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Is this a bed bug? I found it crawling on me in hotel bed
Is this a bed bag? It doesn't have the stripes that I saw in other pictures. I'm traveling and for 5 days I was sleeping in different hotel rooms. What should I do if it is. I searched the bed and found no more.

Nope - it's a tick! If you can get a better photo I can tell you what species - dorsal and ventral surfaces, ideally.

Although probably an Ixodes, I suspect.

Since it's a tick, I would search on your skin, not in the bed. (Meaning: my first priority would be to make sure none of those beasts were attached to my body).

You should check that you haven't been bitten as some (not all) are know to carry Lime disease (http://www.nhs.uk/Conditions/Lyme-disease/Pages/Introduction.aspx)

As already stated in the comments the animal you found is a tick (Wikipedia).
Since they are known to carry diseases you should make sure you have not been bitten or even still have one sucking your blood. So search your body. If you happen to find one still attached, do NOT squeeze it as this may stimulate fluids to flow from the tick into your body (bad). Instead get it out asap using tweezers or even better specialized tools. If you can't do it yourself ask another person preferably a doctor.
If you have been bitten watch for symtoms of an infection such as a red circle. If in doubt always see a doctor since you might require antibiotic treatment.
NOTE: usually nothing happens so don't worry too much but be alert for changes in skin around bites (if bitten that is).
EDIT: since hotel beds are not a typycal habitat of ticks you probably carried it there yourself.

I think it should be mentioned that hotel rooms are not their typical habitat. It's likely that the tick was transferred to the bed from OP's clothes.

Btw., the most dangerous infection would be tick-borne encephalitis which unlike Lyme disease can't be treated. So, prevention (i.e., apart from vaccination, early removal of the tick) is important.

Ticks need humidity to survive, they often just climb onto a leaf or some grass when it's 17-23C degrees and jump on animals passing by. An interesting biological fact is that young ticks that have had a lizard host absorb the lizards lyme antibodies and have far less lyme desease later when they bite a bigger animal.


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Why are the human knees and elbows bent in an opposite direction
I can assume that the hands used to be the same as legs. And they got weaken, and changed direction when human started to walk on two?
Also why do the hand palms facing the body and not facing down like the feet?

What research have you done on this so far?

I just found an article talking about god creation, this wasn't what I was looking for. And I still need to read about why human walk on two.

Do you want to know evolutionarily why or developmentally why knees and elbows point in opposite directions? The latter question is more easily answered.

Your assumption is wrong, hands were never the same as legs.

I am no expert on comparative anatomy, but I will give this a shot. Please edit if you know more about this subject!
The configuration of opposing elbow and knee joints is a feature we humans share with large group of mammals. For example, below is an image of a shrew skeleton.

Opposing joints are course a major feature of mammalian anatomy, and there are many studies on its functions and advantages. Among other things, this configuration allows for characteristic gaits of mammals such as the gallop of a horse, and it allows mammals to rest with legs protected under their body. See this page for some basic information.
Neil Shubin's book Your Inner Fish on human evolution also discusses the opposing joints arrangement, noting that this is a "key feature that gives us the capacity to walk, one we share with other mammals". A preview of the book is here.
A quick literature search turns up many technical articles on this subject, such as this review series. I'm afraid the details are beyond me (again, experts please edit), but I think it's fair to say that there is plenty of evidence for advantages of this joint arrangement in mammals.

Good answer+1 Would be great to have answers to the following question: Do we have an ancestor having knees and elbows bending in the same direction? (2) Did joint on forelimbs and hindlimbs evolved simultaneously? Do they use similar metabolic pathway? (Might be worth eventually opening a new post for these)

@Remi.b I'd add any other mammal species, not only direct ancestors.

you can add any other terrestrial vertebrate, not just mammals.

Unfortunately, your question isn't clear. "Why" could mean different things. What course of events led to it? What benefits does it provide? We could just say, it's not disadvantageous this way, so why not. So perhaps you could clarify.
Evolutionarily, through the stages as our ancestors evolved from small mammal to human, the changes that occurred were sufficiently suitable for the species. The joints are oriented well enough for walking, running, and holding things, and there doesn't need to be more reason. As for the hands, they point away from the arms like they do in other great apes. The difference is that in humans, the feet have a hard time pointing down since they are never used as hands, and hands have a harder time pivoting to be perpendicular to the arm because they are never used as feet anymore. Because of these behavioral differences from other great apes, variations that helped feet be used as hands and hands be used as feet were not selected for, but variations that reinforced walking and running ability and that reinforced object manipulation were selected for.

Good answer. What i meant was that i expcted the 4 limbs to be identical since they all were used for walking. But I got already other good answers here that explained it.

@RonenFestinger Okay well then I guess you have your answer. You might also be interested in asking an engineering or mechanics question about it, as tetrapods walking robots often have front and back joints that are mirror opposites of each other. You might also be interested in asking a question of why other animals have opposite front and back joints. What you should keep in mind is that although front and back legs are all used for walking, they don't have identical functions. Back legs might spring more, front legs might pull more and grab prey more.

It's an amazing question, really. And you might be right about your assumption. In the womb, our legs and arms bent in the same direction. But as the foetus continued to develop, the legs and arms rotated to bend in opposite direction (to each other). As of now, there is no rational explanation as to why this happens.
So I guess all we can do is be grateful to the way our bodies have come into being. If, for instance, our knees bent backward (just like our elbows), our legs would bend forward like our arms and we wouldn't be able to walk the way we do. Apply the same to the arms and we'd be lifting things in an entirely different way, and backwards too! Also, we won't be possessing the ability to write.
You can check out this page for more info:https://answersingenesis.org/human-body/your-legs-are-on-backwards/

Thanks. That's what I found too before asking this question. But I was looking for a different answer than god created it this way.

Well I'm sorry I couldn't be of much help, because there is no scientific theory to explain this as of now. You can always do research on it, though.

"there is no scientific theory to explain this" --- this is clearly not true. See my answer for some basic information and pointers.

When exactly are they bent the same way? http://www.parents.com/pregnancy/what-my-baby-looks-like/ And even if they would change orientation in development, that would mean nothing about God, it would mean something about evolution. For example, turtles in development start out with rib cages, like the reptiles they evolved from, and the rib cages fuse into a shell. This is actually evidence for evolution, because if animals were created separately, it would make no sense to make a rib cage and change it later. Please do yourself a favor and un-brainwash yourself with actual science websites.

I arrived here four days ago. And not to parade my belief in God (I don't see life that way), but to get better, more informative answers of scientific questions. So if you think I blindly swallow whatever's fed to me, I'm sorry. I don't. Or else I wouldn't be here. This was my first answer on this site, and now that I'm here, I look forward to add substance to it. And ironically, your link above doesn't happen to be an actual science website either, so kindly practice what you preach. (I don't mean any offense.)

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What are these tiny insects?
I live in Italy (Emilia Romagna), and my house, seasonally in spring, is full of these guys, someone knows their name and if they could represent a problem?
They are very tiny slightly less than 0,5 cm including the antennae.

It could be Anthrenus verbasci.
These insects are not dangerous, but they can damage carpets, clothing and furniture.

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Cleanliness of cast iron never cleaned between meals
Cast iron cookware has unique benefits. One difference between cast iron and most other cookware is that many people advocate for not cleaning it with any soap between uses, because the soap can degrade the seasoning which protects it. I wonder, how hygienic is that?
The way I understand it, the seasoning on cast iron cookware is a smoothed layer of polymers that prevents food (and bacteria) from contacting and sticking in the iron cookware. Simply scraping it clean, maybe rinsing with some hot water briefly and drying off immediately after, is generally considered enough to 'clean' the cookware.
How is it that bacterial growth on the cookware is never a problem, given they are not washed with soap for long periods of time? I'm under the impression that most kitchenware - pots, pans, dishes, utensils - are susceptible to bacterial growth that could make you sick or transfer illness if you eat with them and don't properly wash off all the food, oils, etc. that gets on them. Does the layer of polymer on cast iron protect it from such growth? The main question here is: Does other cookware really need soap any more or less than cast iron to be used hygienically, and why or why not?

I think we could argue a negative here.  That is, if not washing cast iron cookware was unhealthy, there'd be a lot of sick people :-)

Soap or detergent does nothing to kill organisms. Instead each detergent molecule has two ends, one being hydrophobic (meaning it's repelled by water) and the other end is hydrophilic  (attaching the end to water). When anything is washed with soap or detergent, the oils and dirt on the object - whether it's a dish or your hands - can combine with water as an emulsion and be rinsed away.
Dishes and utensils are only susceptible to bacterial growth if there's traces of food on them. Washing is meant to remove traces of food and oil so bacteria can't multiple on them. The conditions must be right for bacteria to multiple. If traces of food were to be completely dry and hardened on a dish and someone ate off it, the likelihood of any bacteria present on it is close to nil. They need moisture to grow. If dishes had no oily food on them, washing and rinsing with very warm water would be sufficient. I've seen people from other cultures wash dishes with traces of food that are soluble in water. They come out perfectly clean. (As an aside, using a tea towel can often spread bacteria when they're not used properly.) Towels top kitchen contamination hazards list
Bacteria can't multiple in oil. For example, ordinary cooking oil doesn't need to be refrigerated although it can go rancid. A cast iron frying pan is properly meant for frying foods only. No watery sauces should be cooked in them. Even "scraping it clean" shouldn't be done with a sharp metal object as it can remove some of the polymerized hardened oil layer.
I have several cast iron pans that I don't wash. I wipe them out after each use, then I add a little oil nd roughly a teaspoon of salt. With a paper towel, I rub at any bits of stuck on food. If done within a few hours of being used, it effectively removes any food traces, leaving a smooth surface. I usually rinse off the salt in warm water, dry it and then apply a very thin film of oil. I've been cooking in cast iron pans for decades and have never gotten sick or had mild food poisoning (what many people call a 'stomach flu').
Cast iron pans with a layer of proper seasoning and treated like this will definitely not cause sickness. It can't support bacterial growth and as @jeanquilt mentions, the pan gets very hot - enough to blister your skin if you touch them with a bare hand.

'Soap or detergent does nothing to kill organisms.' is incorrect - see https://biology.stackexchange.com/q/39894/1320

@Jude can the alkaline pH of soap or detergents not cause any damage to microbes?

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What are these?
theses are swarming my truck in area southwest of meeker co

Welcome. Do you mean Meeker, CO, USA? Can you add details about when this picture was taken and provide us with some size measures (how large the insects are)?

Looks a lot like a flying ant to me. All criteria met.


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What does testosterone do in a womans body?
I recently took a blood test and had low testosterone. I am looking for information about testosterone in a woman's body.

This is very broad. Googling 'effects of testosterone in females' will give you plenty of info that covers the basics. Is there something specific you're wondering about? Better, on topic questions provide evidence of your own research (quote and link) and a specific question (e.g. testosterone and bone strength) which can be done with an edit. Also, your doctor is the person to talk to about your health, as it's personal and specific to you/your situation. Thanks.


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The minimum oxygen pressure in the synovial fluid of a human joint
It would be greatly appreciated if you would let me know the minimum oxygen pressure in the synovial fluid of a human joint that is considered "physiological" in millimeters of mercury.


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What insect is this ? Is it bed bug or anything else?

This is found in my bed. I have red and some black bumps with itchy rash from last 15 days.

Not a bed bug. Looks beetle-like to me, but not enough detail in the picture for a positive ID.


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Telomere length and cancer
I've been listening to Bret Weinstein talking about telomere length.
He seems to say that long telomeres provide useful tissue repair capacity when young, at the expense of reduced cancer resistance later in life. The has the evolutionary result that short lived creatures have longer telomeres because they do not live long enough to pay the price of cancer later.
This raised a couple of questions in my mind.

If long telomeres meant higher cancer incidence wouldn't we expect to see more cancer in youth than in old age? As I understand it an individual's telomeres get shorter as time (cell division) progresses.

I thought that cancer had some mutation that produced telomerase and so cancer made its own longer telomeres, regardless of the initial length. I cannot see the connection between initial telomere length and cancer probability.

My own observation, unsullied by rigorous research, suggest that cancer works like a lottery throughout life, the longer you live the more likely you are to get it.

You state: "The has the evolutionary result that short lived creatures have longer telomeres" -  Mr Weinstein, in fact correctly states the opposite.

The risk of cancer increases with age largely because it usually takes multiple mutations in order for a cell line to become cancerous. For example, a cancerous cell might have separate mutations that allow it to evade apoptosis, to repair its telomeres, and to divide rapidly. These mutations can accumulate with age until eventually, a pre-cancerous cell acquires the final mutation that makes it cancerous.

As Jiminy Cricket correctly says above, I got that the wrong way around. This makes a nonsense of my first question and I am sorry to have wasted your time.

Perhaps Eonema answered my second question. Given that cancer requires multiple mutations longer telomeres gives those mutations a better chance to accumulate.

There's also what happens when you run-out of telomere; the chromosome starts to unravel and senescence arrives with an increase in metabolic failure of the tissues concerned.


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What do groundhogs and other subsurface-tunnel dwelling creatures do in heavy rains to avoid harm?
I notice groundhogs and many other tunneling creatures in my yard, the same yard which became pretty flooded during heavy rainfall. I don't see wildlife out during rain storms, but not long after, they emerge and return to their regular daily behavior.
What do the creatures living in tunnels underground do to avoid harm from flooding? The kind of harm I imagine them being susceptible to is drowning or damage to their tunnel. It could be that their tunnels get destroyed and they simply dig their way out and make a new one, in which case the only remaining question is how they avoid drowning while sheltering underground from storms. Even that question may be moot if they don't in fact shelter underground from storms, but instead shelter somewhere less susceptible to inundation like up in a tree.
I originally had groundhogs in mind with this question, but if possible, I'm interested in answers that apply to various tunnel dwellers: groundhogs, chipmunks, ants, ground wasps, etc. I know many ground-dwelling insects live there for the moisture it provides, and during storms they'll come to the surface to enjoy the moisture there and avoid drowning (e.g. slugs, worms), but I don't think this applies to all insects and certainly doesn't apply to mammals who generally seek shelter from the rain.


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Why so fewer birds in the yard come late summer and early autumn?
We've enjoyed watching birds in our yard this past summer. We're in a suburb, fairly forested, inland northeastern USA hardiness zone 5. As we scaled up the amount of diversity and net primary production around the house, and added a bird feeder, we notice an uptick in various kinds of wildlife. However, we're surprised to see a stark decline in the amount of birds starting around late summer/early autumn.
What could cause the sudden decline in birds in late summer? Is there a migratory trend starting up around this time; it seems early to me for birds to be flying south?
The birds in question include a family of cardinals, occasional blue jay, downy and hairy woodpeckers mid-summer (some are still around), many various sparrows, yellow finches, chickadees, et al.
We continue to fill the bird feeder as usual. We haven't changed anything about our yard routine. We have a rescued feral cat which goes outside and hunts despite our efforts to stop it, and it has killed many mice and a few chipmunks mid-summer, so perhaps the birds have become wary of him and the dead bodies of small mammals left in forested edges around the yard.

One possible cause is Cooper Hawks. We are in east TX and put out a lot of seed ; we had more birds. Fewer in recent months due to the Cooper Hawk(s). Our yard is a buffet for them ,I hear them often, see them occasionally ;they will perch in the under story.  And we hear birds hit the windows as they panic from the hawk ; it happens 0 to 4 times a day. The hawk has developed a technique of diving and after the small birds when they knock themselves out on the windows , the hawk walks on the patio to pick one up. I have been going out after a bird strike and picking up stunned birds and put them in a shoebox for 30 minutes. They usually recover, had a cardinal yesterday. If you are home during the day , listen for window strikes and watch for sudden flights of all the birds. The Sharpshin Hawk is also here but not a problem.......... And there is a degree of randomness to migrations: Some years we get many Goldfinches, Pine Siskins, Robins, and some years a few or none. And birds like Cedar Waxwings are notorious for their unpredictable movements.


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Have there been any efforts to release opossums as a biological control against ticks?
There's plenty of examples of people recognizing opossums as a great ally in controlling tick populations (here's one example). However, I can't find any examples of opossums being intentionally released or supported in areas specifically to control ticks.
Have there been any efforts documented that deliberately increase opossum populations to reduce tick infestations? If no, are there specific reasons why this has not been done? For the latter, there are of course examples of biological control gone wrong (e.g. cane toads released in Australia), but that doesn't seem to deter all biological pest controls (e.g. nematodes to control fungus gnats).

I think you have given the answer yourself. Opossums can be agressive predators, intentional release in new area's is simply an extremely bad idea from a ecological point of view.

@RHA that's certainly a reason why no one would try this. I wanted to check if anyone has tried it or there's been any serious consideration of it. Maybe it's simply too crazy and no agency has given it serious thought.


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The human has 46 double chromosomes or simple chromosomes?
What I mean: does the human cell have 46 of these:

or 46 of these:

Thank you in advance.

Are you asking about the actual structure of chromosomes ?

the second one. 23 pairs.

Do you mean single chromosomes in your title?

Your first picture shows a chromosome that has been (1) condensed and (2) undergone DNA replication. During G1 interphase (normal cell activity; not dividing), your chromosomes actually do not look like either of the pictures. They look more like a mass of noodles (called chromatin; look at the image provided below); it is only during prophase (step 1 of mitosis, where the cell undergoes division) that the chromosomes condense into the form you have depicted in picture 1. Now, in G1 interphase, you only have single chromosomes. You have 46 of these, which can be grouped into 23 pairs—23 from your father, and 23 from your mother. Remember they aren’t condensed during this stage.

I have also included a diagram of the cell cycle:

In S interphase, DNA undergoes replication, and each of the 46 chromosomes create a double. This double sticks to the original chromosome at a point called the centromere. So long as the two “chromosomes” are conjoined at the centromere, the two “chromosomes” are considered as one chromosome, consisting of two sister chromatids (each like the “single chromosomes” you had previously). Again, in S interphase, chromosomes are not condensed, and look more like noodles than either one of your pictures.
During prophase, the chromosomes look like picture 1. Picture 2 depicts a sister chromatid during prophase (and metaphase), which is considered a chromosome after anaphase (when the two sister chromatids are separated from their centromere). Remember that when the chromatids are not conjoined at the centromere, they are considered each as their own chromosome.
Thus, the human body always has 46 chromosomes. They are “double chromosomes,” as you call them, during S phase of interphase to the beginning of anaphase of mitosis. They are “single chromosomes” from anaphase of mitosis to the beginning of S phase of interphase. As most cells spend the most time in G1 interphase (normal activity), you can say that most of the time their chromosomes exist as single chromosomes. Again, note that most of the time they don’t look like your pictures, except for the times that I mentioned above.

EDIT: To answer the question in your comment:

If during interphase the DNA is not yet condensed and looks like a mass of noodles, then how can we know that there are 46 chromosomes (single ones in this case)?

During interphase, it is indeed difficult to tell how many chromosomes there are. It is only when they condense that they become visible to the eye and can be observed through a microscope. Chromatin, in its noncondensed form, is considered as euchromatin—that is, true (noodly) chromatin. When it is condensed, it can be referred to as heterochromatin. We can only count the number of chromosomes when they are in heterochromatin form; euchromatin is invisible to us. If we align all the chromosomes present, we will get something called a karyotype. Look below.

(You can see each chromosome in each of the 23 pairs are “double chromosomes.” These chromosomes were likely documented during prophase. Some karyotypes show "single chromosomes," most likely taken during anaphase or early telophase.)
In any case, double or single, we can observe that there are 46 chromosomes at all times. If we see "double chromosomes," we would find 46 chromosomes. If we see “single chromosomes,” we would still find 46 chromosomes. In both cases, we would find 46 centromeres, and ergo, 46 chromosomes.

References

Reece, Jane A., Lisa A. Urry, Michael L. Cain, Steven A. Wasserman, Peter V. Minorsky, and Robert B. Jackson. "The Cell Cycle." Campbell Biology. 10th ed. Glenview: Pearson, 2014. 232-50. Print.
https://micro.magnet.fsu.edu/cells/nucleus/images/chromatinstructurefigure1.jpg
http://www.everythingmaths.co.za/science/lifesciences/grade-10/03-cell-division/images/d62a6708a4a3942f21e003500ddf9664.png
https://study.com/cimages/multimages/16/karyotype_karyogram.png

Can you please add some citations (even wiki links will work), especially for the images you used?

Thank you! However, I don't quite understand this: If during interphase the    DNA is not yet condensed and looks like a mass of noodles, then how can we know that there are 46 chromosomes(single ones in this case)?

@MattDMo I have redacted my answer.

@Diego I have made an edit to my answer to answer your question.

The first picture you posted represent a pair of chromosomes. The second one represent a single chromosome. Humans have 46 single chromosomes that can be paired in 23 pairs. In this picture, https://en.wikipedia.org/wiki/Chromosome#/media/File:NHGRI_human_male_karyotype.png, you can see the 46 human chromosomes grouped in 23 pairs. Note that the last pair is formed by different chromosomes, X (the long one) and Y, so you are looking at the chromosomes of a male.

Answer: Both are images of chromosomes. Before a cell divides, we have 46 structures of Image 1. After cell division, we have 46 structures of Image 2 in each daughter cell. They are structures of chromosomes at different phases of cell division.
When the human cell is not dividing we have Interphase, during which chromosomes inside the nucleus look like a network of threads, called chromatin.
Cell division takes place in four phases,abbreviated: P-M-A-T

Prophase: during which stage the chromatin condenses and duplicate themselves. each of this is two chromatids attached at the centromere.

Metaphase: the chromosomes align themselves at the equator
Anaphase: The chromosomes are pulled towards the two poles, each at opposite ends of a cell. Each of this is a single chromatid.

Telophase: contractile ring (a cleavage) starts to separate the two daughter cells.

@Bantu Manjunath - I know a term for it . It's called "chromatid". If it simplifies your answer , you can use it.

When a cell isn't dividing , the DNA is decondensed. So, you can't say what type of chromosomes are present in non-dividing human cells.
But just to clarify ; it can be said if a human cell's DNA condenses into chromosome(without replication) , it will look like 46 chromosomes of image 2.
If it condenses after replication,  it will look like 46 chromosomes of image 1.
And to clarify your next doubt of what's a chromosome-
A chromosome is a structure with centromere present in it. It can have many chromatids in it .
For eg- both of your images are a single chromosome.  The 1st image has 2 same chromatids in it and 2nd image has one.
A chromatid refers to a single DNA molecule.


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How do heredity and regression to the mean work with respect to intelligence?
I am trying to understand the heredity of intelligence between generations in general, and how regression to the mean works in detail in particular. The answer I'm looking for should preferably answer some of the following questions.
When looking at the genetic basis for intelligence, it seems to me that the additive contribution of the genes should not be subject to regression to the mean, and that regression to the mean should rather be due to recessive genes and emergenesis. Is this correct? If so, what do we know about the extents to which these two mechanisms contribute to intelligence?
Towards which mean will a specific child be expected to regress? I have seen various suggestions here, ranging from the mean of the racial groups of the parents, to that of the child's grandparents.
Is it even possible to write down an (approximate) equation for the expected intelligence of a child, in terms of for instance the intelligence of parents, siblings and gransparents?
If someone coould answer these questions, that would be awesome!

I don't think you need this question to be specific to intelligence - you are asking really about regression to the mean and additive genetic variation as a general problem

As @rg255 said, this question has not reason to be specific about intelligence. I think the question is on-topic and not too broad but a very good source of information is the chapter "quantitative genetics" in A short guide to population genetic by Gillespie.

Thank you for your comments, and the reading suggestion. I agree that parts of this question could be answered in a more general framework, but for instance our knowledge of additivity vs emergenesis could be trait specific, no?

Your comment make me think that you might want to start by reading the definition of heritability (see this post). I never heard of the term "emergenesis" before. Reading from wikipedia, it seems to be the equivalent of what we call epistasis in biology. I will try to formulate an answer a bit later today.

I think the question mainly highlight either of two misunderstandings:

misunderstanding about the definition of heritability
misunderstanding why the slope of the regression line is equal to heritability (in the narrow sense).

Definition of heritability
Please have a look at the post Why is a heritability coefficient not an index of “how genetic” something is?.
Notation
Please note that, here I use $h^2 = \frac{V_A}{V_P}$ to designate the heritability in the narrow sense, where $V_A$ is the additive genetic variance and $V_P$ is the (total) phenotypic variance. If anything of what I just said is unclear, please refer to the aforementioned post.
Without any loss of generalization, we will set our scale so that the average phenotype in any studied case is equal to zero. From this starting value, we note X (with a subscript) the contribution of a given haplotype (or allele) to deviate the phenotype of an individual. We will note $E$ (with a subscript) the contribution of a given environmental state to deviate the phenotype of an individual.
An individual phenotype
Let's consider an individual O (stands for offspring, it will makes sense later). The phenotype of this individual is given by the addition of the contribution of each haplotype and of the environment. The expected phenotype of O (called $P_O$) is therefore
$$P_O=X_m + X_p + e_O$$
, where $X_m$ is the contribution of the maternal haplotype, $X_p$ is the contribution of the paternal haplotype and $e_O$ is the contribution of the environment.
Just a note
It might be worth skipping this note and coming back to it once you understood the below calculations (but I did not want to move this note to the end).
In the above calculation, one must assume absence of epistasis and dominance effect. I am not exactly sure how this might eventually cancel out later or whether results would then differ. I would welcome a follow-up in the comments to clarify this point but it might be worth its own post. As the question refers to the heritability of intelligence (assuming this term is defined), I would like to highlight that it is unlikely that we have much understanding about the exact pattern of epistasis underlying this trait as measure of epistatic interaction are often difficult to achieve.
Phenotype of O's parent
Let's note $P_P$, the phenotype of one parent of O'. The below notation applies to the mother but calculations would be the same for the father.
$$P_P = X_m + X_m' + e_P$$
, where $X_m'$ is the haplotype of the mother that has NOT been transmitted to the offspring and $e_P$ is the contribution of the environment experienced by the parent (mother).
Covariance between $P_O$ and $P_P$
The covariance between $P_O$ and $P_P$ (noted $cov(P_O, P_P)$ is just the sum of the covariances of all contributions, that is
$$cov(P_O,P_P) = cov(X_m,X_m) + cov(X_m,X_m') + cov(X_m,e_m) + cov(X_P,X_m) +\
 cov(X_P,X_m') + cov(X_P,e_m) + cov(e_O,X_m) + cov(e_O,X_m') + cov(e_O,e_m)$$
I let you take a few minutes to think about the values of each of these covariances.... They are almost all equal to zero (are independent). There are only two covariances that (under a simple model) can potentially be different from 0; $cov(X_m,X_m)$ and $cov(e_O,e_m)$. $cov(e_O,e_m)$ is teh correlation between the environment experienced by the mother and the one experienced by the father. For simplicity, we will make the assumption that these two environments are independent and therefore $cov(e_O,e_m)=0$. The above, long and hairy equation therefore reduces to
$$cov(P_O,P_P) = cov(X_m,X_m) = var(X_m) = \frac{V_A}{2}$$
Correlation between $P_O$ and $P_P$
By definition the correlation (which is the slope of the regression line) is just the covariance divided by the total phenotypic variance. Therefore the correlation between $P_O$ and $P_P$ (noted $cor(P_O,P_P)$) is
$$cor(P_O,P_P) = \frac{V_A}{2} \frac{1}{V_P} = \frac{h^2}{2}$$
Generalization to any correlation
Following the above logic, one can show that in general the correlation between any two individual phenotypes $P_X$ and $P_Y$ is
$$cor(P_X,P_Y) = r h^2$$
, where $r$ is the coefficient of relationship. For parent-offspring $r=\frac{1}{2}$.
Particular case of mid-parent vs offspring relationship
This is just a study case to show that when consdiering a made-up phenotype such as a hypoethetical mid-parent phenotype, then the math are just a little bit more tricky. If you consider the mid-parent phenotype $P_{mid}$, then you must consider that the total phenotypic variance is half the actual phenotypic variance. The correlation therefore becomes
$$cor(P_{mid},P_O) = \frac{cov(P_{mid},P_O)}{\sqrt{\frac{V_P^2}{2}}} = \frac{h^2}{\sqrt{2}}$$
Conclusion
All of the above mean that if you plot the phenotypes of a series of individual pairs, where each pair is related by $r$, then the slope of the regression line is $r h^2$. For example, if you plot the phenotype of the mothers with their offspring, then the slope of the regression is equal to $\frac{h^2}{2}$. If $h^2=0.4$ (which is a typical value of heritability), then the mother-offspring regression will have a slope of $0.2$.

This is a great answer. You could improve it by explaining some of the equations in more detail and give a conclusion in the end.

I can probably make a conclusion from the last paragraph in ** Generalization to any correlation**. Can you tell me exactly what equation would deserve more details you think? Details about the logic behind the equation, the algebra or the underlying mathematical statistics such as the definition of a covariance? Thanks

Maybe conclusion was not the right term. I was pointing in the direction that it would actually make sense to not stop with a correlation equation but give a sentence or two what this verbally means with regard to the question asked. With asking for more detailed explanations I was thinking of the terms 'covariance' and 'correlation' that make sense to statisticians/population geneticists but maybe difficult to grasp for a more general readership. I also corrected a typo in the cor(P_o,P_p) section. Please re-check as I am not an expert in the field. :)

Thanks a lot for the elaborate answer! As Alex observed, things got a bit abstract though, so before I accept could I perhaps ask you to help me work out an example? Say, if h^2=0.6, and we know that both parents are 2 standard deviations above the mean, if I understand things correctly that would make the expected value of the child 0.6*2=1.2 standard deviations above the mean, correct? What about if we have the additional information that all grandparents are 1 standard deviation above the mean? How would the expected value change?


text:
Forgot to cool slides before washing
I just finished an immunofluorescence experiment and I'm wondering what went wrong. The tissues seem dimmer than they should be.
One mistake I made was: I completed the antigen retrieval step, in a 90 degree sodium citrate bath for an hour. The next step is to cool the tissue in ice for 8 minutes before washing. I forgot to cool the tissue, and just put it straight in the wash.
Could this rapid temperature change have affected my results? How important is this step?

Are you using secondary immunofluorescence?  If you are, the 8 minutes of cooling are probably intended for the signal amplification.  In other words, as you leave it for the time specified, the flourochromated secondary antibodies have more time to attach themselves in greater numbers to the primary antibody without your sample disintegrating.

I do use a primary and a secondary. But the cooling step is before any antibodies are added. Rather, it goes: deparaffinization, antigen retrieval (90 degrees citrate buffer), 8 MINUTES ICE, pbs wash, blocking, primary antibody.
Honestly, I'm not sure what the cooling step is for. I was thinking it was just to prevent rapid cooling of the glass slide, so it doesn't break. But I'm hoping to know if it has anything to do with the tissue.


text:
How do seagulls know it is the 9th inning at a baseball game?
Multiple times that I’ve gone to San Francisco Giants games, the seagulls sensed when the game was ending so they could pick up food. https://youtu.be/LPra_ZfwanU

People give off many cues that are intelligible to animals: https://en.wikipedia.org/wiki/Clever_Hans

Not sure why this is receiving close votes for "opinion-based." It's not the best written question, but it's interesting and, IMHO, on topic here. The current answer should provide context for how this question can easily be answered appropriately. I hope the current answer poster provides additional resources to support his/her answer or that someone else provides some strong support for how bird behavior can be affected by human cues.

@theforestecologist how could it be better written?

Hi Austin. Typically a number of folks here don't like fun and colorful titles and prefer more strictly "scientific" language to be used both in the title and post. The post is also very short, which likely triggered it to show up in the low-quality review queue. I like fun titles (especially when relevant), but I would suggest you expand your post by 1) indicating your own research effort on the subject (show us you tried to look something up on your own), and 2) you can turn your video into a gif to provide directly here by typing "gif" between "www." and "youtube" using your video's link.

I have a seagull-level understanding of baseball, but in the linked video I can see large parts of empty sitting area empty of people but with plenty of garbage. Seagulls don't need to understand the game to see a potential for food at this moment.

Many animals, particularly some birds, are smarter than we give them credit for. Corvids, for example, are known to not only use tools, but are capable of planning and understanding some cause-and-effect scenarios that require patience.
I know practically nothing about baseball, but if it's like any other human gathering, there are probably a lot of clues that the birds learn:

Noise levels. Big events often culminate in some big fanfare with noise (cheering, music, etc.). If the game changes audibly near the end, you can bet the birds have noticed.
Motion/activity: Any large gathering I've ever gone to often has a small percentage of people leaving early because they want to avoid the crowd or traffic. I'd expect a close-scored game has fewer people leaving, but chances are good that as enough people start getting up to leave, it's another signal the birds can use.
Discarded food: Aside from getting up to leave, toward the end of an event many people will start discarding snacks and drinks. Hopefully in the correct bin, but often just on the ground (humans are messy -- which seagulls love). An increased number of people tossing garbage into bins (and missing or they start overflowing) signals a few gulls that there's scraps to be found.
Temporal.  If these events happen regularly, or even irregularly, the birds associate it with food. People filling a stadium or parking lot, playing music, buying food (birds do have a sense of smell, though not as developed as mammals), etc. The birds over time learn: Increased human activity at this location results in more food some hours later.

Gulls are very gregarious, and notice when just one bird has found a morsel. As soon as a few birds get the first discards, the rest of the flock notices and starts to mobilize; circling and calling.
I would argue that the birds don't really know when a game or event is about to end, but they are adept at reading their environment, even if it's an urban one.

Per @theforestecologist's comment, references are requested. While I do not have a reference for each specific behavior described above, the following list covers avian intelligence generally, learning and problem-solving, and physiological adaptations. Many of the described behaviors are products of associative learning and elaborate communication, traits that gulls exhibit in other activities such as dropping clams from heights.
References:

Ravens parallel great apes in flexible planning for tool-use and bartering
Can Kabadayi, Mathias Osvath
Science; 14 July 2017, Vol. 357, Issue 6347
Ecology and Conservation of Birds in Urban Environments
edited by Enrique Murgui, Marcus Hedblom
Springer Nature; 10 February 2017
Cognitive ornithology: the evolution of avian intelligence
Nathan J. Emery
Philosophical Transactions of the Royal Society of London; 7 Dec 2005, Vol. 361
Bird Sense
Tim Birkhead
Bloomsbury Publishing; 2 Feb 2012
Auditory and visual mechanisms in food-finding behavior of the Herring Gull
Hubert Frings, Mable Frings, Beverly Cox, and Lorraine Peissner
Wilson Bulletin 67; January 1955

Nice answer. However, please provide support for your claims. Thanks!

@theforestecologist I've added some references which I believe support the claims.My answer is largely based on my own ornithological studies, albeit at a non-professional level.


text:
calculate elimination rate constant
A patient diagnosed with cancer takes antiproliferative drugs. Suppose the intake of drug(dose) is 250mg and excreted amount 125 mg. Amount of excreted drug as metabolites 1 and 2 are 75mg and 50mg. T1/2 is 4 hours. Calculate its elimination rate constant (K).
My idea is : amount actually used from the body is 250(dose) - 125mg amount excreted= 125mg. Which means that we are at steady state. Steady state is reached after 4 half lives (t1/2). Taking this into consideration we calculate 4 k respectively: K=0.693/4 ; K=0.693/8 ; K=0.693/12 ; K=0.693/16

Just posting the exact same question again just because the previous/first one was closed and downvoted, isn't going to help.

You can use this equation to very generally describe the one-compartment pharmacokinetics of a drug:
Cplasma = (Dose*F/Vd)e^(-kt)
Where F is the fraction that is bioavailable and Vd is the volume of distribution of the drug.  These values can be obtained from the Lexi-comp monograph.  If a drug is administered i.v., F = 1.  k in this equation is your elimination rate constant.

Your description of steady state is not correct.  Steady state is reached with multiple administrations of the drug after 3-5 half lives.  We usually assume steady state is reached in 5 half lives.  Here you are only dealing with one administration of the drug and a steady state is never reached.  The drug will be continuously cleared from plasma until Cplasma = 0.  The time that this takes is usually 5 half lives (50% of initial plasma concentration excreted after 1 half life, 75% after 2 half lives, 87.5% after 3 half lives, 93.75% after 4 half lives and 96.875% after 5 half lives).

Without any plasma concentration data, a route of administration, volume of distribution and bioavailability, a proper elimination rate constant cannot be calculated.  Consider the case where an oral drug is only 75% bioavailable.  This means that 75% of the administered dose reaches the plasma and systemic circulation while 25% is cleared initially by stomach acid, digestion, poor absorption from the GI tract, etc.  The elimination rate constant for this drug will be different than for one that is 100% orally bioavailable.


text:
Activity driven model threshold
So I am trying to figure out a threshold for an activity driven model. That is described in this paper: https://www.nature.com/articles/srep00469
That is I don't see how the researchers got R0 to be between 0.2 and 0.5 (page 6). If they are using gamma=-2.1 and epsilon=10^-3 and threshold is defined in equation 4, my calculations give me threshold of 2.020396043515874.
Now if the power law distribution (activity) is a random number i.e. this:
http://mathworld.wolfram.com/RandomNumber.html
this yields average activity of 0.005489691793543477 using this equation:
((1-gamma)/(2-gamma))*((1-(epsilon**(2-gamma)))/(1-(epsilon**(1-gamma))))

so then following equation 4, the threshold is 2.020396043515874, but that's not what Figure 4 (B) is showing so I'm very confused.
I would really appreciate if someone could clear this out for me.

can you fill in a few more steps of your calculation?  Where does your average activity formula come from?  I'm getting 0.59 following the mean and variance formulas from https://en.wikipedia.org/wiki/Pareto_distribution - but in any case your question will be much more useful with more details

@BenBolker Average activity formula comes from $\int_{\epsilon}^{1}af(x)da$. At each time $t$ a node will be activate with probability $a$, which is between $\epsilon = 10^{-3}$ and 1 and each active nodes will get m links. We then infect 1% of node, i.e. 1% of 10,000 and run SIR model on that.

I think you just get some calculations wrong, maybe for the second moment $<a^2>$ of the activity distribution.
All the calculations are just simple algebra and definite integrals of powers.
For a power-law distribution $F(a)\propto a^{-\gamma}$ with $a\in[\epsilon,1]$, in order to have $\int^1_\epsilon F(a)\:da=1$ i.e. the correct normalization, we have:
$$
F(a)=\frac{\gamma-1}{\epsilon^{1-\gamma}-1}a^{-\gamma}
$$
The moments of the distributions $<a^n>=\int^1_\epsilon a^nF(a)\:da$ are:
$$
<a^n>=\frac{\gamma-1}{\gamma-1-n}\frac{\epsilon^{1+n-\gamma}-1}{\epsilon^{1-\gamma}-1} \quad if \quad n\ne\gamma-1
$$
The case $n=\gamma-1$ have a logarithm and it is not relevant in our case.
For $\gamma=2.1$, $\epsilon=.001$, $n=1$ and $n=2$ we get:
$$
<a>= \frac{\gamma-1}{\gamma-2}\frac{\epsilon^{2-\gamma}-1}{\epsilon^{1-\gamma}-1}= 0.00548969179354348\\
<a^2>=\frac{\gamma-1}{\gamma-3}\frac{\epsilon^{3-\gamma}-1}{\epsilon^{1-\gamma}-1}=0.00061164650162922
$$
With these numbers I get:
$$
R_0=\frac{2<a>}{<a>+\sqrt{<a^2>}}=0.36330095782279
$$
which is between $0.2$ and $0.5$.
I'm not the best at explaining things, so let me know if there are any doubts! Goodluck!

How will the threshold change on a directed graph please?

How directed? In the sense that infection can occur only if the active vertex is infected ?

Directed in a way that an infected node will be able to infect another, but not vice versa.So if node A is infected, and it has a direction to node B, A->B, the infection can travel from A to B, but not back (if A would recover). At the moment the graph wasn't directed, which made it bidirectional really A<->B, but now I want to introduce that direction in which infection can travel, which would change the threshold

If I understood well you question, you should get R_0=2 . Can you run simulations of such a system?

I get R_0 = 2 as well, does that value change for you if you have different values of m?

(A little too long for a comment, and maybe useful)
Assuming that a is supposed to represent the degree of a node, and
using the formulas from Wikipedia for the Pareto distribution, I have

mean (which I'm assuming is <a>)  =  gamma*epsilon/(gamma-1)
and
variance (equal to <a^2>-<a>^2, or <a^2>= mean^2  + var) = epsilon^2*gamma/((gamma-1)^2*(gamma-2))

Translating into R code (rather than doing the algebra):
pmean <- function(gamma=2.8,epsilon=0.001) {
    gamma*epsilon/(gamma-1)
}
pvar <- function(gamma=2.8,epsilon=0.001) {
    epsilon^2*gamma/((gamma-1)^2*(gamma-2))
}
prms <- function(gamma=2.8,epsilon=0.001) {
    sqrt(pvar(gamma=gamma,epsilon=epsilon)+ pmean(gamma=gamma,epsilon=epsilon)^2)
}

When I use the value of gamma=2.1 in the figure caption and feed it into equation (4):
2*pmean(gamma=2.1)/(pmean(gamma=2.1)+prms(gamma=2.1))

I get 0.588 (still not right, but closer ... ??)

$a$ is the activity of a node at time $t$ if a node is active, it will connect with $m$ other nodes (in this case 2). The activity is a power law from the link I've got above.


text:
What's the minimum, if any, concentration of atmospheric nitrogen needed by plants?
What's the minimum, if any, concentration of atmospheric nitrogen needed by plants?  Would plants be able to grow in an atmosphere with just carbon dioxide and oxygen?

So, where would the plants get nitrogen from?

@GrahamChiu plants do not get nitrogen from the air.

@John I never said they did.  Bacteriae and fungi fix nitrogen and then supply the plants.

@xusr with no nitrogen cycle?

https://space.stackexchange.com/q/20153

@xusr so please explain how a nitrogen cycle occurs with no atmospheric nitrogen.

@xusr  http://www.azotictechnologies.com/index.php/technology/n-fix/ and exactly where is the nitrogen for the harber process coming from?

@xusr you continue to evade the question. The Haber process uses atmospheric nitrogen which can not happen since this scenario says there is none. And the link I provided is a process of plant fixation of nitrogen using intracellular bacteriae.

Zero if you are supplying them with solid nitrates in their growth medium, plants can't use atmospheric nitrogen. Some soil bacteria can and create nitrates the plants can use but this can and often is supplied by other means.
But as Graham points out you will need another inert gas to fill in the atmosphere as high concentrations of CO2 or Oxygen are both toxic.

If there is not nitrogen, then there will need to be another gas as an excess of either Co2 or O2 will cause problems.


text:
Why can plants handle extra chromosomes much better than animals?
Why can plants handle being polyploid way better than animals, where it is almost always fatal?
I found a 2004 paper while searching about this topic, but I'm wondering if there have been any recent discoveries and if scientists are still actively looking for a definitive answer.


text:
Log2 vs Quantile normalization
I am learning normalizations, I wonder when log2 and quantile normalization is used in each situation, may I ask if there is any material that compare these two types especially in microarray expression matrix for differentially expressed gene analysis? Thank you!

Welcome to Biology.SE. I'm voting to close this question as off-topic because it is not about Biology but about statistics.

Note that the tag 'human-biology' that you chose does not apply


text:
What are the interactions between mtDNA and nucelus' DNA?
In an exam situation I have been presented with the following question by the teacher:

What are the interactions between the mitochondrial DNA and the cell's nuclear DNA?

To my knowledge there is no such interaction. At the best you could say that the nuclear genome provides the mitochondria with some proteins and vice versa the mitochondria may participate in intrinsic apoptosis by releasing cytochrome C. Unfortunately this answer was not accepted by the teacher and I was not given an explanation. My question is wheter there is an actual interaction I've never heard of or if maybe the poorly worded question was alluding to something else.

IMO, the question is rather broad and a little vague. Knowing the subject of the course may help us. What was the subject of the course?

Hello. I am studying medicine in europe. The exam in question is just a first year Bio & Genetics course.

Sounds as if you have a good grasp of the biochemistry of mitochondria. Probably better than your instructor, who may be embarrassed at his poor question. Certainly there are no contemporary physical interactions, although if you are considering evolution then mitochondrial genes were lost to the nucleus. Move on.


text:
Trying to clarify how mutation is passed to offspring
In popular documentaries there is an often-used example related to mutation and natural selection. I want to clarify my understanding.
One such example is polar bears. It is being white as a result of genetic mutation and the gene is passed to offspring and they have an advantage in the snow, etc. There are many other similar examples. My question is (unless it is critical, I just want to focus on the essence of the question): Should I understand that genetic mutation made that bear white also? Or, is it the offspring that was the one that became white? Or is it the case it could be either? (Or, maybe the mutation happened in the reproduction, etc.?)

Animals are made up of cells. Each cell has a copy of DNA that contains all the patterns needed to produce the proteins that cells use to function.
Animals grow by cells dividing. In the process of division, a copy of the DNA is made. If the DNA in one cell is changed due to a copying mistake or damage (like from UV sunlight), that change only affects that one cell and any cells that come from it.
Gametes are a special type of cell used in sexual reproduction. Each contains half of the DNA of a normal cell, so when you put two together you get one cell that has a full set of DNA. That one cell, the fertilized egg, divides and the daughter cells divide etc such that all the cells of the new animal originally came from that one egg cell.
If a mutation happens in a cell that does not produce gamete cells, that mutation can't be inherited by the next generation. To have a heritable mutation, it must affect the gametes. So, most heritable mutations involve the gametes directly. Mistakes or damage in a gamete will then be in all cells of a child organism, because all cells in the child (including their gametes) will derive from the gamete's DNA.
https://en.wikipedia.org/wiki/Cell_(biology)
https://en.wikipedia.org/wiki/Heredity
https://en.wikipedia.org/wiki/Gamete


text:
What’s the difference between normal ZZ plant and “Raven” on the DNA?
I didn’t find about it on Google. Does anyone know or guess about that?
I’m thinking maybe it would be the same as the difference between green algae and red one but I don’t know if they don’t have the same pigments molecule.
And I also assume that they originally have like the anthocyanin but it just didn’t express.
I really want to know what causes mutation of black from greens or what the mutation caused the difference on DNA.

Please clarify your specific problem or provide additional details to highlight exactly what you need. As it's currently written, it's hard to tell exactly what you're asking.

I assume you want to know the gene that causes the Raven variety 's distinctive black-purple coloration and how the gene make the leaves black. Firstly the color may be coded for by several different genes, not just a single gene. Secondly, the changed genes turn the leaves black by causing the plant to produce large amounts of a dark pink-purple pigment - most likely an anthocyanin.


text:
What species of a spider is it?
I found this specimen in my garage in Idaho:

Does anyone know what species is it? Is it venomous?

My guess:
Schizocosa mccooki
You can go to the website inaturalist.org and set location and type of animal, then you can compare.
Its a type of wolf spider and has medically insignificant venom.
https://www.inaturalist.org/taxa/230594-Schizocosa-mccooki
https://www.webmd.com/a-to-z-guides/what-you-need-to-know-about-a-wolf-spider-bite
https://pictureinsect.com/wiki/Schizocosa_mccooki.html


text:
Papers regarding the use of radio in brittle stars
After stumbling on this article, I have been looking for additional research into the possible use of radio by sea stars for some time now.
However, I haven’t been able to find anything regarding the subject, so I’m wondering if anyone here knows of any papers either confirming or disproving the use of radio in brittle stars.

What were your search terms? Try  - use of "radio" frequencies by brittle stars, with the quotes. That was the only search I did and I got one result.

I wasn't able to find anything at all on this subject, either with Google Scholar or Pubmed.

The only Pubmed hit for '"brittle star" radio' is referring to radio-isotopes, not radio frequency communication/sensing
similarly, Google Scholar hits for '"brittle star" radio' give mostly stuff about radioisotopes and radiolabeling, while '"brittle star" "radio frequency"' covers topics like use of imaging and tracking.

I looked at the Google Scholar profile of the principal investigator of the DARPA grant, and noticed only these relevant pubs:
Thackston, Kyle A., Dimitri D. Deheyn, and Daniel F. Sievenpiper. “Limitations on Electromagnetic Communication by Vibrational Resonances in Biological Systems.” Physical Review E 101, no. 6 (June 1, 2020): 062401. https://doi.org/10.1103/PhysRevE.101.062401.
———. “Simulation of Electric Fields Generated from Microtubule Vibrations.” Physical Review E 100, no. 2 (August 15, 2019): 022410. https://doi.org/10.1103/PhysRevE.100.022410.
The first paper looks particularly relevant: here is the (abridged) abstract:

Previous research in biology and physics speculates that high-frequency electromagnetic fields may be an unexplored method of cellular and subcellular communication. The predominant theory for generating electric fields in the cell is mechanical vibration of charged or polar biomolecules such as cell membranes or microtubules. The challenge to this theory is explaining how high-frequency vibrations would not be overdamped by surrounding biological media. ... While many resonators have been studied and simulated, the general limitations on communication imposed by energy transfer arguments have not been considered ... We determine the flexing mode of microtubules as an identified resonance in the literature which meets our criteria. Our results
suggest the major obstacle to meeting our criteria for effective electromagnetic communication is the trade-off between the Q [quality] factor and the plasma frequency: Resonators must be large enough to have a large Q factor, but small enough to resonate at frequencies greater than the plasma frequency.

To me this sounds like "our ideas didn't work out [DARPA projects are supposed to be high risk, so many should be expected to fail!], but here's the beginning of a theoretical framework for why they didn't work and what avenues someone interested in this area should pursue ..."


text:
importance of pigments involved in photosynthesis
How do the accessory pigments(chl-b and carotenoids) help in during the process of photosynthesis? Can I please get a detailed explanation about it. I know that it helps in increasing the efficiency and protects chl-a present at the reaction center but how? Why all the shield pigments go to the excited state when only chl-a is needed to transfer the electron to the primary acceptor.

Hi and welcome. This is a good question, but on this site, evidence of research in an attempt to answer your own question (a quote and a link) is required. We don't know how much you already understand, and in order to avoid unnecessary explanations, we need to know the starting point of the answer. Wikipedia has articles on the various accessory pigments. A link to the one you are most basically confused by, and why the article doesn't answer your question, would help us give you the answer you need. There are entire books on photosynthesis. We can't write a chapter here as an answer.


text:
Is there a formal definition of signature of natural selection?
I’ve searched for a definition of signature of natural selection. Unfortunately, I haven’t found any formal definition of it.
The signature of positive selection on standing genetic variation. I found this post that links to an article measuring the signature with an Fst and a Linkage Disequilibrium test.
Are we looking at only some frequency of alleles in different populations? Is the signature only a fixation of alleles in a population where this allele was positively selected?
Another article says:

A single beneficial substitution can be detected in polymorphism
  data, so long as it occurred recently. The fixation of a favorable
  allele in a population distorts patterns of variation at linked
  sites, thereby leaving a distinguishing signature that lasts up to
  about 104 generations in humans or about 106 in Drosophila
  melanogaster (Przeworski 2002). In principle, targets of positive
  selection can therefore be identified by searching polymorphism data
  for regions that harbor this signature (Nair et al. 2003; Wright et
  al. 2005).

Is it always in linkage disequilibrium?

Here is how I would personally explain what a genetic signature is:

A genetic signature of a certain type of evolutionary history (type of selection or demography) refers to the effect that this specific type of evolutionary history has on genomic properties of populations today.
We are interested in understanding such signatures because knowing the association between a number of evolutionary histories and their genetic signature allows us to reconstruct the evolutionary history of a population just by looking at the genomics of this population.
For example, recent selective sweep, population expansion after a recent bottleneck and/or linkage to a swept gene are all causing negative Tajima's D. Balancing selection and/or sudden population contraction are causing positive Tajima's D. In this example Tajima's D is a statistics that is used to measure this so-called signature of the different process.

The above was NOT a citation. I am NOT aware of any publications defining rigorously what a genetic signature is. I think it is not so uncommon for authors to use a term without strictly defining it. As long as the unclarity of the definition does not yield to limit cases and misunderstanding, then it is totally fine.

Do you have a reference to this? I mean, is this a quote? Is it like the gene signature or the genomic signature?

Nope I don't! Feels like we already had this discussion on another post $\ddot \smile$ This is why I said I would explain... and I am not aware of any publication defining rigorously what a genetic signature is. I tried to make this point even clearer.

Haha! Thanks a lot for your contribution! I'm going to continue the research until I find something. This concept is, most of the time, used with selective sweep, right? For instance I found Nielsen, R. 2005. Molecular signatures of natural selection and Hohenlohe, P. A., P. C. Phillips, and W. A. Cresko. 2010. Using Population Genomics to Detect Selection in Natural Populations: Key Concepts and Methodological Considerations with nice figures (fig 1 and 4 respectively) Seems that these images could represent a "signature".


text:
Making a hole in a tree is okay? Or does it damages the tree?
I am watching a TV series named "Treehouse Masters." What they do is make houses on trees or around it getting physical support from a big strong tree, like this:

But to make the support strong, they make a big hole in the trunk of a tree

Then they put a steel beam into it, like this:

In some cases, they make more than one hole. So, does this affect the tree in any way?
If anyone makes a hole that big or even bigger but doesn't fill it with any other thing(like the beam), will the tree heal itself?
I have heard that trunk is the most important part of a tree. So I am curious to know if this act is cruel towards the trees or not.

Trees don't have nerves or brains, so anthropomorphizing the effects of an action upon them as "cruel" is misguided. Yes, trees can be damaged by injuries that are too many or two large. However, they can also heal quite well if they are healthy overall. While the trunk is extremely important for holding up the tree, the bark and the layers just under it are the most important for delivering nutrients in between the leaves and roots. The inside wood of a tree is avascular, and essentially "dead", so the difference between a 5 cm deep hole and a 30 cm deep hole of the same diameter is small.

It can have a negative effect if parasites are able to take advantage of the holes in the tree.The bark is the first line of defense against parasites and making holes without covering them tend to have a negative effect.Furthermore, the bark also protects the plants against adverse weather conditions.


text:
Length of anopheles chromosomes?
Where can I find the length of each anopheles chromosome? I've obtained data in which the length of each 2L chromosome for several anopheles is 39101648. I'm looking for an article that gives the length of 2L so I know my output is correct.

I came across this paper (Holt et al. 2002), does this answer your question? Look at Table 2 and 3. In this paper the lenght of 2L is  52393056 bp.


text:
Summary statistic that can distinguish between migration from pop2 to pop1 vs. pop1 to pop2
Given two sister populations that diverged some time ago, say pop2 migrates to pop1 and breeds there, giving offspring with sequence segments similar to those from pop1 but not in pop2. There are stats to find how similar two populations are; for instane, mean dxy takes the average of number of pairwise sequence differences between the two sister populations. Say if there is no migration, mean dxy at a locus of length 10000 is 100. Then with migration, say mean dxy at that locus is 300. Detecting a dxy that's unlikely under the null hypothesis of no migration indicates migration and interbreeding occurred.
I've been thinking for a while on if there are summary statistics which can distinguish between migration from pop2 to pop1 vs. migration from pop1 to pop2 (assuming only one of these events occurs). Do such statistics exist? Without loss of generality assume pop2 members migrate to pop1. Then pop1 will have members that are more similar to pop2 compared to if no migration occurred, but pop2 will be as if no migration occurred.
If we run simulations of a population w/ no migration, we can expect to see some value of pi and # of segregating sites. These measurements may be different in pop1 when pop2 migrates into pop1; some members of pop1 will have SNPs that pop2 do not have, and thus there would be more genetic variation (higher pi and ss) in pop1 compared to its expected pi and ss under no migration. So dxy can say that there's some similarity between pop1 and pop2 that's not expected under null hypothesis, and then pi or ss can say which of the two has a higher genetic variation than expected. Can some statistic that depends on dxy and pi distinguish between migration from pop1 to pop2 vs migration from pop2 to pop1?

Yes, migrants affect patterns of genetic diveristy
Immigrants yield to higher effective population size and therefore higher genetic diversity. They will also affect the site frequency spectrum and I would expect that if the migrants are numerous enough, they would yield to positive Tajima's D.
Therefore, unidirectional migration will definitely yield to differences in patterns of genetic variance among populations (that can be measured by any summary statistic of the site frequency spectrum).
Existing methods for detecting directional selection
I have never had to do such inference so I am not able to do a good review of the existing technics.
You should probably read Slatkin and Maddison 1998 and more importantly Beerli and Felsenstein 2001. Beerli and Felsenstein 2001 has been cited 1,341 times and you should probably quickly see whether some of these papers suggest more recent methods. John Novembre has some very interesting work on how to estimate migration rate between any two populations (e.g. Novembre and Stephens 2008). He might have done something of interest to your problem.
You can always use Approximate Bayesian Computation (ABC;see for example Jeffrey Jensen's work for example of inferences with ABC in population genetics) to figure out what pattern of migration is most likely. With a simple enough model, a good ABC algorithm is not that long (with good computing ressources). The question then is what statistic(s) to use for the rejection algorithm. Again for that, you should have a look at the existing literature to come up with a set of potentially useful statistics.


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Is vitamin D a vitamin or a hormone?
Some people like to say that vitamin D is a hormone.
A simple set of differences between hormones and vitamins is described here.
Vitamin D is not (for the most part) absorbed through food but created by our body when our skin is exposed to the sun, so it does look more like a hormone than a vitamin.
Another difference listed is whether it has catalytic action or not (that I don't know what it means - answers with an explanation would be nice).
So, is vitamin D a hormone? And if so, why is it called vitamin D?

It's called "vitamin" D because it was discovered before scientists knew it could be created by the body. In a way, it's both, as it can be created by the body or provided through food.

@BillDOe the link I provided offers another differentiating statement, i.e. whether it has catalytic action. Do you know the answer to that question?

From researgate chat related to this topic they rather call vitamin D biomodulator vitamin, which means it is capable of gene regulation

@user, a catalyst is a chemical that helps enable a chemical reaction that otherwise wouldn't occur without the catalyst, or different physical conditions, and itself remains unchanged from initiation of the reaction and the end, though it may be modified during the reaction itself. So as far as how vitamin D transports calcium, magnesium, etc. I'd have to answer that it seems to fit the definition of a catalyst. However, this and that article both call vitamin D a hormone.

There's an open access article "From vitamin D to hormone D", which explains the difference(s). Vitamin D is a family of substances, but for humans the most important one from this family is vitamin D3 aka cholecalciferol. "Hormone D" (1α,25(OH)2D3, the substance that normally regulates calcium etc.) aka calcitriol is closest to vitamin D3. So if one wants to be technical about it, the vitamin(s) and the hormone are slightly different substances. Vitamin D itself is more aptly called a prohormone (i.e. a hormone precursor):

Vitamin D[3] is not technically a vitamin, ie, it is not an essential dietary factor; rather, it is a prohormone produced photochemically in the skin from 7-dehydrocholesterol. The molecular structure of vitamin D is closely allied to that of classic steroid hormones (eg, estradiol, cortisol, and aldosterone) in that they have the same root cyclopentanoperhydrophenanthrene ring structure. Technically, vitamin D is a secosteroid because one of the rings of its cyclopentanoperhydrophenanthrene structure has a broken carbon-carbon bond.

The above view is also endorsed by Horst et al., but they have a much more detailed discussion, including the fact that in vitamin D poisoning, calcifediol (25(OH)D3)--an intermediate compound in the pathway between the vitamin and the hormone--can itself act as a hormone, i.e. it has some binding affinity to the calcitriol receptor, but only at at very high doses.
As for how the vitamin label came about, "historical accident" is one way to put it...

Considering the fact that now we accept that the biologically active form of vitamin D [what the other paper calls "hormone D"], namely 1a,25(OH)2-vitamin D3, is a steroid hormone, it is somewhat ironic that vitamin D, through a historical accident, became classified as a vitamin. It was in 1919/20 that Sir Edward Mellanby, working with dogs raised exclusively indoors (in the absence of sunlight or ultraviolet light), devised a diet that allowed him to unequivocally establish that the bone disease, rickets was caused by a deficiency of a trace component present in the diet. In 1921 he wrote, "The action of fats in rickets is due to a vitamin or accessory food factor which they contain, probably identical with the fat-soluble vitamin." Furthermore, he established that cod liver oil was an excellent antirachitic agent.
Shortly thereafter E.V. McCollum and associates observed that by bubbling oxygen through a preparation of the "fat-soluble vitamin" they were able to distinguish between vitamin A (which was inactivated) and vitamin D (which retained activity). In 1923 Goldblatt and Soames clearly identified that when a precursor of vitamin D in the skin (7-dehydrocholesterol) was irradiated with sunlight or ultraviolet light, a substance equivalent to the fat-soluble vitamin was produced. Hess and Weinstock confirmed the dictum that "light equals vitamin D". They excised a small portion of skin, irradiated it with ultraviolet light, and then fed it to groups of rachitic rats. The skin that had been irradiated provided an absolute protection against rickets, whereas the unirradiated skin provided no protection whatsoever; clearly, these animals were able to produce by uv irradiation adequate quantities of "the fat-soluble vitamin", suggesting that it was not an essential dietary trace constituent. In parallel studies, Steenbock and Black at the Biochemistry Department of the University of Wisconsin found that rat food which was irradiated with ultra violet light also acquired the property of being antirachitic. However, because of the rapid rise of the science of nutrition -- and the discovery of the families of water-soluble and fat-soluble vitamins -- it rapidly became firmly established that the antirachitic factor was to be classified as a vitamin.

As an amusing parallel to this, calcifediol was identified in 1968 as an active metabolite of the vitamin, but it wasn't until 1971 that calcitriol was properly identified as the metabolite that exercises the hormonal action under normal circumstances. (cf. DeLuca)


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Help understanding cell replication animations
I often come across these animations about molecular biology showing for example how cell replication works, how virus infection works etc. Take this video as an example
https://www.youtube.com/watch?v=odRyv7V8LAE
HIV virus infects T helper cells using receptors on the cell surface which are cd4 molecule, it binds to the receptors using envelope protein. But the video shows you a little ball with some hooks that attaches to another little ball with other hooks.
I understand this is an useful abstraction, but could someone recommend a book or other materials to a novice like me who would like to understand how this really works? Question is probably too general but I am really interested in basics only. Hopefully someone could help
Thanks

When these animations are made by experts, they are actually not abstractions. Animations like this one [https://www.youtube.com/watch?v=X_tYrnv_o6A] actually don't show you an "idea" of how this looks but the actual shape of the individual molecules involved.
The reason we can now for many proteins draw pictures of how the molecule looks on the tiny scale that it is, is the field of structural biology. The scientists working in this field use techniques like X-ray crystallography, nuclear magnetic reconance spectroscopy and cryogenic electron microscopy to determine the structure of a protein at resolutions down to 2.7 Å (Angstrom, 1Å = 0.1nm). Once they manage to get a reliable picture of how a protein molecule looks, they publish their work and submit it to the world-wide protein data bank, which you can access freely using one of three websites: PDBe, PDBj and RCSB.
I tried searching for the proteins in your animation (CD4 and the HIV envelope protein gp120). Some structures do exist for them (e.g. http://www.ebi.ac.uk/pdbe/entry/pdb/2ny1) but they seem to contain only part of what's shown in the animation. Often certain parts of proteins can't be identified by structural biology for technical reasons, but we know they must be there based on the genetic information we have, and we can make some educated guesses about what those bits of the protein might look like. It seems in this animation, there was quite a bit of educated guessing involved.
A lot of biological science nowadays goes by the paradigm "seeing is believing". Many modern animations are reproduced from actual recordings where the process shown in the animation can be seen happening in reality. Cell divison for example is an intensively researched process that has been filmed using many different microscopic techniques and focussing on many different parts of the cell, figuring out what each protein or other molecule does during the process. Putting together knowledge from many different teams, you can generate a full picture of what everything is doing at the same time.
As far as reading recommendations go, any basic molecular biology textbook like Molecular Biology of the Cell by Alberts et al. (pick it up from a library), or lectures freely available online should allow you to gradually wrap your head around it.


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ATP production via aerobic respiration
Just started learning about aerobic respiration today, specifically Glycolysis.
We were told that aerobic respiration produces 38 ATP, while anaerobic respiration produces only 2.
However, we're also told that:

Glycolysis produces 2 ATP
Link reaction produces 6 ATP
Krebs cycle produces 24 ATP (18 from NADH, 4 from FADH, and an extra 2)

This only adds up to 32 ATP, so where is this other 6 coming from? Or is this information incorrect.

In short, the difference stems from different values regarding the number of ATP attributed to the electron carriers in the electron transport chain (ETC).
My guess is that your class didn't go too far in depth on the subject, and also that your class or text is using mixed sources of information.

I have overviewed (general) glucose metabolism here, but feel free to skip this section if you don't need it.
Glucose metabolism is generally composed of 4* processes:

Glycolysis: a 6-C glucose molecule is broken down to 2 pyruvate molecules producing a net gain of 2 ATP and 2 NADH (electron carrier) molecules. Note that this is a net gain.
Pyruvate Dehydrogenase Complex (PDC): Here Pyruvate is made into Acetyl CoA, which enters the Krebs Cycle (step 3). This is the Link reaction step that you mentioned. This step produces a 1 NADH molecule per pyruvate.
Krebs Cycle (TCA): The Krebs cycle is central to cell metabolism and produces a lot of electron carriers, netting 1 GTP (ATP energy "equivalent"), 3 NADH, and 1 "FADH2" (electron carrier) PER Acetyl CoA entering the TCA.
Oxidative Phosphorylation (ETC): This step converts your electron carriers into ATP. It does this by using the energy released by electron transfers (e- are transferred from your electron carriers NADH, FADH2 to intermediate compounds to oxygen. This provides the energy to actively transport protons) to pump protons (H+ atoms) across a semi-permeable membrane to create a electro-chemical gradient. These H+ atoms will flow down this gradient through the channel of the ATP synthase, creating ATP. Currently, it is pretty widely accepted that an NADH molcule provides enough energy to net 2.5 ATP, and a FADH2 molecule provides enough energy to net 1.5 ATP.

As a result, we get the following:

+2ATP, +2NADH
+1NADH x2
(+1GTP, +1FADH2, +3NADH) x2
-10 NADH, +2.5ATP x10; -2FADH2, + 1.5ATP x2

This yields 2+2+25+3=32 ATP, which is what you obtained in your calculation.
However, a previously accepted value states that the 4th step nets 3 ATP/NADH molecule and 2 ATP/FADH2 molecule. Running the same calculation, we obtain 2+2+30+4, netting 38 ATP, causing the discrepancy you notice. I wouldn't say either set of values is universally accepted, but I would say that 32 ATP is generally recognized as the "right" answer.

In other words, 32 ATP is the result of the more recently accepted equivalences of 2.5ATP/NADH and 1.5ATP/FADH2 in oxidative phosphorylation, whereas 38 ATP is the result of the older pair accepted equivalences of 3ATP/NADH and 2ATP/FADH2.

Some notes and caveats:
Please note that in (most) Eukaryotes, the NADH produced in the cytosol (Glycolysis) is "reduced to FADH2" via the mitochondrial shuttle as the high energy electrions enter the ETC. This means that each NADH produced by glycolysis only nets 1.5 ATP, resulting in 30 ATP/glucose in majority of eukaryotes.
It is also important to note that the numbers that I have provided are mostly used in classroom calculations for general systems. Real organisms will often deviate for a multitude of reasons. Further, some organisms may not follow this rule at all.
*A few sources might classify the PDC as part of glycolysis or as part of the TCA.

Fine, but you misuse the word “convention”. You are takling about “accepted values” for the equivalence of NADH and FADH2 with ATP. At one time they were thought to be 3 and 2 (i.e. these values were generally accepted), but more recent work gives values nearer 2.5 and 1.5 (which are now generally accepted). It is now usual in eukaryotes to consider the mitochondrial shuttle, so a value of 30 (rather than 32) is cited, e.g. in Berg et. al.

@David I went back and edited out the word "convention." I'm usually pretty bad with choosing my words, so I'm not surprised to hear that I misused the word. However, I was wondering what made you say that "convention" was used wrong?

A "convention" refers to a normal or usual manner of proceeding, and in science usually refers to nomenclature or representation. The reason for not using it in the way you did originally is that it concerns the representation of an object rather than the object itself. Examples are 1. Writing nucleic acid sequences (e.g. GTTC) — 5′ to 3′ direction, phosphodiester linkages omitted; 2. Writing of species in papers — italicized, first mention in full with second part in lower case (Escherichia coli) subsequently first part abbreviated (E. coli).

I think that sort of makes sense to me. Just to check, the object itself is a convention, but a representation of the object is not a convention?

— I would put it the other way round. The object is a tetranucleotide and its representation is GTTC according to the current convention. If you look at early books on nucleic acids it would have been written GpTpTpC — an earlier convention, but the object is just the same. However as an analogy for the values for NADH/ATP conversion, consider that this was a discrete molecule the structure of which had been wrongly determined and, say, the C was later found to be methylated. Then the object has changed.

@David: How can a molecule of NADH give rise to 2.5 molecules of ATP? (i.e. how can 1/2 ATP be formed). Or is it like, 2 molecules of NADH gives rise 5 molecules of ATP.

@user237650 —  SE would regard this as a side discussion, but, in brief, it relates to the way ATP is synthesised by the chemi-osmotic mechanism and the structure of the ATP synthase. If you have access to it and your background is appropriate this paper might help. Otherwise it is a valid query and you should consider asking it as a separate question.

I dont know how much do you know this metabolic paths but i am going to try to get that 32 ATP out of 38 ATP step by step.

First off all in glycolysis you have to activate sugars with phosphate (glucose;fructose). This process is done by hydrolysis of  two ATP. So we have 36 ATP left.

I am going to move forward to the ratios of kofactors. Ratio ATP:NADH+H and ATP:FADH2 in oxidatice phosphorylation is not actually 3 and 2 ATP, but 2.5 and 1.5 ATP respectively.

ATP synthase produces 1 ATP from 3 H+. However the exchange of matrix ATP for cytosolic ADP and Pi (antiport with OH or
symport with H+) mediated by ATP–ADP translocase and phosphate carrier consumes 1 H+ / 1 ATP due to regeneration of the transmembrane potential changed during this transfer, so the net ratio is 1 ATP / 4 H+-

The mitochondrial electron transport chain pump 10 H+/1 NADH+H+ and 6 H+/1 FADH2. In the end it is that 2.5 ATP for NADH+H and 1.5 ATP for FADH2.

Sum it. FOr 1 molecule of glucose comes from substrate-level phosphorylation 2 ATP and 2 ATP (GTP) from Krebs cycle dicectly. 2NADH+H from clycolysis (2x 1.5 ATP or 2 x 2.5 ATP from malete aspartate. 8x 2.5 ATP from dekarboxylation of pyruvate and last but not least 2x1.5 ATP for FADH2 from Krebs cycle.
4+3 (or 5)+20+3= 30/or 32 ATP.

Source: https://www.saylor.org/site/wp-content/uploads/2013/04/BIO101A-6.2.3-CellularRespiration.pdf


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What kind of worm is this?
What kind of worm is this? I’ve seen them in my bathroom and kitchen which are both ceramic tile. This morning I walked in the kitchen and this one just so happened to be dead.

Welcome to Biology.SE. Where do you live (country/region/type of ecosystem)? What is the approximate size? Did you notice any behaviour of interest? How fast do they move? Any other info?

I'd say that isnt a worm but a nonvenomous blind snake specie named Indotyphlops braminus
(Indotyphlops braminus)  .(Brahminy Worm Snake )


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What is the difference between infected and infectious in epidemiology?
I am studying the SIR model and in the infected class I, both infectious and infected individuals are included, as stated here
I know that the model uses the assumption that the disease has an insignificant incubation period so infected individuals are capable of transmitting the disease as soon as they become infected. But what is the specific difference between these two terms? Does infective mean anything different?

(The document you link to says "see Chap. 1 for distinction between infected and infectious individuals", but I'll assume you don't have access to that - I certainly don't.)
Infected individuals have been infected by a pathogen.
Infectious individuals have the potential to transmit a pathogen to
others.
Note that the definition given for "infected" in the source you link to is actually wrong: hosts may have a subclinical infection, in which case they are not "now sick with it".


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Why are worker ants not clones of the queen?
Currently worker ants of most species share only three quarters of their genetic code. It seems like worker ant clones would be better, as it would remove all genetic conflict of interest between them. Then they would be like our body cells. Only queens (and possibly males) would be produced sexually.

Yes, worker ants have a relatedness of 0.75 between each other (haplodiploid with shared parents).

why has evolution not produced perfect X can usually be answered by the correct mutations have not occured. evolution is about jury rigging good enough not perfection.
you are assuming ant are free to change how related they are, they aren't, they cannot rebuild their reproductive system from scratch they can only modify what they have.

Hypothetically, there could be disadvantages to making worker ants clones of the queen. In that case, an unfertilized queen could start a colony. Even if that colony was successful, how could the queen produce a new queen and new colonies? If we assume parthenogensis could answer those problems, then we would probably see much less genetic diversity over time, which could potentially lead to massive die-offs if the genetically homogenous ant population couldn't handle some new pathogen or environmental change. Forcing queens to mate before forming a colony ensures greater genetic diversity.

You are assuming my question is rhetoric, when you say "you are assuming ant are free to change how related they are". There is no such assumption in my question.


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Can organ-accumulated iron get shed again?
Hemochromatosis can lead to an accumulation of iron in some organs. If the accumulated amount is not too high, will it go down again upon correction of blood iron levels?

What research, if any, did you do to answer your own question? I believe this is very easy to answer with a quick search.

@anongoodnurse I did quite a bit of googling, and reading articles. I might not be using the right keywords.

Please cite an article on the treatment of  hemochromatosis which you read that didn't answer the question. Then I'd be happy to share what I know.

@anongoodnurse https://hemochromatosishelp.com/iron-overload/

I'm sorry to be so picky, but that is not a reputable source; it's a for profit blogsite that sells supplements. The Mayo clinic is reliable and easy to understand.

@anongoodnurse sure, there you go: https://www.mayoclinic.org/diseases-conditions/hemochromatosis/symptoms-causes/syc-20351443 (it still doesn't answer my question)

Did you read the second page? The answer is there.

@anongoodnurse It doesn't. Nowhere does it say specifically whether iron accumulated in organs gets eliminated. It only talks about outcomes (e.g. "Phlebotomy will not reverse cirrhosis", which of course it won't since cirrhosis is about tissue scarring). And to me, "reduce your iron levels to normal", sounds like blood levels, although it's unclear. Maybe some organs shed the excess iron much more slowly, just like they would with e.g. lead. This is my last reply to you, as your comments are starting to border on trolling. If you don't want to or can't answer, that's fine.


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Evolution of multicellular eggs
Which animals where the first in which ova were not simply released, but instead provided with some additional nutrition and/or protection in the form of a larger egg?

What animals are you talking about? Unless I am mistaken, eggs are, by definition, single cells.

@kmm the term 'egg' is also used for the vessel surrounding the ovum. I don't know if there is any other term for what we commonly call the egg (for example a chicken egg).


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Is it possible to Interpret Nerve Signals As to Where They Are Going In The Human Body And What Their Task Is?
I have recently watched some anime, (yes, anime, probably a huge cause to lots of questions asked on the internet), and it got me thinking. We can intercept nerve signals throughout the body, but could we interpret their task, as to whether they are meant to contract or relax a muscle, and their destination, as to which muscle they are meant to travel a signal to.
Extra Inspiration:
I have seen an article by Chris Brooker about the theory of intercepting optical nerves to benefit augmented reality, so it got me thinking, what if we could intercept all nerves in one go, the brain, but I realised, that's a stupid idea, they travel to the brain all over, so the next best location was the Central Nervous System (The Spine).
On top of Anime super inspiration, and some articles which helped further my theory, I thought more and more about how nerves travel around the body as impulses, so I theorised maybe they use different currents or charges to travel to different parts of a body, which brings me to my conclusion, is there anyone who would be willing to carry this experiment out? And then give me the results? If this is true we may be able to make a huge breakthrough in the virtual department, even if incorrect it can still be a starting stone for a new hypothesis.
However this entirely bases on the idea that all nerves start from one point on the cns, however the start to this would be to gain a test subject and patch a circuit into a nerve. on the circuit would be an ammeter and a voltmeter, and then have the subject move the muscles connected to the nerve.
The second step would be to find a lone point in the cns where all nerves touch or cross paths to identify the Sweet Spot (( ͡° ͜ʖ ͡°) I named it myself) and differentiate different nerves for different purposes.
Keep in mind this would be no small discovery, this would help engineer a better future in the virtual department, however this is only a small part to this, imagine being able to truly see or hear without the help of heavy machinery, or be able to walk with actual legs again, or be able to play catch with family again as this would engineer the greatest part to prosthetic engineering where we could actually move lots of different gears as if we contracted or relaxed a muscle.
If my hypothesis is completely off as my science is incorrect than please let me know. I currently do not have the facilities to go further into this as I am still in High School ((̿▀̿ ̿Ĺ̯̿̿▀̿ ̿)̄), and am busy with studies, but I hope I am correct and thus would have contributed to science which can help thousands of people everyday.
Please contribute to this topic even if it is criticising it.
Thanks,
IbnJalal

you've done a lot of thinking about that, and the wording is informal, talking about animes, high school. you should prepare yourself to know that this is a relatively formal science forum, where people prize concision and prior research for the wording of questions. sounds like, once you have armed yourself with lots of knowledge you will be contributing to science of many people.

I agree with previous comment from com.prehensible but I would like to change the emphasis ever so slightly.
Its great that you 1. get inspired by experiences you find in the world 2. you think about them and 3. you reach out to other people to check if your ideas are correct. This is basically how any scientific project starts.
I don't think that an informal tone is detrimental to serious and precise scientific discussions on any topic, quite the opposite, so I wouldn't worry about talking about animes or high school. Ask away and as you talk more and more with people with the same interests your language will automatically change to reflect more precise and specific objects/subjects.
Nonetheless, and to the point of the previous commenter, I'll try, instead of general statements of form, to point out some specific things you might want to look at in order help you think about your question:

A precise statement of your hypothesis is a must. You almost make a precise hypothesis about different charges and currents. A lot is known in terms of neuronal communication, both at the single cell level as at the group level. I would start from the wiki entry on action potentials it might help you understand exactly how neurons "talk" to each other. Also it might be useful to have a more specific insight on how these cells are physically organised. Again the wiki on the CNS is a good place to start.
You should have a specific idea of a particular experiment that would allow to you to test your hypothesis. Thinking about the experiment will require you to know what is possible and what is not. Usually animes, movies, and books are quite a bit more advanced in terms of what is nowadays possible, hence the word "fiction" in science fiction. Thinking of an experiment also allows you to operationalise your hypothesis, which is science speak for deciding exactly what you will measure and how. This will tell you if you can answer your question as you stated it and is super important to plan an experiment.

If you have these 2 things i.e., a good idea and a doable experiment that would answer your question the hard part is done!
Well... then you will probably need time and money, but that is a different problem altogether...
Answering your question though, yes, it is possible to interpret nerve signals, both in terms of their targets or downstream areas, as in terms of information content they might relay in order to accomplish a particular task. There is a whole field of Neuroscience that studies neural coding and its trying to solve how neurons transmit messages to each other or how they can encode information in general. However looking at the signals by themselves is usually not enough and people are very careful about the particular behavior that is going on while these signals are being recorded, basically it turns out that one needs context to properly interpret the messages that are intercepted.
Good luck :)