perhaps it's the queen piping? I'm really grasping with this one. I don't even know if that species' queens pipe or even have the ability to pipe.

Any excited entomologists wanna fill me in?

Okay, perhaps the sound issue isn't resolved yet. this video shows a rather similar species also demonstrating that sound!

Firstly, those aren't bumblebee faces ... those are big fly eyes. Those are Bumblebee Hover Flies (Volucella bombylans):

The noise in the first part of the video is identical to a fly flying around your head and the noise at the end sounds like what a fly would sound like when you press it against a surface like a wall or screen (or a newspaper, apparently)

I thought those compound eyes were rather 'fly-like', I just couldn't put my finger on it. Thanks for the species identification! As for the sound, I had someone remark the sound was similar to a fly on its back flapping its wings.


text:
Worm Identification
Please identify the attached worm and larvae.
Location:  Payette, Idaho
Approximate size:  1 mm
Found in home.

Note:  I have photos of dozens of these, "things."  The samples were gathered using a lint roller.  They are on my bed.  I use a $20 lens with a USB port to my laptop camera.  I am unsure of the magnification.


text:
How does the Endoplasmic Reticulum scale with Cell Volume in Epithelial Cells?
I am working on a mathematical model of a biological tissue (drosophila pupal notum; an epithelial tissue) where the tissue is built up from cells all described by the same cellular-model. The tissue is generated using a somewhat random process, and so each cell in the tissue has a different size (volume, surface area, etc.)
The model focuses on the movement of particles both between cells as well as between the cytosol of each cell and internal stores (like the Endoplasmic Reticulum (ER)). In order to use the same parameters across the entire tissue, I need to know the ratios of various volumes and surface areas, such as the ratio of the volume of the cell to the volume of the ER, or the ratio of the volume of the cell to the surface area of the ER.
So my question is, if we have a cell of some volume $V_1$, and we look at another cell with volume $V_2$, what can we say about how the volume of the ER of cell $1$, $V_{\text{ER},1}$, or the surface area of the ER of cell $1$, $A_{\text{ER},1}$, compares to the volume and surface area of the ER of cell $2$, $V_{\text{ER},2}$, and $A_{\text{ER},2}$? For example, would we expect $V/V_\text{ER}$ to remain constant across all cells in the tissue? Or maybe we would expect $V/A_\text{ER}$ to be a constant across cells in the tissue? Or maybe both of these ratios follow some other sort of scaling law?

Do we speak about volume-ratios within the same cell-types at different cell-states or do we compare different cell-types? I think this question is too specialized and you won't receive an answer. It could help if you provided allowed generalizations; i.e. you tell us what cell-types (or what one specific cell-type) you are interested in, and I am quite sure there will be people who can tell how those ratios behave in similar cell-types/tissues, that are not exactly drosophila pupal notum.

@KaPy3141 I'm not thinking about various cell-states. As for cell type, do you mean like epithelial cells?

But what would case different cell-volumes? Different points in the cell-cycles? Different cell-types that naturally have different sizes?

@KaPy3141 Or just cell-cell variability. The tissue I'm considering has the same cell type throughout.

Ok, I see. At least that is now defined. Maybe someone has data.

Please consider this "answer" as an enlarged comment. I can't answer your question, but it's possible that my speculations or considerations could be helpful in your particular situation, in the early phase of building a model.
First of all, I doubt that general formulas that link cell-volume to ER-volume of different cell-types can exist. Dependent on the specific cell-type, (dependent of the protein production need in the rough ER), the ER/total ratio can strongly vary (i.e. compare neurons (strongly protruding ER), red-blood cells (no ER), pancreatic cells (large ER), endothelial-cells..). Thus, any correlation may just be chance, without the general meaning that you truly seek.
Therefore, you should focus on such volume-correlations within the same cell-type at different cell-cycle stages.
In this context, I can think of mathematical considerations, that could help your model: When cells divide, they effectively half their membranes (membrane-lipid count). Mathematically, this means that the overall volume of the cell should reduce to around 35%. In contrast, the volume of the ER as a highly condensed structure could scale linear with its surface area, if we see it as a long tube that gets separated. From this, you could build an easy mathematical model, in which ER volumes are relatively bigger, when cells are small.
However, according to cell-size measurements this is not true; cell-volumes get halved [1] when cells divide, which should indicate relative stretching of the membrane. Unfortunately, I could not find any data on how the stretching of the cell-membrane relieves over time. Further, the volume (quite) linearly increases over time until the next division can take place [1].
This means the cell-membrane keeps a constant weight/V before and after cytokinesis, while the surface-area increases by root 2. Given, that the ER-membrane-mass is also halved when the cell divides, and there is no apparent mechanism that should cause swelling, it is still quite difficult to predict how the ER volume would change. Again, the ER is no simple sphere, but has a highly collapsed shape.
However, I found this source, that deals with changes in shape and volume of the ER during the cell-cycle. Apparently, there is a membrane exchange between nucleus and ER and the ratios in volume between ER and nucleus is constant throughout the cell-cycle. You can study this yourself in more detail, but I would take this observation as an indication, that the ER volume behaves as would be inferred from a mathematical standpoint; to the third power of the diameter of the cell.
To sum it up, I initially expected smaller cells seem to have relatively larger ER volumes, and I suspect, that you had a chance to fall for the same trap. However, if the volume-ratios are not constant, they should rather behave the opposite way: ER takes less cell-volume after division, when the cells are small.


text:
How do the maximum rates of calcium pumping compare between the calcium ATPases SERCA and PMCA
Two important Calcium ATPases found within cells are the Sarcoplasmic reticulum Ca2+ ATPase (SERCA) and the Plasma membrane Ca2+ ATPase (PMCA). Both use ATP to help maintain resting calcium concentrations within cells as well as play important roles in calcium signaling.
How similar are these two calcium pumps? More specifically, how do their maximum pumping capacities compare to each other? I would assume that just because they are both calcium ATPases it does not mean they are similar in all properties. For example, the Wikipedia page linked above even mentions how

The endoplasmic reticulum calcium pump...[is] inhibited by the tumor-promoting agent thapsigargin, which does not affect the plasma membrane calcium pumps.

Have any studies been done that compares the pumping capacities of these calcium ATPases? Or maybe is there a way to determine it based on their structure, roles, etc.?

I am not sure why this is being voted to be closed as a homework question. Can the close voter give pointers?

I didn't vote to close, but the rationale is likely as follows. Posters are expected to show that they have thoroughly researched a question before posting — "Tell us what you found and why it didn’t meet your needs". This is not my field, but faced with this problem I would search for reviews of calcium ATPases — general and specific — using, say Google Scholar. Just restricting yourself to a very short Wikipedia article is hardly enough.

Thanks @David, will do!


text:
Where does this equation in the electrophysiology literature form come from?
In my studies I keep coming across the form of an equation that is used in many different mathematical models for voltage gated ion channels. The most general form I have found is in the 1977 paper Reconstruction of the action potential of ventricular myocardial fibres by Beeler and Reuter. Each ion channel has a gating variable $y$ whose differential equation depends on functions $\alpha$ and $\beta$, both of which take on the general form:
$$\{\alpha,\beta\}=\frac{C_1\exp[C_2(V_m+C_3)]+C_4(V_m+C_5)}{\exp[C_6(V_m+C_3)]+C_7}$$
where $V_m$ is the membrane potential and each constant is determined to have different values depending on the channel, system, etc.
My question is where does this form come from? In all of the papers I have come across they seem to just use this form with numbers chosen to fit their data without explanation as to why this form is actually used. The Beeler and Reuter paper cites the 1952 paper by Hodgkin and Huxley, but it seems like H&H use simpler forms of this equation primarily motivated by just fitting the data rather than illuminating any underlying mechanisms. Therefore, I do not understand where this form in the B&R paper comes from that so many papers later on use as well.
Does this form come from assumptions about the workings of the ion channels, if so, what are these assumptions, and how do they give rise to this form? Or is this just a general form found to fit many data sets fairly well, and if so why was this chosen over other functions that could probably do the same thing?

They chose that equation mainly because of numerical simplicity. It can fit the rates $\alpha$ and  $\beta$ for all the ion channel particles in the model.
The theoretical foundation for the equation, as in the H&H model, are loose. It resemble the equation derived for the movement of a charged particle in a constant field. But it is not an equation derived from the ion channels biophysics. We can't blame them, considering that at that time (1952) they don't even know for sure that ion channels where proteins.
In page 183:
 In order to simplify the reporting of the actual values used in this model, we have expressed the alphas and betas entirely in terms of a generalized function, with eight defining coefficients. Table 1C gives the equation, and the defining coefficients for al rate constants.
For the generalized function note that in every case at least some of the coefficients are zero: this generalized formula is just a way to collect both possible forms for the H&H rate constants.
I have read papers using Eyring equation for a theoretical formulation of transition rates, based on thermodynamics.

This is partly true, in that in the HH model the theoretical foundations are at best loose, but I would not say they are non-existent: they refer to Goldman for example and all relate to Boltzmann equations. The choice of the generalized function in the Beeler and Reuter paper is mostly motivated by algebraic simplicity. That said, all are approximations to more modern biophysical models.

Goldman equation refers to the ion reversal potential not to the ion channel dynamic. $\alpha(V)$ and $\beta(V)$  are not Boltzmann function in H&H model. As far as I know, they are just phenomenological. If you know any derivation for them please let me know.

@heracho Bryan isn't referring to the Goldman equation. I think a paper by Goldman in 1944 is being referred to, which is cited by the HH paper when discussing a lose physical interpretation of their equations for $\alpha$ and $\beta$

@BryanKrause Are the biophysical models these are based on just as explained in the HH paper of a charged particle moving in a constant field? Or are there other models you are referring to?

Basically HH compare their results to Goldman's results for a charged particle, i.e. an ion moving across some boundary; they note that their equations similarly evoke a charged something moving within the membrane, which is both a fairly accurate if abstracted notion of what really happens now that we have fuller models of ion channels, and also makes a whole lot of sense for how you could implement a biological ion sensor. So to @AaronStevens "Are the biophysical models these are based on just as explained in the HH paper of a charged particle moving in a constant field?" - Yes.

@BryanKrause  Thanks for the hint. In H&H 1952: "First, it is one of the simplest which fits the experimental results and, secondly, it bears a close resemblance to the equation derived by Goldman (1943) for the movements of a charged particle in a constant field. Our equations can therefore be given a qualitative physical basis if it is supposed that the variation of $\alpha$ and $\beta$ with membrane potential arises from the effect of the electric field on the movement of a negatively charged particle..."

@heracho Yeah, that's the sentence I was referring to; they also talk about how it doesn't quite fit Goldman (I think in the next sentence, or maybe next paragraph), because the voltages that they fit are not symmetrical. They basically punt and say "we don't know what exactly is going on" which is pretty fair given they are writing this in the 1950s (fair enough for a Nobel prize at least ;) ). I think if you add this comment discussion to your answer and summarize this comment discussion a bit it would be a good answer.

@BryanKrause, I edited trying to summarize the discussion. Please feel free to edit further.


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At what calcium concentration does the Sodium-Calcium Exchanger (NCX) "turn on"?
I am interested in the comparison between the Plasma Membrane Calcium ATPase (PMCA) and the Sodium-Calcium Exchanger (NCX) which are two pumps on the plasma membrane of cells that serve to move calcium out of the cell and maintain relatively low resting calcium concentrations. Typically, I see the statement that the PMCA has high affinity for calcium but a low pumping capacity, whereas the NCX has a low affinity for calcium but a high pumping capacity.
In the literature, I can find relatively simple models of the PMCA as well as data of estimated dissociation constants for it. However, I am having a much harder time finding the concentration of calcium where the NCX becomes relevant. It might be because the NCX also depends on sodium concentrations, membrane potential, etc., which gives rise to much more complicated models. However, there must be some research that backs up the "NCX has a low affinity" claim.
So, what is the typical calcium concentration range where the NCX becomes relevant, such as a calcium dissociation constant where the pump is at 50% of its maximum capacity?

Check https://en.wikipedia.org/wiki/Sodium-calcium_exchanger

@PCM I don't the the answer to my question there.

I'm not sure but I think you will find that these are "always on" pumps, so at any concentration they can be pumping. By relevant you mean physiologically?

@bob1 Good point. More quantitatively, I'm asking about something like a dissociation constant where we would expect the pump to operate at 50%. I know that's a huge simplification for the NCX, but I feel like there should still be some sort of estimate.

I could not find the $K_d$ of NCX proteins in KEGG BRITE, BRENDA, SuperTarget, DrugBank, Uniprot, or PDSP Ki databases...
(Also, I cannot understand the use of the word 'relevant' in the question you asked.)
Still, the requested thermodynamic constants can be found in publications.
Taken from Z.Li et al.(1994)

NCX2 ($Na^+$) : the $K_d$ values for $Na^+$ $(28 \pm 2 mM, n=2)$ are very similar before and after $\alpha$-chymotrypsin treatment and are somewhat higher than those measured for NCX1(e.g. Hilgeman, 1990; Matsuoka et al., 1993)

NCX2 ($Ca^{+2}$) : The fitted $K_d$ values are 1.6 and 1.4 $\mu$M with Hill coefficients of 2.4 and 1.1 respectively. The reason for the shift in the Hill coefficient is unclear.

Also, B.Linck et al.(1998) studied NCX1,NCX2,NCX3 comprehensively. They reported the $K_d$ of these proteins in various situations and environments. These two results seem conflicting... Maybe because they worked on different types of tissues in their studies...
Taken from B.Linck et. al.(1998)

Exchange currents recorded from NCX2-expressing
cells (Fig. 8B) were not as well regulated as those
previously reported from oocytes (22) [=> Z.Li et. al. paper] and were smaller
than those obtained from NCX1-expressing cells.

Looks like B.Linck's paper is much more reliable, though. But I may not share all the graphs of the paper here.(copyright stuff)
I skimmed through the papers, honestly... So feel free to dive into these papers yourself. Cheers!


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Why does UV radiation from the Sun cause skin cancer?
What is the specific mechanism makes non-ionizing UVA and UVB radiation carcinogenic? Can lower energy light, like visible light, be carcinogenic because of this mechanism, or is there some kind of threshold within spectrum at which electromagnetic radiation does not induce cancer in humans?

Ionizing radiation can be mutagenic, which can cause cancer. However, this only applies to high-energy electromagnetic radiation with photon energies exceeding about 5 eV, or about 248 nm. (The FCC defines this threshold even higher at 10 eV, or about 124 nm!) These photon energies correspond to UVC, which is blocked thoroughly by the atmosphere, meaning Sunlight does not appreciably contribute to the ionizing radiation we receive on Earth. Therefore, the mechanism with which solar UV radiation induces cancer must be different from higher energy electromagnetic radiation, right?

https://pubmed.ncbi.nlm.nih.gov/21436607/

Some more useful links: https://pubmed.ncbi.nlm.nih.gov/20883261/ ... https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2564815/

It's not an answer which is acceptable on this site, but the best explanation of the electromagnetic spectrum I've ever seen is ElectroBoom on YouTube. This is in relation to 5G but explains why radio is safe and why UV-C isn't: https://www.youtube.com/watch?v=i4pxw4tYeCU

Rather than 'breaks' caused by high energy radiation, UV radiation causes chemical modifications of the bases ('letters') that make up DNA. There are four bases in the DNA alphabet abbreviated to A,T,G or C belonging to two classes. A & G are guanines while T & C are pyrimidines.
When you have pyrimidine bases next to each other on a DNA strand, they can react to form photoproducts or pyrimidine dimers. These block transcription and replication and need to be repaired by nucleotide excision enzymes (only route in mammals) or photolyase enzymes (plants, many other organisms). TT dimers are the most frequent but dimers with a C cause more trouble as they can be imperfectly repaired causing a transition mutation. If they don't get repaired in time they can cause stalled replication which causes all kinds of trouble and can result in mutations that lead to cancer. You can find more on the wiki page.

There are very many photochemical reactions: Up to 50–100 mutagenic reactions on DNA per second might occur in a skin cell during exposure to sunlight, but are usually corrected within seconds by photolyase reactivation or nucleotide excision repair. (That's just DNA, excluding O2 and other cell constituents)
chemist ref and wiki ref
Molecules that absorb photons can adopt transient excited states whose chemical and physical properties differ greatly from the original compounds.
New chemical species arise, which can cleave, glue in different places, change structures, combine with other molecules. They can also transfer electrical charge, protons and hydrogen atoms, to other atoms.
The elevated states of compounds are stronger acids and reductants than the ground states.
Free radicals from UV have an indirect effect on DNA:

Superoxide is partitioned by the enzyme Superoxide dismutase into O2 and H2O2, eventually giving way to hydroxyl radicals OH.
Hydroxyl radicals can attack the deoxyribose backbone and bases, potentially causing a plethora of lesions that can be cytotoxic or mutagenic.
UV's can also detach iron atoms in the mitochondria, which can breach the mitochondria and cause havoc inside the cell.
Cyclobutane pyrimidine dimers are the most common DNA mutation cause by photons.

Two "T" bases forming thyamine dimer:

it can also be thiamine-cysteine.
UVB is a lot more reactive with DNA, and recent studies find that UVA travels deeper and can also cause CPD dimers.
Photochemistry in cells is a bit like throwing a spanner at a billiard table, reactions can occur with hundreds or thousands of organic compounds, one of those being DNA.
The following is the answer I posted prior to that:
Radiation/electromagnetic waves are an extended version of the visible light rainbow spectrum, which go from radio waves to X-rays and Gamma rays.

The lower energy waves (longer wavelengths) can raise electrons to higher energy levels in the atoms. The higher energy waves (shorter wavelengths) can knock electrons totally off of the atoms, leaving a positively charged atom (a positive ion) and an electron. Since electrons are often shared between two atoms of a molecule like an atomic glue, knocking an electron away can sometimes reconfigure or cleave molecules in two.

The ionisation line is also the Lyman-alpha line, which is the wavelength absorbed by hydrogen atoms, the smallest atoms. All radiation shorter than hydrogen absorption is known as ionising radiation.
https://en.wikipedia.org/wiki/Ionizing_radiation#Health_effects
Some illustrations.

Thank you for updating your answer with the photochemistry specifics! Apart from the fact that UVB is more reactive, how do photon energies play into this? Is there some threshold wavelength at which photoproduct generation begins, or does it drop off logarithmically with respect to energy after the peak reactive wavelength? To what extent does lower energy light than UV, like visible light, cause these reactions, if at all?

Infrared photons transmit 0.001 to 1.7 eV which can change the quantum states of molecular vibrations and temperature, so infrared can accelerate chemistry including events that lead to molecular instability, and the higher energies make electrons jump multiple orbits upwards to where they are less tightly bound. https://en.wikipedia.org/wiki/Hydrogen_spectral_series#/media/File:Hydrogen_transitions.svg ... Search g.images for the "absorption spectra of DNA", i know blue light can damage DNA, https://www.jbc.org/article/S0021-9258(20)61544-7/fulltext I think it's logarithmic, don't know sorry

@aliential Better to write "to higher energy levels" rather than "multiple orbits upwards to" as technically they're not moving in "orbits" or "upwards".

@Armand The average distance of electron orbitals is a good way to illustrate the energy state, because most biologists will be familiar with the atomic orbital schematics rather than average electron radial distance graphs, the average radial distance tends to rise and electron is further away, and the energy level is also said to rise. https://chemistry.stackexchange.com/questions/15208/difference-between-actual-position-of-electron-and-radial-distribution-probabili

Physics/Chemistry aside, as @mimat and @aliential awesomely explained, it's always good to keep in mind that cancer, in general, is a statistics game, in the sense that at any time, there's a cell suffering mutation in your body, and it is not manifesting as cancer simply because your body evolved to deal with those situations.
You can take a walk on the beach normally without any worries about developing skin cancer, just because this acute dose of UV radiation is minuscule in comparison with your expected lifetime. The real problem is the chronic exposition to those radiations, which leads to more chance of mutated cells appearing, and from those, more of them that would suffer mutations in the specific genes that allow them to trick your cell's defense systems and immune response.
Cancer is a very complex pathology that cannot be explained just by one factor (UV degradation of DNA in the case of skin cancer). There's a lot of variables like the individual genetic predisposition, to cite just one of them.


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What kind of insect does chirp like this?
I live in Japan. Recently I hear chirp coming from Wisteria floribunda at every night. Please check this sound that I uploaded for this question.


text:
Is there a survey on whether people have gained or lost weight as a consequence of lockdown?
I am not sure if this is the right forum for asking such a question. Moderators can of course close it if it isn't and please migrate it to relevant site.
Is there a survey/study that statistically checks whether people have gained or lost weight as a consequence of lockdown?
Of course, it would be a complicated as there would be a need for number of controls such as age, usual changes in lifestyle of subjects (independent of lockdown), etc.

Weight is not usually something surveyed. The female part of the population will not answer, half of the men don't know nor care and a good proportion of the rest will answer with a wrong number. Weight is something you really need to measure. I expect that what you are after will come out of controlled studies that measure weight routinely and need to account for the confounding effect of the pandemic.

Thanks for your comment. I have edited the question accordingly.


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DNA and Genes, which consists of which? It seems that the hot answer on quora is different to the nih post
This quora's answer has got 8.3k views and 20 Upvoters.
"Genes are a part of the DNA."
per nih, "Genes are made up of DNA, which is telling the truth."
in my understanding, the quora version indicate that

DNA consists of Genes, and DNA is bigger than a gene, in the context of same living thing, such as a specific escherichia coli.

while the nih version indicate that

Genes consists of DNA, and a gene is bigger than DNA, in the context of same living thing, such as a specific escherichia coli.

did I misunderstand somewhere?

What difference does "part of" and "made of" makes in your mind? How does it change your conception of what DNA and genes are and aren't?

@Remi.b Which one is bigger in your mind, in the context of same species, such as escherichia coli?

Bigger between what and what? The expression "made of" cannot be said to be bigger/smaller than the expression "part of". I don't understand your comment.

Oh did you mean "is DNA bigger than a gene?". The question has bad semantic but anyway... yes DNA is bigger than a gene. DNA is a massive molecule. Specific locations on this molecule cde for proteins. These sequences are called genes.

@Remi.b thanks for your reminder, I've updated the post.

I don't find the text you quote on the linked page. Also, can you add a more informative title for your question?

As @kmm points out,  the quote you include doesn't actually appear in the NIH article you link to. You may want to go back to that article and re-read it. Were you reading a Google Translate version of it by any chance?

DNA is a large molecule which is particular interest relies in the succession of nucleotide that composes it. The genetic information is contained in the succession of nucleotides (I will ignore epigenetics here for simplicity). A given position of any length on the DNA molecule is called a locus.
A gene is typically defined as a protein coding sequence. In other words, a gene is a locus. A gene is not so much a structural element that makes the DNA, it is rather a functional element.

Thanks for your answer. Take this example, AADACL3 on chromosome 1, thanks again for that question, is a gene. in the meanwhile, is it also a DNA? it seem to be not, "DNA basically contains two copies of 23 chromosomes each" from that quora post.


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In a Chromosome, 2 nm is the length of what?
this figure comes from the nature

2 nm at the top right hand corner is the length of what?

DNA is a long, thread-like molecule. 2nm is the approximate width of the DNA molecule.


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Consider gene is countable, can anyone give a concrete example of "a gene"?
gene is a countable noun but people always say genes, so what is A gene?
for instance, Each chromosome contains many genes, so, which part of the chromosome of Escherichia coli could be A gene?

Welcome to Biology.SE! It is expected that you will demonstrate that you have done research on your own before asking questions here — for example you could start with this: https://ghr.nlm.nih.gov/primer/basics/gene ——— Please also take the time to check out the tour: biology.stackexchange.com/tour and then the help pages on how to ask questions on this site: biology.stackexchange.com/help/how-to-ask. Thanks!

There are about 20,000 genes in the human genome. Here are the first 5 genes (following alphabetical order) on chromosome 1:

AADACL3: Arylacetamide deacetylase-like 3
AADACL4: Arylacetamide deacetylase-like 4
ACADM: acyl-Coenzyme A dehydrogenase, C-4 to C-12 straight chain
ACTL8: Actin-like 8
ADGRL2 (1p31.1): adhesion G protein-coupled receptor L2


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What species is this fast-moving spider?
This is a frame from a recent recording:

Location
Forest in Central Europe at around 1pm.
Abiotic factors at the time of recording

Temperature = 23°C
Humidity = 38%
Wind = 6 km/h

Description

Approximate size = ~3 cm including limbs
Semi-transparent limbs and cephalothorax, opaque abdomen
The abdomen presents a pattern which reminds me of the coat pattern in giraffe G. camelopardalis tippelskirchii
its general morphology makes me think it might be part of Pholcidae family but I'm not entirely sure because the height of the abdomen seems a bit too bulbous on the Y axis
web structure rather irregular

Observed behavior
Very short reaction time (dropped a piece of leaf on top of its web), very fast moving spider. I can't provide a better estimation for the speed, but here's is the 3rd frame after the one above (on the previous two frames it just very slightly flexes its limbs):

And one frame later it's already gone.
Internet search

Google image search: no results using the first image you see in this post
Google text search: different sentences like "long-legged transparent forest spider" only returned the usual daddy long legs you can find at home in urban areas.
Finally I tried https://spiderid.com/spiders/ selecting white and brown but none of the displayed spiders matches anything that resembles the frame above.

Any help will be much appreciated. I guess the pattern on the abdomen is key to identify this species but I haven't had a lot of luck while looking for abdominal spider patterns.

Go to iNaturalist and type in "spiders" as well as your country, then go to the species tab and scroll down until you find it.

It looks like a male Linyphiid, most probably a Frontinellina frutetorum

Source: https://ednieuw.home.xs4all.nl/Spiders/Linyphiidae/Linyphiidae.htm
Thanks to John Robinson and Ed Nieuwenhuys who helped get a probable match for this spider.

Pawelek;
Unfortunately, I'm not very experienced at European spiders, but I suspect you're looking in the wrong place.  First of all, this appears to be an adult male spider (large ball-like structures at the ends of the pedipalps, in front of the 'face'), so the body pattern is probably going to be a bit different from the one you see on the females.  Male patterns are often an afterthought in identification references, unfortunately.
Secondly, this doesn't look much like a Pholcid to me - I'm getting more of a Linyphiid impression, from the shape of the abdomen, the visible patterns on cephalothorax and abdomen, and the filmy sheet it's hanging under.
I wish I could be of more help than this - but perhaps Ed Nieuwenhuys can help.  Here's a link to his site; if you look down toward the bottom, there's a contact link you could send him a photo and this question:
https://ednieuw.home.xs4all.nl/Spiders/spidhome.htm

Hi, Pawelek - for some reason, the answer dropped the "Hi," I had put before your name, and it refused to let me add it in later.  Most odd and unfriendly!  At any rate, please don't think I would simply start right in in that brusque fashion.  I'm a grouch, but not an unfriendly one!

Stack Exchange discourages "hi" and such salutation on the post though.

John, I wrote to Ed and he confirmed it is a linyphiid as you suggested. He said it looks like a Frontinellina frutetorum. If you modify your answer to reflect this I'll be happy to mark it as accepted. Thanks for the help!

Hi, Pawelek;  That's a nice offer, but I would feel a bit dishonest if I modified my post to give a suggested species that I don't, in fact, know.  I'm glad Ed gave you a probable ID!

I suggested so because I wouldn't have been able to get such a close match if you hadn't pointed me to Ed's site :) (for which I'm thankful). I'll answer it then for the sake of not letting the question "hanging" after having managed to get a probable match.


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What species is this burrow-digging insect?
These are frames from a recent recording:

Location
Urban area in Central Europe.
Abiotic factors at the time of recording

Temperature = 27°
Humidity = 51%
Wind = 16 km/h

Description

Approximate size = 6 cm 4-5 cm
Elongated shape
Distinctive orange-ish abdominal segment near the end of the abdomen
6 legs
One pair of wings (I think it's very possible that it has two pairs of wings, though, hard to see on the video or pictures)

Observed behavior
The insect seemed to be digging burrows in one of my pots (so far there are 3 holes in one pot and I also saw another burrow in a second pot). Every time I've seen it, it was alone so I assume it's not a social species.
Internet search
I ran these images through google search images and the results were (in order):

hymenopteran
insect
pest
carpenter ant

I think the closest match was the first picture but I wasn't able to get a specific species so I would appreciate any insight from experts on the matter.

That is clearly a type of wasp.  Some digging leads me to think it could be something in the genus Ammophila (a type of "thread-waisted wasp") for example Ammophila sabulosa:

However, 6 cm is huge for a wasp and twice the size of Ammophila sabulosa — are you sure about that length?

The page you linked states 15 to 25mm. https://www.google.com/search?q=Ammophila+sabulosa+ruler&tbm=isch&ved=2ahUKEwiTpMiW562BAxWruCcCHR28BLgQ2-cCegQIABAA&oq=Ammophila+sabulosa+ruler&gs_lcp=CgNpbWcQAzoECCMQJzoHCAAQGBCABDoECAAQHlCxDFjQIGDRImgCcAB4AIABdIgB6wWSAQM4LjGYAQCgAQGqAQtnd3Mtd2l6LWltZ8ABAQ&sclient=img&ei=n-0EZdPYCqvxnsEPnfiSwAs&bih=580&biw=1242#imgrc=mVGVyPlWqFlclM


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What happens to silverfish when we throw them out the window?
I'll find a silverfish from time to time in my flat. I don't mind them but usually I catch them and throw them off the balcony (second story) into the bushes and lawn below.
I was wondering, since they seem to live in the water conduits in the house, if they can survive outside or if they die/get killed instantly.
Thx for your help!

They can definitely survive outside. Remember, houses haven't existed for much of history at all, so what did they do for their ~400 million years of existence before the advent of houses?

Well, they could have lived in caves or next to rivers?

Yes, they can and do, but my point is that they can survive the outside, as you asked.

Are you sure those are silverfish? In my experience, it is quite difficult to catch them alive. I find it hard to believe that you do that regularly.

@Roland Yes, quite sure. I put a glass over them, when they are exposed somewhere and then a piece of paper below. The very young and tiny ones are harder but the adults are fine.

Silverfish prefer high humidity and warmth. Ctenolepismacalvum (Ritter, 1910) was recently found in Japan at a temperature of 20-30°C and 50-60% RH. As long as there are pieces of bark, wet grass or other organic or human-made structures that retain humidity after each raining event, the likelihood that they will survive long enough to complete their cycle is high.
They could face dessiccation if they are not able to find a damp spot in time, depending on their tolerance to it. However, it was not possible for me to find information about their dessiccation tolerance.
The Zygentoma (silverfish order) have high tolerance to low humidity and most of the species inhabit dry and hot environments (it's just a few that like humidity), which again makes me think that those silverfish propelled out the window will survive.

References
Shimada M, Watanabe H, Komine Y, Kigawa R, Sato Y. New records of Ctenolepismacalvum (Ritter,1910) (Zygentoma, Lepismatidae) from Japan. Biodivers Data J. 2022 Nov 3;10:e90799. doi: 10.3897/BDJ.10.e90799. PMID: 36761636; PMCID: PMC9836529.
Kulma M, Bubová T, Davies MP, Boiocchi F, Patoka J. Ctenolepisma longicaudatum Escherich (1905) Became a Common Pest in Europe: Case Studies from Czechia and the United Kingdom. Insects. 2021 Sep 10;12(9):810. doi: 10.3390/insects12090810. PMID: 34564251; PMCID: PMC8471186.
Querner P, Szucsich N, Landsberger B, Erlacher S, Trebicki L, Grabowski M, Brimblecombe P. Identification and Spread of the Ghost Silverfish (Ctenolepisma calvum) among Museums and Homes in Europe. Insects. 2022 Sep 19;13(9):855. doi: 10.3390/insects13090855. PMID: 36135556; PMCID: PMC9505982.


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What are the environmental conditions for larval Haemonchus contortus to survive?
What is known about the environmental limits for Haemonchus contortus to survive outside of a host organism in its larval stages?
I'm interested in knowing:

temperature tolerance levels
preferred humidity levels
pH tolerance
how long can it survive outside of the tolerated ranges?

Lowest temperature
2, 3, 4 and 5 week beakers containing eggs and non-infective larvae in lamb faeces didn't develop into infective larvae (L3) when exposed to fluctuating temperatures ranging from -1 to 15°C:

[...] there were no signiﬁcant differences in the number of harvested larvae
at the different time points for the faeces incubated at 15°C.
However, at 5°C and -1 to 15°C no development of eggs occurred,
although it was found that a small proportion developed into infective
larvae when incubated at 25°C for an extra week.
(1)

Highest temperature

Temperature of 40ºC negatively correlated with the survival rates of
H. contortus L3. [...]
Decreased motility was observed on day 10 after heating. [...]
Heating of L3 at
higher temperatures (45ºC and 50ºC) caused 100% lethality as early on
hour 48 and 24 of exposure
(2)

Desiccation
When it comes to dessication, there are three main things to take into account:

whether the larvae are in exsheathed or ensheathed state matters
they can survive several dessication/rehydration cycles
it is best survived below freezing temperatures

The experiments on desiccation survival showed that, after a few hours
exposure to 47% R.H., all exsheathed larvae died and all ensheathed
larvae survived. (3)

Desiccation protected the larvae against death on storage at
temperatures below freezing, but it was harmful at temperatures above
freezing. (4)

Ruminant larvae were able to survive up to 7 desiccation/rehydration
cycles, and, during anhydrobiosis, metabolic activity was decreased
and survival of the larvae was prolonged both in the laboratory and in
the field. (5)

pH

The effects of temperature on survival and development of the
free-living stages of H. contortus have been studied both by faecal
and by agar-culture methods. [...] with a pH range from 6.5 to 8.5 (6)

How long?
As usual, depends on the current environmental variables and current state of the organism and so forth. Read above sections. The article by P. T. Iliev, A. Ivanov, P. Prelezov has a few tables that can give you a good idea of these times (at least for temperature and humidity).

(1) The development and overwintering
survival of free-living larvae of
Haemonchus contortus in Sweden,
K. Troell, P. Waller and J. Höglund
(2) Effects of temperature and dessication on survival rate of Haemonchus contortus infective larval stage, P. T. Iliev, A. Ivanov, P. Prelezov
(3) Desiccation Survival of the Infective Larva of Haemonchus Contortus,
C. ELLENBY
(4) Effect of dessication on the survival of infective Haemonchus contortus larvae under laboratory conditions,
Kenneth S. Todd, Jr., Norman D. Levine and Paul A. Boatman
(5) Anhydrobiosis increases survival of trichostrongyle nematodes (abstract only),
S E Lettini, Michael Sukhdeo
(6) Trends and Perspectives in Parasitology 2 (page 84),
B. A. Newton


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How often do birds steal from fish traps?
Does anyone have any solid information about how often birds (e.g. cormorants, mergansers, gulls etc) steal fish from any sort of fish trap? Fish traps include, but are not limited to, fyke nets, pound nets, gill nets etc. I'm not looking for info on birds getting caught in the traps, rather any cases where the birds actually take the fish in the trap.
Ideally I'm looking for published articles, but grey literature or any reports are useful.
If you can think of anything more or less suitable, please let me know.

taken that fish and fishtraps are under water it is unlikely that birds can open a trap under water.

@trondhansen Cormorants and mergansers at least do their hunting under water normally. These are not necessarily closed traps that need to be "opened"; I'm not familiar with all of them but a gill net for example is a net where the fish swims partway through and then gets stuck past the gills, so that they cannot move forward (body too big) nor backward (gills caught). There's a half of a fish sticking out either side.

@BryanKrause i was unaware that a fishing net can be seen as a trap,but atleast i now know  the definition of a trap.maybe this question can be narrowed down by focusing on just a few types of traps.birds do take fish from nets every single day and many birds get trapped in the nets and drown.

@trondhansen OP specifically listed the sort of instruments they are considering.

@trondhansen, Could you provide any reasearch or reports about birds taking fish from nets? Especially if you have info on the amount of fish taken and what species of birds took it.

I think that would be a pretty nice line of research. Thievery in birds (corvidae and psittacidae especially) has to be well documented. However, something as specific as what you're asking seems hard to find with some initial research. I'll try to give it a shot tomorrow.

@pawelekzzz Thnaks, I appreciate it. I've been looking for a while now, but with no luck.

Since kleptoparasitism, that is, stealing food from other entities that have procured that food earlier for themselves, is a widespread strategy in animals, it is no surprise that birds also engage in this kind of behavior (up to 856 accounts of some sort of interspecific thievery). Food stealing skills is even related to parental quality in Sterna dougallii. Honest parents had lower productivity. Additionally, in parrot-owner behavioral problems dynamics, stealing human food got a 2.34 in a 5-point Likert scale where 5 = always.
On top of that, theoretical ecology tells us that behavioral dynamics are characterized by a cooperation/conflict tension where a behavior such as theft may thrive (while also depending on many other factors, e.g.: larger thieves tended to get the highest payoff, and bear in mind size is but one factor). So I think a bird will maximize stealing if the opportunity is present to it and whether it's physically capable of doing it.
In Larus argentatus, head turns, approaches, and angular body position were three behavioral markers identified in an ethogram to measure attention to anthropogenic food-based contexts. I think this article is the one that is key to your question, considering how difficult it is to find statistics for how often thievery from anthropogenic sources happens. It is key, because combined with theoretical ecology, and the amount of bird intelligence research nowadays, it shows intuitively that birds will probably steal from human fish traps 1) if they have knowledge about it, and 2) as much as they can.
Anecdotally, birds, (both known and unknown to me) have also stolen from me several times in varied environments (many of them could be considered "traps" or at least "food containers that require a certain degree of skill to operate or get to"), but not fish traps.

References
Anne Tygesen & Björn Forkman (2023) The Parrot–Owner Relationship and Problem Behaviors in Parrots, Anthrozoös, DOI: 10.1080/08927936.2023.2238434
David A. Shealer, Jeffrey A. Spendelow, Jeff S. Hatfield, Ian C. T. Nisbet, The adaptive significance of stealing in a marine bird and its relationship to parental quality, Behavioral Ecology, Volume 16, Issue 2, Mar./Apr. 2005, Pages 371–376, https://doi.org/10.1093/beheco/ari008
Feist F, Graham P. An ethogram identifies behavioural markers of attention to humans in European herring gulls (Larus argentatus). Biol Open. 2023 Jun 15;12(6):bio060016. doi: 10.1242/bio.060016. Epub 2023 Jun 13. PMID: 37309817; PMCID: PMC10281265.
Hadjichrysanthou C, Broom M, Rychtář J. Models of kleptoparasitism on networks: the effect of population structure on food stealing behaviour. J Math Biol. 2018 May;76(6):1465-1488. doi: 10.1007/s00285-017-1177-7. Epub 2017 Sep 18. PMID: 28921258; PMCID: PMC5840298.
Morand-Ferron J, Sol D. and Lefebvre L (2007) Food stealing in birds: brain or brawn? Animal Behaviour, 74, 6, 1725-1734. https://doi.org/10.1016/j.anbehav.2007.04.031
Phillips JA, Peacock SJ, Bateman A, Bartlett M, Lewis MA, Krkošek M. An asymmetric producer-scrounger game: body size and the social foraging behavior of coho salmon. Theor Ecol. 2018;11(4):417-431. doi: 10.1007/s12080-018-0375-2. Epub 2018 May 1. PMID: 30931016; PMCID: PMC6405016.

Thanks, I'll look into the references you provided


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Protocol to transform _Staphylococcus aureus_
I'm working on transforming Staphylococcus aureus and I'm
totally lost on bypassing the RM systems. I have a plasmid already constructed, but I think I want to pass it through DC10B E. coli so that it loses its methylation and is staph-compatible.
Let me know if this is a feasible plan. Are there any known protocols for this task?

I'm not particularly familiar with S. aureus genetic transformation protocols, but it looks like a quick search reveals some articles related to the topic.


text:
If blood vessels mostly aren't supplied by parasympathetic nerves, how effects through M3-ACh receptors are mediated?
Blood vessels throughout the body mostly aren't supplied by any parasympathetic fibres. But the effects of ACh through M3-ACh receptors would infact release NO (which acts on VSM and causes vasodilation), which is demonstrated after ACh intravenous administration.
My question is how is it physiologically mediated? (i.e. the ACh mediated vasodilation)
*VSM= vascular smooth muscle
*NO= Nitric Oxide
*Ach= Acetylcholine
*M3 (Muscarinic type 3) Acetylcholine receptor

ACh=acetylcholine? NO=nitric oxide? M3-ACh? Might be useful to spell out acronyms/abbreviations the first time you use them (I see you have VSM at the bottom), since odds are the average user of this site is not in your field

Thank you! I've edited the question.


text:
Myelination of 1st Order Neurons in Spinal Cord Ascending Tracts
When a 1st order sensory neuron enters the Dorsal Column Ascending Pathway (i.e. Spinal Cord), does it get its myelination from Oligodendrocytes (as inside CNS) or it retains Schwann Cell myelination?

Is anyone at least up for a discussion?

Welcome. I think this is a great question. What have you found so far?

I haven't come across any text addressing this issue. But I think when the 1st order neuron enters the spinal cord it should retain Schwann Cell myelination (Considering Embryological Origin). But it contradicts with the statement that inside CNS oligodendrocytes myelinate Neurons. :(


text:
Why severely increased Ligand (eg Hormones) concentration downregulates the Receptor?
As an example continuous high blood level of GnRH in humans causes a suppression of LH and FSH. This is due to the fact that increased GnRH downregulates GnRH-Receptors . My question is how this is done and why? What are the probable molecular mechanisms underlying this effect?

Kumar P, Sharma A. Gonadotropin-releasing hormone analogs:
Understanding advantages and limitations. J Hum Reprod Sci.
2014;7(3):170-174. doi:10.4103/0974-1208.142476
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4229791/

Hi A.N. Ψ, Could you provide more resources on continuous high blood level of GnRH in humans causes a suppression of LH and FSH? Or on the fact that increased GnRH downregulates GnRH-Receptors?

Go through the paper. I have added it to the Question

Gonadotropins are hormones synthesized and released by the anterior pituitary gland, which act on the testes and ovaries to increase the production of sex hormones and stimulate production of either sperm or ova.
The hypothalamus contains Gonadotropin-releasing hormone (GnRH). Intermittent released of GnRH is responsible for the biosynthesis and secretion of follicle-stimulating hormone (FSH) and luteinizing hormone (LH) from the anterior pituitary gland.
LH stimulates interstitial cells to release testosterone, which triggers spermatogenesis. The rising level of testosterone exerts negative feedback control on the hypothalamus and pituitary glands.
GnRH has been shown here in a negative feedback loop
This feedback loop has great interplay with the number receptor levels as you suggest.
(From a quick search) I found one paper (behind a paywall) that states the following information when studying rats:

We observed an acute reduction of both GnRH and GnRH-R mRNAs 24 h after the injection [of GnRH agonist (triptorelin)] (about 38% of control).

Transcription does not equal translation, but it seems that acute increased levels of GnRH cause a reduction and mRNA of GnRH and GnRH-R and therefore potential reduction (down-regulation) of protein levels of GnRH-R.