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What type of genetic changes occurs when ovaries or uterus are removed from female body?
I saw so many women which have present dermoid cysts in their ovaries or uteruses. Doctors operate and mostly the ovaries and uterus can not be saved and the doctors remove the ovaries or uterus.
Which type of genetic changes occur in such type of women?

welcome to biology stackexchange!
In the classical way we think of the body, there won't be a lot of genetic changes if the ovaries, uterus (or the testes for that matter) are removed from the body.
The main effect would be that the sex hormones that are produced in these organs would no longer be present and this would have a profound effect. So the broad answer might be 'no genetic effects but large endocrine changes'.  Endocrinology is the study of glands and their function in the body. Growing cysts, tumors as well as other effects seem like reasonable effects to see for such a drastic change in the body as removing the reproductive organs.
If I were hard pressed though probably this might end up with some small genetic effects compared to an individual who had never had the organs removed.  Mutations happen frequently in many of our tissues and also they respond to the environment to methylate the genome and modify it in non-genetic ways ( known as epigenetic effects).  This is purely conjecture but its also found that nearly everything has some effect on the cells.
hope this helps.

Answer simplified to match OP level
There are two different parts of biology in this question:

Genetic changes, only happen when the DNA changes (in a person's genes). But in general, this is fixed before your birth (when you are conceived), and what happens in your life does not change it any more.More accurately, genetics can change, or be changed, but not just by removal of a body part like this question asks.
Removal of organs like the ovaries and uterus will mean that hormones they produce, and actions they are involved in, may be reduced or stop.  That can change a persons life a lot, because hormones and other functions play a major role in our body. But it doesn't change the person's genes, or genetic makeup.

A way to think about this is, if a doctor had to remove your leg, or your tonsils, and then you had a child, your child would have the leg, or tonsils, even if you didn't. Because that is in your genes, and has not been changed.


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Why is melanin black?
I understand that the function of melanin is to protect individuals from sunlight, and that people living in sun exposed areas are darker due to increased production of melanin. But why is the melanin pigment black in color? Wouldn't it have been more useful if melanin was white?
From my understanding, black absorbs more sunlight than white, so if melanin is black, it will tend to absorb more heat (which isn't a good thing in areas with a lot of sun exposure). This will lead to production of more melanin (tanning).
Instead, evolutionarily wouldn't it have made more sense if melanin were white, since not only would the pigment protect the person from sun exposure, but also prevent more sunlight from being absorbed?

As phrased, the question is not a biological one, but one for chemistry or physics: melanin is black because of the way its chemical structure interacts with photons.  Perhaps you meant to ask how mammals evolved to produce melanin, and how humans (among others) have evolved to use it as protection against the harmful effects of intense sunlight?

Let's do a quick mind experiment. Imagine a ray of UV light hitting a white molecule in the skin. White generally reflects light, so that UV light would bounce off, and potentially could hit something much more critical. Black, on the other hand, absorbs light, so the energy in the UV light would be absorbed by melanin rather than other, more sensitive molecules. According to this article:

eumelanins are capable of dissipating >99.9% of absorbed UV and
  visible radiation through nonradiative means.

Eumelanins are the most commmon type of melanin. Incidentally, not all melanin is black.
Another quick note, somewhat relevant: Try not to think of evolution as having a goal or purpose. Melanin being black is a result of random changes that happened to result in a beneficial phenotype. It didn't conclude that something was needed to counteract UV light and try to reach that goal.

source: Stack Exchange

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

sort: votes


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Does eating beans of a mother cause flatulence on babies?
Is it true that if you eat beans it could cause flatulence on babies (when breastfeeding them)?
I can't find any research or scientific facts about that topic.
I thought the body of the mother would filter "bad" ingedients.

When the mother eat beans, the fiber (oligosaccharides) from them is not digested in the small intestine, so it travels to the large intestine, where normal intestinal bacteria break it down to some absorbable nutrients (like short-chain fatty acids) and gas that is largerly expelled (fao.org). Some gas can be absorbed into the blood and then removed by the lungs (PubMed).
This means that neither the fiber nor the resulting gas ends up in the mothers breast milk, so it cannot give gas to the baby.
Breast milk contains human milk oligosaccharides (HMO). HMO is undigestible, but bacteria in the infant's intestine can break it down and produce gas. However, the amount of HMO in the breast milk is not likely related to the amount of beans or other high-fiber foods the mother consumes, but is genetically determined (PubMed).

Is it true that if you eat beans it could cause flatulence on babies (when breastfeeding them)?

Yes and no. It primarily comes down to if the mother has the necessary bacteria in the large intestine to break down the oligosaccharides in beans.

I thought the body of the mother would filter "bad" ingedients.

Flatulence from consuming beans is a result of bacteria in the large intestine breaking down oligosaccharides, those of which don't get broken down in the "initial" stages of digestion. There's nothing inherently "bad" about oligosaccharides.
Regardless, oligosaccharides are naturally found within human breast milk whether the mother consumes beans or not. In fact, they're the third most abundant solid in human break milk (behind fat and lactose).
Ultimately, if the mother does not have the necessary bacteria to break down the oligosaccharides but the infant does, then yes, it's theoretically possible that flatulence exhibited by an infant could be a direct result of the mother consuming beans.

So that mean to avoid beans as a mother would reduce the risk for the infant for flatulence?
And second, how can one easily determine if the bacteria exist in the large intestine?
And third, if the bacteria exists, can a mother eat beans without having an effect on the infant?
Your answer is awesome anyway ;)

I don't agree with these conclusions. The amount of oligosaccharides (namely human milk oligosaccharides or HMO) in the mother's breast milk is NOT related to the amount of oligosaccharides in the beans (or other foods) the mother consumes or to the extent to which these oligosaccharides are broken down by her intestinal bacteria. Mother eating beans or not does not influence the gas in the infant.

@Peter, every health human (except newborns) has intestinal bacteria that break down oligosaccharides. They are part of the normal or beneficial intestinal flora.

@Jan Matter of opinion that you disagree. If you have some literature that supports your beliefs, then please provide. Theoretically, it is possible.

@Charles, I have added 2 links into my answer. All 3 sources together explain that fiber is not absorbed, but decomposed (as you also stated correctly). The end result is that fiber does not go into the mothers blood and milk. If you assume that some mothers do not have enough bacteria to decompose fiber, the fiber will be then excreted with the stool and will not be absorbed and will not reach the baby. It is the last paragraph in your answer that is problematic and is not based on any evidence.

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


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Why do both the mango and the bee have "Indica" in their binomial name?
In my textbook, it is written that the binomial name of mango is Mangifera indica and the binomial name of a bee is Apis indica. Now in the name the second part is the name of species. But mango and bee are not the same species. One is a tree and the o,ther is an animal. Then why is their second name the same?

In short, we do not think about the uniqueness of the second part of the binomial (the species epithet) but about the uniqueness of the binomial itself (the genus and the species epithet). Thus, the unique binomial of mango is Mangifera indica and the unique binomial of bee is Apis indica. For more detail, see this question.
To complicate matters  slightly, plants and animals are governed by different nomenclatural codes. So it is possible for a plant to have the exact same binomial as an animal. These are called "hemihomonyms." For more detail, see this question. However, a plant cannot have the same binomial as another plant, and an animal cannot have the same binomial as another animal.
In this specific case, the authors probably chose to give both species the epithet indica because they are associated with the Indian subcontinent, which is the root of that word.

That is the species name it is often the same for unrelated organisms, that is why we use a two name system. Binomial nomenclature (literally, two term naming system) goes Genus species respectively.
The first part of the binomial identifies the genus (which should not be the same unless they are closely related) and the second is the species name which is often little more than a descriptor, you would be amazed how many species names translate to simple concepts like colors or one of the most common, familiaris which just means household or common. In dinosaurs many many end with carnegii because Andrew Carnegie funded so much paleontology and scientists knew who buttered their bread. In your case indica literally means "from India" in latin so it is not surprising many things carry it.
Mangifera indica means 'mango from India', Apis indica means 'honeybee from India;' guess where they were first discovered.
In short, the second name really doesn't matter as long as it does not match anything else with the same genus name. As long as the combination of the two names is different and unique. The first name, the Genus name, however should not be the same unless they are related.

Think of a binomial as a first and last name. Both the genus (first name) and specific epithet (second name) can vary, but both together indicate an individual [species]. Additionally, like most names at some point in their origins, the specific epithet (and often times the genus) "names" can have meanings (and so, in a way, act as adjectives). In your case, indica simply means that each taxa originated (or at least was first described) in India.
See here for further [easy to understand] explanation.

Just like namespaces in programming

Indica in binomial nomenclature means "of India" - from classical Greek and Latin.
Apis indica is more specifically the binomial name of the Indian honey bee, one of the predominant bees (most common bees) found and domesticated in India - differing from the western honey bees (Apis mellifera - mellifera is the Latin word for "honey-bearing") one of the first domesticated insects and most common honey bees around the world.
Mangifera indica or "Indian mango", has been so widely distributed around the world that it has become known as "common mango" and remains one of the most widely cultivated fruits within tropic regions.


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To what extent does the distribution of nerual transmiters in the brain vary human to human?
Suppose $x$ is a position in the brain, and $n_i(x)$ is the density of neuro recepter $i$ around that point. Any given human will have some distribution of neruo recepters $n_i(x)$ through out there brain.
I am wondering what do we know about the statistics of these densities, or how they vary from person to person?
For example, is there a variance in the amount of serotonin receptors in the brain between healthy or unhealthy people?
How does one go about measuring this?


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How exactly does mitotic recombination help repair damaged DNA?
I understand the utility in crossovers during meiosis, but how exactly is mitotic recombination useful for dealing with DNA damage? If one sister chromatid is damaged, the other can supply a functional replacement for the defect part, sure, but then the donor chromatid will lack that section. Isn't that a zero-sum game? What am I missing?

Note: the technical term is homologous recombination (as DNA repair is actually its primary function), and this answer focusses on lesions affecting both strands at approximately the same level (as a lesion affecting only one strand at a particular location can easily be repaired by using the clean strand as a template), such as symmetrical double-strand breaks (where both strands of the double helix are severed at the same level; commonly caused by [and responsible for the main lethal effects of] overexposure to ionising radiation; used as the example type of damage for the purposes of this answer).
Short answer
The homologous DNA serves as a template for synthesis of new DNA to repair the damaged area.
Long answer (paraphrased from here)
If both strands of a chromosome are severed at or near the same location, special enzymes unwind the broken ends, and other enzymes then clip off a length of one of the strands from each end (the strand that gets clipped off is always the one with the exposed 5-prime end, in case you were wondering), leaving an exposed single-stranded flap on each side of the break.
At this point, other special proteins grab onto these flaps, and take them looking for an intact homologous piece of DNA (that's why it's called homologous recombination), which can be either a sister chromatid (which is guaranteed to be either identical or very nearly so, and is, thus, the preferred solution when possible) or a homologous chromosome (which is always available, except for haploid cells [such as human gametes], but is virtually guaranteed to be not-quite-identical, and, thus, is a less-optimal solution).
With the help of the aforementioned special proteins, one of the flaps then butts into the homologous double helix, base-pairs with the strand it's complementary to (forming a structure known as a Holliday junction [well, technically, seven-eighths of a Holliday junction, as one of the junction's four arms has only a single strand, rather than two]), and kicks the other strand out of formation.  The displaced strand forms a single-stranded loop hanging off to the side (known, unsurprisingly, as a displacement loop, or D-loop), while a DNA polymerase latches onto the bare 3-prime end of the invading strand and lengthens it, using the homologous DNA as a template.1
At this point, things can go in either one of two ways:

In the simpler pathway (the synthesis-dependent strand annealing, or SDSA, pathway), the polymerase simply continues to lengthen the invading strand until enough DNA has been added to the end to bridge the gap between the two broken ends and base-pair securely to the flap on the other end; at this point, the invading strand backs out, allowing the invaded DNA to reassume its double-helical dignity, and the newly-lengthened flap grabs onto the complementary flap on the other broken end.  More DNA polymerases fill the remaining gaps, and a ligase seals the helix back up.  The SDSA pathway is the major homologous-recombination pathway for cells not planning on undergoing meiosis.
In the more complicated double-strand-break repair (DSBR) pathway, the exposed flap on the other broken end also gets in on the action, base-pairing to the exposed D-loop and likewise being lengthened by a DNA polymerase.  When enough new DNA has been synthesised to completely fill the single-stranded gaps, the exposed ends are joined together by ligases, forming a structure with no exposed ends and two complete Holliday junctions.  To turn this back into a pair of separate bog-standard double helices, two of the four strands in each Holliday junction are cut by endonucleases, causing the two DNAs to separate.  (There are rules as to which two strands are cut; either both of the two strands that cross over in a given Holliday junction, or else both of the two strands that don't cross over in said junction, but never one crossing and one non-crossing strand [as this would merely create a new double-strand break at the location of the junction].)  Depending on how the Holliday junctions are severed, the portions of the two chrom[atid/osome]s distal to the original break may or may not be exchanged between the chrom[atid/osome]s; if both junctions are severed on their crossing strands, or both on their non-crossing strands, this distal DNA will not be exchanged, while, if one junction is cut on its crossing strands and the other on its non-crossing strands, said DNA will be exchanged.  Due to its possibilities for swapping bits of genetic material, this is the preferred pathway for cells that are planning on undergoing meiosis (although it also occurs to some degree even in somatic cells).

Here's an image to illustrate the process:

(Image by Emw at Wikimedia Commons.  Blame them for the typo in "Strand invasion", not me.)

1: This is why the 5-prime strand got pruned back, and not the 3-prime strand; all DNA polymerases known to science lengthen DNA strands in exclusively the 5-prime→3-prime direction, and can only add nucleotides to exposed 3-prime ends (exposed 5-prime ends need not apply).


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What is this insect

This was found in my house in florida

Welcome to Biology.SE. Your question seems fine, but could you add the size of the animal (and maybe give a somewhat more precise title to your question - e.g. What is this x cm winged insect found in Florida, US?), please? That makes it more likely for you to get an answer.

That is a Milkweed Assasin Bug, Zelus longipes. Order Hemiptera, family Reduviidae. Here is a good website that describes a lot about them. http://entnemdept.ufl.edu/creatures/beneficial/bugs/zelus_longipes.htm


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Can people with AIDS/HIV be vaccinated?
If there is no immune system,it  seems like vaccines wouldn't do much since there is no adaptive immune system to develop antibodies and memory cells. But can people with AIDS/HIV still be vaccinated? It is expected that a normal person will have antibodies to attack the minimal infection produced by the vaccine and generate memory cells, but without an immune system I expect vaccines to be deadly.
Is that right?

Can people with AIDS/HIV be vaccinated?

Yes. Immunization is an important part of the overall treatment strategy for HIV positive individuals. HIV infection is a risk factor for a number of vaccine preventable infectious diseases. Immunization in these patients is particularly important because of their increased risk of developing disease. (See Cecil Medicine Ch 396)
Can the immune system still mount a response to the vaccine?
Yes. HIV infection does lead to a decreased immune response. Though the primary deficiency is a decrease in both CD4+ (helper) T-cell count and function, there is, perhaps consequently, B-cell dysfunction as well. This would suggest that vaccines are less immunogenic. When this is studied directly, as would be expected, we see that vaccines are less immunogenic, but they are still effective.
Which vaccines are given?
Specific recommendations are based on both the age of the individual and their immune status. As a rule, vaccines are more effective when given early in the natural history of an HIV infection or after immune reconstitution with HAART, but there is some effectiveness and little risk of heat killed or subunit only vaccines even in highly immunosuppressed individuals. While live attenuated vaccines are contraindicated in individuals with a CD4+ cell count below 200, these vaccines are given routinely to other HIV positive patients. Current guidelines are found here. Here is the main figure from those guidelines:

Can people with HIV still be vaccinated?

No (most of the time) if the vaccine is an attenuated vaccine, this means it contains living organisms that have been modified in order to reduce their virulence. The reduction would keep a healthy individual unharmed while still inducing an immune response to form antibodies, however it is considered dangerous to administer these kinds of vaccines to HIV positive people. Some physicians will decide to administer these kinds of vaccines if the patient has had excellent control of his/her disease and is strong enough to take for example, the influenza virus vaccine without any major complications.
Yes if the vaccine is not an attenuated vaccine. Being HIV positive doesn't mean "no immune system" right away. The damage to the immune system goes in function with the viral load and the CD4 count; if the viral load is low the HIV positive individual can still benefit from vaccination, moreover he should be vaccinated because he is more exposed to infections than an average person.

source: HIV InSite, University of California San Francisco.
I would suggest also reading more about CD4 count in HIV patients and viral HIV load.

I think I don't understand. If the vaccine is atenuated, they can't be vaccinated; but if the vaccine IS NOT atenuated they CAN be vaccinated? It's the opposite of what I would expect.

@Gabriel the missing information here is that the alternative to live attenuated is killed or antigen component only. Vaccines that are not live vaccines cannot replicate in the vaccinated individual. There are no non-attenuated live vaccines.

To clear things up vaccines that don't belong to the group of attenuated vaccines do not contain any sort of living organisms and use other agents to induce immunization (polysaccharides, inactivated toxoids, etc.) and hence are safer to use in an individual with a compromised immune system.

@DeNovo, there are no non-attenuated live vaccines any more.  The original vaccine for smallpox was the live cowpox virus.

@Mark vaccinia, in that instance was effectively an attenuated variola.

A person with AIDS cannot be vaccinated. The immune system is no longer functional and is unable to mount an immune response to your vaccine.
If the vaccine is a "live vaccine", the person will get a dose of viruses that body can no longer fight against. And the live vaccine would probably give the AIDS patient an infection of what the vaccine was suppose to protect against
However if the vaccine is an attenuated vaccine (which is the case for most vaccines made today), then all your be introducing into the body is parts and pieces of a virus or bacteria. These piece can trigger an immune response in a healthy person but as they just pieces, are not a live cell or a functional virus. So in a person with AIDS, the attenuated vaccine will be harmless.
A person with HIV can be vaccinated. The HIV virus is in the body multiplying. However the immune system while damaged is still functional.

"if the vaccine is an attenuated vaccine (which is the case for most vaccines made today), then all your be introducing into the body is parts and pieces of a virus or bacteria."

It sounds like the opposite of what the other answer said.

Most vaccines contain dead virus today. Attenuated viruses are alive (as far as you can say that for a virus) but usually do not cause full blown disease. An example for this is the oral polio vaccine.

With genetic engineering, its not possible for the immune system to be "completely" non-functional. This is because the body is constantly producing immune cells from non-terminal differentiated cells. These cells are almost never specifically targeted. Whatever is left can, with time, clean up the infection.


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Is it possible to contract the plague by kissing a wild chipmunk?"
I watched  this cute video and I came to conclusion that the lady in the video is putting her life in danger. She kisses a wild chipmunk.
As I know, they have fleas, and fleas have a black plague. Am I right? But maybe the risk of infection in contact with just one chipmunk is low?
How dangerous is such behaviour?

Very dangerous. Cute videos rot the mind (of those that watch them).

I suggest replacing the question title with the one you're actually asking: "Is it possible to contract the plague by kissing a wild chipmunk?"

I was going to vote close for opinion-based, but apparently this is actually a risk: https://www.cdc.gov/plague/resources/PlagueEcologyUS.pdf

@Armatus Yes, transmission risks are generally well studied and not opinion based. If you get a VTC as opinion based itch, hold off for someone who has specific knowledge

@DeNovo "As I know" is a signal phrase for opinion basis, but as you can see I do double check

@Armatus a quick search is not always a good way to tell whether something is or isn't opinion based. Be wary of the opinion based VTC, which is often a "not my field" VTC.

@Armatus this was a great suggestion!

The causative agent of the plague, Yersinia pestis, can be indirectly (via a flea vector) or directly (via exposure to infectious fluid or a bite) transmitted by rodents. In the western United States in particular, Y. pestis is endemic, and ground squirrels, prairie dogs, chipmunks, and woodrats are important reservoirs (see Cecil Medicine Ch. 320). US National parks have signs warning against feeding squirrels and chipmunks for this reason. You can read more about it in a national park brochure . Chipmunks and squirrels indirectly and directly transmit a variety of other diseases as well, including Tularemia (Cecil Ch 319) and various tick and flea borne encephalitides.

Can you also tell how dangerous is it for that lady? I mean except for kissing the chipmunk, she doesn't seem to be a poor medieval peasant. Not even a poor modern day folk. Maybe if she is generally clean, such cute act poses a low risk? And if she contracts plague, how doomed is she? I wonder how much darkness lurks in this cute video.

@user46147 Y. pestis infection is treatable, though it can cause loss of limb or death, especially if diagnosis is delayed. It's not a common disease. There are a few thousand cases globally every year. Exposure to the chipmunk is a risk factor, regardless of whether she is a medieval peasant or royalty, and it is a risk factor for more than just the plague.


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How to tell petiole apart from stem?
How to tell petiole apart from stem? Is it by the rule that there is usually a pair of stipules at the base of a petiole?

Petioles typically have the presence of one or more of the following:

Stipule at base of the stalk
Axillary bud between the stalk base and attached stem
Leaf scar when removed

Source: Miami University

Source: Wikipedia
None of these characteristics would be present if the stalk you were looking at is a stem.

However, they are not always each visible on every species...
From: Oregon State University Dept of Horticulture:

It is not always easy to find the bud at the base of a petiole, it may not be visible early in the growing seaon and sometimes a mature bud is “hidden”, such as being enclosed by the petiole base.

From Wikipedia:

although in many species the stipules are inconspicuous or entirely absent (and the leaf is then termed exstipulate)

Leaves are usually borne from petioles and rarely from the stem itself -- so presence of a leaf (or compound leaf parts) is usually indicative of a petiole as well. However, sometimes plant leaves lack a petiole altogether, as in the case of sessile leaves.
In other instances, specifically those of compound leaves, the stalk of compound leaves (i.e., the rachis) will lack the properties previously described for a petiole, but following the compound leaf to the nearest stem typically will result in locating the petiole with one or more of the above mentioned characteristics at its base connecting the compound leaf to the stem.


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Is gut bacteria Succinivibrionaceae's low methanogenesis understood well enough for GM of cattle gut bacteria to be considered?
After watching the Periodic Table of Videos episode linked in this question I watched the episode Wallabies and Methane where Sir Poliakoff says (a bit after 02:00):

So the point of this paper was that Wallabies have different bacteria in their stomachs, which instead of producing methane, produced succinic acid, which is the diacid of butane.

 Succinic acid, Source
The paper he references seems to be Isolation of Succinivibrionaceae Implicated in Low Methane Emissions from Tammar Wallabies Pope, P. B. et al. Science 29 Jul 2011: Vol. 333, Issue 6042, pp. 646-648 DOI: 10.1126/science.1205760
Question: I can not understand the abstract, and the paper is paywalled. Presumably much more work has been done since its publication in 2011. How well is  Succinivibrionaceae's low methanogenesis understood; well enough for the genetic modification of cattle gut bacteria to be considered?

Abstract
The Tammar wallaby (Macropus eugenii) harbors unique gut bacteria and produces only one-fifth the amount of methane produced by ruminants per unit of digestible energy intake. We have isolated a dominant bacterial species (WG-1) from the wallaby microbiota affiliated with the family Succinivibrionaceae and implicated in lower methane emissions from starch-containing diets. This was achieved by using a partial reconstruction of the bacterium’s metabolism from binned metagenomic data (nitrogen and carbohydrate utilization pathways and antibiotic resistance) to devise cultivation-based strategies that produced axenic WG-1 cultures. Pure-culture studies confirm that the bacterium is capnophilic and produces succinate, further explaining a microbiological basis for lower methane emissions from macropodids. This knowledge also provides new strategic targets for redirecting fermentation and reducing methane production in livestock.

I may need help with tags; I didn't see genetic-engineering or genetic-modification. I can not think of a shorter but still accurate and descriptive title, help is appreciated there as well, thanks!

Old question, but: it's worth noting that there is substantial variation in methane emissions even among ruminants such as cattle. And indeed, even among cattle, Succinovibrionaceae are associated with lower methane emissions. So quite possibly you don't need to do any engineering, though there are apparently a large number of (then) poorly described metabolic genes that might be relevant:

Lower emissions were accompanied by higher Succinovibrionaceae abundance and changes in acetate and hydrogen production leading to less methanogenesis, as similarly postulated for Australian macropods. Large numbers of predicted protein sequences differed between high- and low-methane-emitting cattle. Ninety-nine percent were unknown, indicating a fertile area for future exploitation.

Instead of sorting through all those proteins (which might be fun but would probably take a lot of work), it might be more effective and easier to simply make cattle rumens better places for low-methane bugs to live, if your goal is to reduce methane. Possibly unrelated to these bugs, but for example feeding seaweed to cattle lowers their methane production by affecting their microbiome through antimicrobial activity.
The old adage in microbial ecology is often wrong but always helpful to remember: "everything is everywhere, and the environment selects". So set up an environment that selects for the kind of bug you want!

This is probably a better answer than an answer to the question as-asked, +1!

The question — which I would regard as off-topic as not being about a problem in biology — was about whether science had progressed sufficiently for some unspecified genetic manipulation (I assume GM does not stand for General Motors) to be performed. Your information is not without interest, but provides a non-answer to a non-question.


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Why do we have an immune system?
My daughter asked a question that I could not answer.
If you have a cold, you have symptoms such as fever, cold and sore throat. These symptoms, however, are the reactions of the immune system to bacteria, viruses and other germs.
So my question is: What would happen if the immune system did NOT respond? I know that bacteria can produce certain poisons. And viruses can capture human cells and make them produce more viruses.
Now to the naive part: But what's wrong with that?

Are Viruses dangerous because these cells would then no longer perform their function?
Without any immune system: Would a virus simply take over all human body cells?
Is it not the organism in the first place, who puts itself in mortal danger (such as high fever or inflammations) because of the defense reaction?

Thanx!

I hate to say it but, it depends. There may well be some pathogen which would otherwise be harmless, if not for the body's defense mechanisms. However, we are talking about a system which has evolved over thousands of years. In turn, the pathogens have also been evolving for thousands of years. There have been countless variations over the years. One thing is for sure, people who have an issue with their immune systems tend to die from pathogens which people who have healthy immune systems do not die from.

Basically you would rot from the inside out, as bacteria and viruses destroy your cells.
Fever is your body using heat to denature the viral proteins (viruses don't have chaperone proteins like us so they are more vulnerable to heat) Sore throat is you body killing infected cells before the virus can reproduce inside them, normally the virus will reproduce inside the cell until the cell bursts or simply runs out of resources and dies both release huge numbers of the virus.
Check out the virus life cycle. https://en.wikipedia.org/wiki/Viral_life_cycle


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When two amoeba cells form from one amoeba, does spindle fibers form?
When two amoeba cells form from one amoeba, does spindle fibers form? Some sources say that spindle fibers do not form while an amoeba cell is undergoing cell division. If spindle formation does not occur, than how are the chromosomes pulled apart? Which intracellular transport mechanisms are used?

Amoebas undergo binary fission, which is a much more simplistic process than mitosis. In binary fission, the duplicated chromosomes simply separate as the cells is pulled apart. There are no spindle fibers used in this method of cell division.
Ok - so some of my references were a bit older, and I went through and looked through the literature a bit further - and found this great newer (ish) reference that actually used optical imaging to document the process of cell division: https://link.springer.com/content/pdf/10.1134/S1990519X16010041.pdf   Demin, S. Y., Berdieva, M. A., Podlipaeva, Y. I., Yudin, A. L., & Goodkov, A. V. (2016). Optical tomography analysis of Amoeba proteus chromatin organization at various cell cycle stages. Cell and Tissue Biology, 10(1), 84-94.
The process by which they undergo chromosomal separation is  a bit different in that there is no clearly identified kinetichore, but it looks as if microtubule spindles are involved. My error!  The process of DNA replication and other stages are quite different in this process that in typical mitosis.


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What is an accessible book about plant evolution for a non-biologist?
I have an acquaintance interested in learning about the evolution history of plants. This person has a wide knowledge on botanics, from personal reading and taking care of plants, but E is neither a biologist or a biology student.
Based on this, which is an accessible book to non-biologist that can be used to learn about the evolution of plants?

Can you please provide additional details like: what extent of information do you expect, what topics should it cover etc. If a person is a non-biologist then they can simply start with a general book on evolution. There are many popular books for non-biologists (or even non-scientists). This website is also a good place to start. Unfortunately, the answer to your question would highly depend on the personal opinions of people. Unless you ask very specific recommendations, literature suggestions would be off-topic.

I have Fossil Plants by Paul Kenrick and Paul Davis, published by The Natural History Museum in London.  It takes the reader through a well-researched but accessible illustrated history of the evolution of plantlife from the beginnings to now.  There are photos of many key fossils, and artist's renderings of what the landscapes of the past would have looked like.

It is possible to download it as a pdf from researchgate. https://www.researchgate.net/publication/248686492_P_Kenrick_P_Davis_2004_Fossil_Plants_216_pp_London_The_Natural_History_Museum_Price_1695_paperback_ISBN_0_565_09176_X

@John, that is a review of the book, not the book.

So it is, my mistake, still helpful so I'll leave the link.


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Why isn't Fluorine, or Neon, the final electron acceptor in cellular respiration?
I'm a Chemistry student learning about periodic trends. I know that in (many organisms') cellular respiration, oxygen serves as the final electron acceptor due to its high electronegativity.
However, applying the periodic trends, fluorine is more electronegative than oxygen, and the noble gas neon even more so than fluorine. Why aren't either of these the final electron acceptor? I know that in some organisms, the final electron acceptor is sulfur. But I've never heard of it being fluorine or neon. Why?

One of the main reasons that modern(!) biology uses oxygen as an electron acceptor is availability.
Around 2.45 billion years ago, oxygen (O$_2$) started being built up in the atmosphere (which actually killed off a lot of the lifeforms/bacteria at that point). Since then, oxygen consuming lifeforms were able to establish themselves. Before that, most organisms probably used mainly (elemental) hydrogen as electron acceptors.
Apart from not really being available in the atmosphere, there are other reasons why fluorine or neon don't make for good biological electron acceptors:

While elemental fluorine (F$_2$) is indeed extremely electronegative, this makes it so reactive that it:
a) could not be controlled by biology [the reactivity of oxygen is why it killed so many bacteria in the first place] and
b) just does not occur (or at least remain in) in the elemental state in nature (there is no measurable F$_2$ in our atmosphere).
Neon (and other noble gases) are in theory also quite electronegative, actually so much so, that they never* occur without their electrons and therefore don't react at all.

*It's somehow possible to form noble-gas compounds, but it requires very specific chemical reaction conditions, that mostly occur under controlled man-made conditions (and are not good for biological life forms).

I suspect another reason is simple availability.  Oxygen is the most abundant element in the Earth's crust, fluorine is relatively rare (> 0.1%), and tightly bound in compounds.

There are instances of fluorine gas found in nature (within certain minerals) but they are pretty rare. YouTube and press releases 1, 2

Note that oxygen was available to organisms well before the GOE, merely in bound form.

Yeah, try breathing F2, it won't be fun.

Availability and applicability.

Availability.
In the beginning, there was CO2. It was abundant in the atmosphere, and later, the oceans.
Fluorine and neon weren't, and so respiration evolved around what was (and is) available.
Ref.: Paeloclimatology / History of the Atmosphere.

Applicability.
The other point about oxygen is that it works rather beautifully both ways. Chloroplasts can easily split up CO2 and H2O into glucose and O2 with a bit of sunlight. Hemoglobin can combine both O2 and CO2 with just a little difference in partial pressure. Mitochondria can run through the citric acid cycle without getting destroyed in the process.
Once fluorine has taken hold of another atom and formed a molecule, it will be pretty hard for an organism to make it let go again, and if it does the fluorine will want to react with something, anything really, whether that's good for the organism or not.
On the other end, neon doesn't want to react with anything.

So while chemically there's a point to be made for the more energetic oxidizer, evolution / an organism is not "interested" in the energy content alone. The substance must be available, and the process must be somewhat sustainable. Oxygen ticked those boxes, fluorine and neon didn't.
Even rocket scientists, who are really looking for the most energetic compounds they can get their hands on, dropped the idea of fluorine as a propellant because it's not safe to handle in uncombined form. There's a lesson in there.

Availability isn't the fundamental issue with neon. Even if half the atmosphere were neon, we wouldn't be using it in respiration.

@DavidRicherby: You could say the same about fluorine. Both factors -- inavailability and chemical unsuitability -- apply. Either would be enough as an explanation on its own.

I think the rocket scientist example is flawed, because these rocket scientists happen to belong to a biological system that has evolved using oxygen. Reasoning after the fact of evolution under oxygen availability is not telling that evolution under predominant fluorine availablity couldn't have lead to (other, functioning) biological systems. To point out another example: H₂O is really a very aggressive and corrosive solvent. But we are perfectly adapted to deal with it and use it, and thus it is fine for us, whereas, say, H₂S is not. However, already if you'd ask some  sulfur-oxidating...

... bacteria, their "point of view" will differ considerably.

@cbeleites: Which on the one hand takes us right back to "availability" -- H2O was on this planet long before life was, so naturally life evolved to be tolerant of H2O. Predominant fluorine "availability" would mean abundance of fluorine compounds, and you'd still face the problem of breaking those up for an organism to actually do anything with the fluorine (that doesn't destroy the organism). I'm open for a demonstration of a viable "breathing cycle" corresponding to photosynthesis / citric acid cycle that works with fluorine.

@DevSolar: of course. As modern chemist I'd start by guessing cell walls of teflon to contain HF solution. I.e., while of course I cannot say how nor whether things would have evolved, I'd expect a fluorine-based biology to be all in all more "harsh" (in a similar sense as that our oxygen-based biology uses more harsh chemistry than the sulfur based (nowadays) niche biological systems), but then the whole organisms would probably be more "fluorinated" and thus able to cope with fluorine/HF. (Also, on the one hand the difference in electronegativity between oxygen and fluoride is less than that

between sulfur and oxygen, but at the other hand, there's the step from divalent to monovalent which would be a major difference). Also, the aggressivity may be offset to a certain extent because we may be looking at systems that work in much colder temperatures: 20 °C is the boiling point for HF, melting point is below -80 °C. Stepping down a few 10s of °C may be slowing down reactions to a suitable pace. Who knows? Summary: HF/F₂ based biology would surely look quite diffrent from "our" biology. But that doesn't mean it cannot work.

@cbeleites: ...but not on Earth, or anything even remotely similar to it. So... as far as the answer to the OP's question is concerned, is there anything that would "need" editing?

@DevSolar: no, sorry: I like your answer - no need to edit. The point of my comment is just that the alien rocket scientist (or combustion engine engineer) from the HF-planet may think fluorine a totally normal oxidizing agent... (and may have trouble if that bit of H₂O they have gets into the HF in their system...)

The atomic radius of fluorine is just slightly larger than that of carbon.  When a fluorine atom bonds to a carbon atom that is part of a carbon backbone, the fluorine atom covers up not only the C-F bond but also the adjoining C-C bonds.  This makes it impossible for biological enzymes to access these bonds to break them, and is why fluorinated compounds are biologically inert.
This is the reason why we fluoridate water and toothpaste; bacteria have no enzymes that can break down enamel that is formed with fluorine!  It is also why teflon (repeating units of -CF$_2$-) is not biodegraded yet saturated fatty acids (repeating units of -CH$_2$-) are easily biodegraded.
All elements that are used biologically have ecological cycles where they are reused for other purposes.  Because fluorinated compounds can't be broken down, such an ecological cycle would rapidily come to a halt.  Therefore, fluorine has an evolutionary disadvantage over other elements.
I agree with the other answers that neon can't be an electron acceptor because it won't form into compounds.  I disagree with their "oxygen first" argument; evolution doesn't care which mechanisms evolve first.  If a fluorine metabolic pathway had been more effective than oxygen's, its pathway would eventually surpass the earlier-evolved pathway.  Furthermore, there are plenty of trace minerals (e.g. selenium) that are used by life.

Evolution does somewhat care about which mechanism evolves first: it tends to seek a local optimum, not a global optimum.  If the benefits of an oxygen pathway and a fluorine pathway are similar, and both are a major advantage over whatever came before them, evolution is likely to get "stuck" on whichever one evolves first.

@Mark True, but then you get something like the evolution of photosynthesis, and everything gets thrown out of whack planet-wide. It's not inconceivable that the same thing could happen with something like fluorine, if it were available. The availability argument is much stronger - regardless of utility, life can't use it if there's no source for it. The proportions of elements in life are pretty close to the proportions of biologically available elements (e.g. including the "no enzymes" argument) in Earth's soils and oceans.

Neon just does not work as an electron acceptor. It is that inert that there are currently no known Neon compounds at all.
Fluorine would work in principle, but it is rare compared to oxygen and its strong reactivity makes it a very dangerous substance in elementary form. So it seems very natural that life chooses Oxygen and not Fluorine.

Of course, oxygen is also a horribly dangerous substance - it's just that evolution created life that's able to cope with it. Even then, it's a balancing act and oxygen (and oxygen compounds) are responsible for quite a few cell deaths and cancerous growths :P The Great Oxygenation Event killed of almost all life on Earth's surface/oceans. But granted, coping with fluorine would be even worse, and perhaps impossible (under standard pressure and temperature).

The reason is, free Fluorine does not exist in nature and Neon is a noble gas. I would make the assumption, that oxygen is the only free and abundant electron acceptor in our biosphere.
1) Fluorine reacts with every element with only a few exceptions (some noble gases) and will thus be bound instantly even if it is constantly produced somewhere.
2) Because of its electronegativity the energy to free Fluorine from complexes is very high, so efficiency of photosyntheses will be shitty.
3) Under the assumption there would be an atmosphere of fluorine gas, carbon based life could not exist, because fluorine reacts with carbon already below room temperature.
The comment below stating that fluorine is rare is plain wrong. It is not as common as oxygen, but doesn't need to be. E.g. carbon is also rare in comparison to oxygen. The main problem is lack of accessibility due to stability and high energy necessary to free it, connected with the fact that it would destroy every protein. A suitable electron acceptor must be metastable and be able to co-exist with carbon based life.

Free oxygen also didn't exist in nature when life first formed. It needed to be liberated through photosynthesis. The more important thing is that fluorine is very scarce even in compounds, compared to something like oxygen. While its abundance would be enough if it had a micro-nutrient role, it certainly isn't enough for something like being the final electron acceptor. And then there's the other tens of reasons why fluorine wouldn't work, like the fact that it (and its compounds) don't dissolve in water...

Whatever, free fluorine never existed and therefore it never was an option. It will also never be an option, because even if it would be produced by plants, it would react instantanously with something else. This means it will be never a free electron acceptor. Nowhere in the universe.

This source request is silly.


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How does fish breath under water?
How we will describe the whole mechanism of fish breathing under water? How they absorb oxygen and and then remove oxygen through a process known as gas exchange?

Did you read articles like this about respiration in fish already? If so, could you please edit your post and add, what exactly remained unclear?

Fish are able to obtain oxygen that is dissolved within the water, and exchange it along with Carbon Dioxide through their gill structure, called filaments.  The gills are located adjacent to the mouth and filaments include a large amount of blood vessels.  Those blood vessels (capillaries) are close to the gill filament surface and move in the opposite direction to the water flow, which they are exposed to by means of the fish drawing in water through it's mouth.  The tissue that comprises the filament is porous and allows for diffusion of these small molecules (oxygen and carbon dioxide) across this tissue and into the blood vessels.  Each red blood vessel consists of four "Heme groups," which are designed exclusively to bind to oxygen and transport it through the body. A process called the Root effect (Bohr effect in other vertebrates) in hemoglobin regulates the "drop-off" of oxygen by recognition of low pH values.
Hughes, G. M., & Morgan, M. (1973). The structure of fish gills in relation to their respiratory function. Biological reviews, 48(3), 419-475.
Bonaventura, C. E. L. I. A., Sullivan, B., & Bonaventura, J. (1976). Spot hemoglobin. Studies on the Root effect hemoglobin of a marine teleost. Journal of Biological Chemistry, 251(7), 1871-1876.


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Do Colorblind People Have Stronger Sensitivity in Their Other Remaining Cones?
I came across this paper Color defect and color theory. The paper explained about how unilateral color blind (people who color blind only in 1 eye) actually see less bright in their color-blind eye (in graph : filled bullet) compared to the normal eye (in graph : white bullet). Especially to the scene that corresponds to the missing cone (in this paper, Deuteranopes. Missing cones = green)

I have 2 questions regarding this brightness loss in color blind people.

Green cones response are near the red cones response, and they are overlapping. How is it possible that Deuteranopes loss brightness in Green and Blue (which will make more sense if they also loss brightness in Red, thus loss brightness in the whole spectrum) but instead, still achieve the same amount of brightness in Red ? Despite Red and Green color-blind have the same color combination possibility (gamut mapping) that they can perceive ?
Could it be that color-blind people have stronger sensitivity in other cones (for example : stronger in red) and then this red opsin actually replace / fill the missing cones stimuli in retina, so their retina still able to perceive the same amount of brightness on that excessive cones ?

Kudos for Delta-S in Reddit for enlighten me. Original post is here.
The answer is no, color blind people don't have stronger sensitivity in their other remaining cones. This goes back to the Photopic Sensitivity Graph below.
As you can see, human vision are most sensitive to green. All responses of green cone are within the photopic sensitivity as well as most response of the red cones. And despite few responses of red cones are outside the Photopic sensitivity, the peak sensitivity of red cones is very close to the peak of Photopic sensitivity (560nm and 555nm).

Peak Photopic Sensitivity: 555nm
S cones peak  : 420nm
M cones peak  : 530nm
L cones peak  : 560nm

So, in case of Deuteranopic, depending on which wavelength is loss (defected) from their eye, if it closer to the red response then they will likely to experience luminance loss as well. However, if the green cone that is defected is far from the red response, the red cones still have possibility to maintain the luminance they can achieve.
Unfortunately in the paper, it's not mentioned which sensitivity wavelength was defected from the unilateral participant. It is only mentioned "result indicate that she was deuteranopic".


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How does vasodilation slow blood flow?
During inflammation, cytokines and histamine cause vasodilation to increase blood flow to the inflamed area. However, it is also said that vasodilation slows blood flow which facilitates the adhesion and movement of leucocytes through the blood vessels and into extravascular tissue. My question is how does it slow blood flow? To me it would seem that there would be less drag force for a given volume of blood which would increase the speed of flow. There would also be less resistance.

The measurement that decreases during vasodilation is flow velocity, $v$, or a change in distance over change in time $\frac{\Delta x}{\Delta t}$. Prior to a reflex response, the same rate of flow, $Q$, or $\frac{\Delta V}{\Delta t}$ enters the capillary bed (here we use a capital V to represent volume, where $\Delta V$ is a change in volume, and $\frac{\Delta V}{\Delta t}$ is the change in volume over change in time. Because volume is area times a third distance dimension (e.g., if we say area is height times width, then volume is area times depth or thickness), we can describe flow as flow velocity times cross sectional area ($Q = A \cdot v$, or  $Q = A \cdot \frac{\Delta x}{\Delta t}$). If you increase the cross sectional area, $A$, and maintain the same flow, $Q$, then flow velocity, $v$, has to decrease.
A more intuitive explanation would involve turning on a garden hose and covering part of the end with your thumb. The smaller the opening you allow, the greater the flow velocity through the end of the garden hose. The same volume of water leaves the hose per unit time. It's just moving at a faster flow velocity if you decrease the cross sectional area (and at a slower flow velocity if you increase the cross sectional area).
This is discussed in Chapter 4 of Costanzo Physiology, in the section on hemodynamics.
The actual physical measurements end up being more difficult to predict in a situation with parallel capillary beds and reflex responses. $Q$ does not stay constant, for both the specific capillary bed, and for the entire circulatory system. However, you can say that, as a general rule flow velocity, or $v$, will decrease when cross sectional area, $A$, increases. As @BryanKrause points out in particular, provided the series resistance for a capillary bed doesn't change, the initial $Q$ for the capillary bed won't change, which means this caveat isn't relevant.

You might improve the answer by considering an entire branch of the vascular tree from artery to capillary. Because resistance does not occur in one cross-section, local vasodilation has a bigger effect on velocity than flow, even when the overall pressure is distributed in a parallel configuration with other branches of the tree.

@BryanKrause could you be more specific with your suggestion? This is textbook level material, and I'm honestly not certain if in a local (vs. systemic) inflammatory response there are good measurements that show resistance clamped upstream of a dilating arteriole, enforcing a constant $Q$.

It doesn't have to be upstream or downstream specifically, if there is any part of the vascular tree that is not affected (or less affected) the effect on velocity in the affected area will be bigger than the effect on flow, because flow is dependent on the series resistance whereas velocity depends on the local cross-sectional area.

I don't have time to grab a reference but I think the important vasodilation for leukocyte infiltration is on the venous side.

@BryanKrause local mediators of inflammation have different actions on venules than on arterioles, but the question is about the relationship between dilation (i.e., increased cross sectional area) and flow velocity. If you have a specific suggestion for how to change the answer, I'd be happy to incorporate it, or you can feel free to edit. I trust your physiology knowledge.

@BryanKrause incidentally, I just looked it up in Robbins, and histamine, at least, does appear to clamp resistance upstream. I'm not sure that an increase in resistance downstream would hold flow to a capillary bed constant, at least initially, since there is an low resistance path out of the capillaries into the tissue


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How can i count my E. coli colonies?
I did a test which involved growing e. coli on a petri dish. I did not dilute the sample, and this resulted in growing hundreds of small, overlapping colonies. However, they still can be counted, but it has been tedious work. Does anyone have tricks for counting small colonies? Also, I've read people will just write >300 if their colony count is too large. Is this data sufficient? I need to compare the colony count for several petri dishes and they all have quite a lot. If i just write ">300" for 80% of my data, it won't be a very good comparison. Can anyone help me out here?

I had once learned of a method where you can observe through a microscope and do a calculation. However, I can't remember the exact procedure over the top of my head. Do a google.

Read this on why people report >300. It’s acceotable depending on what you are doing. If you need an actual count, you need to dilute the original culture.

I'm seeing an opportunity for some image analysis here. Sounds like you could tweak some basic segmentation methods to at least approximate the number of seeds on your plate, but you'll need to work yourself into FIJI (https://fiji.sc/) or a similar image analysis software. Might be able to get help at the forum at https://forum.image.sc/tags/fiji

Actually, Cell Profiler (http://cellprofiler.org/) might have out-of-the box functions that could count your dots, but the image format might need some adjusting.

Divide the plate into equal sectors. Count one sector as accurately as you can then multiply that number by the number of sectors. This assumes the colonies are roughly equally distributed.


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Glycolysis step 5: isomerization by triose phosphate isomerase
On the 5th step in glycolysis, triose-phosphate isomerase converts dihydroxy-acetone-phosphate to glyceraldehyde-3-phosphate.
Now my question is: Why?
Most books and sites I've read only say that glyceraldehyde-3-phosphate has a direct pathway compared to dihydroxy-acetone-phosphate. Anyone with additional info on this would help much if they shared.

Can you please clarify your question? Actually I am not sure, if I understand what you are asking.

Welcome to SE Biology. Unfortunately your question is unclear and does not yet meet our standards. It could be made to do so if you edit it. First, as a new poster, you should take the Tour and read the Help on Asking Good Questions. You should also look at other questions on the site where you will see that we use standard English here, not textese. Most important, we cannot explain statements you encounter in your reading unless you quote word for word and name the source (with a link if possible).

Thank you .I'm new, I will read through the guidelines and try to rephrase the question.

"a direct pathway" to what? If you consult a text to complete that phrase you will most likely see the answer to your question yourself. In any case wiithout completing it your question is still unclear, regardless of any scatter-gun answers that are posted.

"Why" questions in biology tend not to make sense-
https://en.wikipedia.org/wiki/Teleology_in_biology
But perhaps if I narrate the reaction it will connect with your intuition.
Let's look at the reactions in question:

https://en.wikipedia.org/wiki/Glycolysis#Summary_of_reactions
Step 4 in glycolysis cleaves fructose 1,6-bisphosphate into two molecules that are isomers. One isomer (glyceraldehyde 3-phosphate, GADP) is a reactant in step 6, and fuels the “payout phase” where glycolysis reactions begin to yeild ATP and NADH. So what happens to dihydroxyacetone phosphate (DHAP), the other product from step 4? How can we extract energy from this?
Reaction 5 is the interconversion of GADP and DHAP. So as GADP is consumed by reaction 6, reaction 5 will, by Le Chatlier’s principle, lead to net conversion of DHAP to GADP. The GADP produced by this isomerization then also feeds reaction 6. In this way, both of the products of reaction 4, GADP and DHAP, are channeled down the chain to fuel NADH and ATP production.


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Why are semi log graphs used in drug Dose response curves?
Why are Dose response curves, as well as most biological graphs shown in semi log graphs and not normal graphs? What is the advantage of semi log graphs over regular graphs? I still haven't gotten an intuitive sense of the answer, can someone explain, maybe with a diagram?

The reason is to make it easier to determine a suitable dose from the graph.
Normally, using a arithmetic scale, the response curve is a hyperbolic, with most of the information squished together in a small section of the graph. By using the log the function usually becomes somewhat sigmoid, with a relatively linear section in the transition from low-high response. This means that this dynamics in this section can be studied more carefully.
See e.g. this example (with data from https://www.idbs.com/media/396649/dose-response-comparison-example-hr.jpg), where I have reversed the x and y-axes, and used a secondary y-scale to show the log dose (so the graph is flipped compared to a normal dose-response curve). Here, the orange line shows a semi-log dose-response curve, and the blue line shows the same data using a normal arithmetic scale. Note that the orange line (log dose) should be read against the right scale and the "normal" dose against the left scale):

Here it is obvious that the normal scale doesn't give any possibility to interpret the region where the dose is effective, while this is obvious in the log graph.
The statistical modelling of these data is to some extent a separate issue though, where probit model or logit models along with data transformations are often used to analyse the data. Note also that the "usefulness" of the semilog-plot only lies in the visual presentation, and whether it will add anything depends on the dose series used in an experiment. If the doses used are not exponential (as in this example), the semilog-plot will not add much. In the statistical test of an effect the log dose is also usually not important, and I suspect (as someone not working in pharmacology) that the semilog plot is to some extent a historical artifact from the time before computer analysis of results, when the appropriate dose was determined in  a more manual way (e.g. linear analysis of the middle portion of the semilog graph).
Example data:
dose (conc.)    response
0.00001         0.993
0.0001          1.02
0.001           3.12
0.01            6.36
0.1             31.97
1               51.2
10              75.96
100             89
1000            97.932
10000           98.8

Regarding your point about the historical background of the semi-log graphs, there's a few more factors. Namely, adding a competitive antagonist causes a parallel shift to the right in a semi-log graph - this is much simpler than the change in a graph that isn't semi-log. It also allows you to make a Schild plot comparing the amount of the parallel shift with the concentration of the antagonist, which can tell you the strength of the antagonist.

It also allows similar advantages for the analysis of noncompetitive antagonists and partial agonists.

@Jam Thanks for the additional background, and feel free to add to and edit my answer. Good to hear from somebody with more specific knowledge on dose-response curves than me.


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Do Squirrels have 4 legs OR 2 arms and 2 legs?
Do squirrels have four legs, or two arms and two legs?
I first asked this question many years ago, and it has since unearthed a whole array of conundrums and questions that I have struggled to get a conclusive answer to.
See a squirrel (often described as a quadruped, 4 feet, which implies 4 legs) can stand on its back two legs and hold a nut in the paws of its front two legs - but those front legs are jointed in a very similar way to arms, look like arms and are being used as arms.
When a squirrel runs, it uses all four limbs - but then so does a gorilla, and that definitely has arms.
So in trying to answer this seemingly simple question I ended up lost in a world of definitions and further questions - questions like "what is an arm anyway?"  "what is the difference between a paw and a hand or foot?" - and after trying to find out the answers to those questions I ended up in a much stranger world.  Octopuses have arms, but no hands - bats have hands, but no arms (I will spare you one of the resulting conversations which wanted to know how long a nose has to be until it's a trunk, especially concerning anteaters).
I could be wrong but it seems to me that if your front paws are called hands, then you have two arms and two legs.  Koalas, for instance, are often described as having hands despite also being described as quadrupeds.  Perhaps the differences are merely linguistic choices rather than anything relating to the biological nature of these limbs.  I just don't know anymore, and at this stage, I am starting to wonder if I have given this question way too much thought, time and energy.
Can anyone help me out?

Very sorry if this question isn't appropriate here - if there is a better group for this question on Stack Exchange please let me know.

@fileunderwater that is specifically about human biology, and I want to know about squirrels/animals - humans have distinctly different arms and legs, however this is not the same with animals, so that question and it's answers won't help me here.

I disagree. That question is asking about the general case, and is referring to humans, cats and apes as examples. The answer is hardly ideal though, but that doesn't mean that it is a good idea to have overlapping and duplicate posts. Hopefully, somebody can add a better answer to the previous question, that answers both that question as well as yours.

In scientific text the terms, "forelimbs/anterior limbs" and "hindlimbs/posterior limbs" are used instead of hands and legs. Hands and legs are quite anthropocentric terms. So, I would say that this question is more about language than biology.

in litterature and science they generally have limbs.


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Struggling to make sense of Km
So I have two substrates for one enzyme and I measured the product formation-> michaelis menten kinetics. The Vmax for both substrates is the same, the Km however is higher on substrate number 2.  What can I conclude from this in terms of enzyme-substrate interaction?

Homework questions are discouraged on here.

The situation you described is entirely normal. $V_{max}$ is the same, so when described with a graph of initial reaction rate vs. substrate concentration, both curves will asymptotically approach the same maximum level. $K_M$ is higher in one than the other, so the exact shape of the curve as it goes from 0 to $V_{max}$ is different. As you may know, you can interpret $K_M$ as the substrate concentration that causes the initial reaction rate to be half of $V_{max}$. This means the substrate with the higher $K_M$ will have a shallower first half of the curve.
You can read more about these parameters and initial enzyme kinetics in Berg biochemistry or at khanacademy.

This does not answer my question of enzyme-substrate interaction though :), thank you for the effort nonetheless.

@Flip you'll have to clarify your question then.

@DeNovo : Seems like the question of OP is to describe the enzyme substrate interaction when Vmax is same and Km is different.

@user237650 that still needs clarification. As I understand the words of that question, this answers it (the difference between the way those two substrates interact with the enzyme is that the initial reaction rate increases more gradually for the second substrate) but there must be something else the OP is looking for.


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Why is the spirit bear/Kermode bear a subspecies of the American black bear Ursus americanus?
The Kermode bear Ursus americanus kermodei is only found in British Columbia,Canada. The Kermode bear has single nucleotide polymorphism at the melanocortin 1 receptor gene (mc1r) locus which cause the white color. 1 out of 10 indviduals are white and are refer as Kermode bear. However, is the black version of the Kermode bear still a Kermode bear Ursus americanus kermodei? If not, why?

It is because somebody wrote a paper that described it as such, and the paper was published. I don't mean to be flip. Its just that taxonomy is done through publication, not committees (although the peer reviewers could be considered a kind of committee). Subspecies are less stringently regulated than species, and this subspecies does have a particular unique set of gene frequencies that occasionally (as you mentioned) show up in the phenotype. The fact that it has been culturally recognized as special may also have something to do with its subspecies status. A subspecies need not be reproductively isolated from its parent species, and need not have any fixed characters.


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Does consistency in minor allele frequency of a SNP across populations imply selection?
If a particular SNP has very similar MAF value across multiple largely non-overlapping populations, with the assumption of no gene flow between the populations over many generations, would that then suggest that there is a selective pressure that is keeping the MAF stable in these populations?
Are there methods to test that can parse out the drift and selection effects in such cases?
Also, does it matter in this context if the MAF value is high or low - since I believe a low MAF SNP is more likely to disappear than a high MAF one?
Thanks in advance for any insight.

Your are not saying but I would assume you are specifically interested in cases of balancing selection?

I would assume you would need a vast number of independent populations and/or small population sizes in order to be able to deduct from the constance of an allele frequency alone that balancing selection is at play.

Yes that was what I was meaning to, sorry for not being very clear...do you know of any literature or probabilistic methods that can deduce if balancing selection is at work versus random drift. Thanks for your answer.

No, I am afraid I don't know of any literature on the subject. I would tend to think though that with population genetic data only, it will be very hard to get a good signal of balancing selection but I might be wrong.


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What kind of mite is this?
I found this (mite?) on my head skin close to hair. Is it a common dust mite or something else? Photographs under a simple microscope (10x objective) are below. Size is in the order of tenths of mm. Some of the hair sticking out are as long as the body. It was not that translucent enough to be well visible in bright field, only as a black spot.
Also, what could be the large round white object on the back an the brown spot to the left and right in the first picture?

Note: One month ago I was treated for scabies and my head is still itching (although scabies is supposed to not affect heads of adults). But I do not think this is Sarcoptes and I think it likely does not cause the itching.

related: How many species of mites live on the human body?


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Why is DNA polymerase added at the end of PCR reaction?
PCR reaction is used to amplify DNA fragment. Each reaction requires a DNA template, buffer, dNTP mix and a unique pair of primers, one ''forward'' primer and one ''reverse'' primer. The DNA polymerase should be added last to the reaction, just before starting the PCR programme.
My question is, why is DNA polymerase added right before the PCR starts? Is it because it can begin to amplify DNA before adding the reaction to the thermocycler? How could it amplify the DNA when the DNA is not denaturated until added to the thermocycler?

True, the template is double stranded, but the primers could begin amplifying themselves, and any other stray DNA. You don't want any nonspecific amplification in the early stages that could compete with the target fragment. Also, even though Taq polymerase is a very hardy enzyme, it is standard practice to treat enzymes with special care, on ice so they don't degrade (although I have forgotten them on the bench overnight, and they survived that).


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How to determine the number of parameters in a phylogenetic model?
I want to calculate the AIC for a phylogeny that I inferred via maximum likelihood. To calculate the AIC I need to know the number of parameters in the model. But how do I determine this?

Biostar forum... bio informatics forum is a popular place which specializes in phylogeny statistics data researchers questions and answers https://www.biostars.org

The number of parameters depends both on the number of taxa and model of sequence evolution. The topology is not typically considered a parameter in the usual sense of statistical inference (as it is the a priori specified topology the likelihood was calculated on).
So, for example, if you infer a tree from nucleotide data for 25 sequences under the General Time Reversible (GTR) model with gamma distributed among-site rate heterogeneity and empirical stationary frequencies (this is commonly called GTR+F+G), then you would have 56 parameters with the following breakdown: 2n - 3 = 47 branch lengths (where n = 25, the number of tips), 3 frequencies (because these sum to 1, once three are known the other is automatically known, so we only count 3 estimated parameters), 5 substitution rates (there are actually 6 substitution parameters in GTR, but it is typical to set one, usually G > C, to 1, and estimate the others relative to this, hence only 5 estimated) and 1 alpha parameter for the shape of the gamma distribution of rates (gamma distributions actually have two parameters, alpha and beta, but for phylogenetics we usually constrain them to be equal).
In total, this gives 47 branch lengths and 3 + 5 + 1 = 9 model parameters, and 47 + 9 = 56

Thank you, @NatWH! This is extremely helpful. In any of the phylogenetic classes of objects in R (e.g., phylo) is there a way to extract the number of parameters?

I don't know - R objects of class phylo don't store model specifications, so I doubt it. But there may be a function somewhere. If not, it should be simple enough to write your own.


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What are the advantages of iTRAQ/TMT technology over electrophoresis?
I'm currently working on the paper regarding proteomics research. I've listed a lot of questions that freshmen may have during their study. Can anyone explain (based on your experience in the lab) the advantages and disadvantages of iTRAQ/TMT technology and electrophoresis? Which technique is better?

I believe this paper can answer your question: Q&As About Proteomics (Q1-Q5). It says that 2-DGE is a protein separation technology developed along with MALDI-TOF technology. In theory, the total protein can be separated one by one with the difference of isoelectric point (IEF) and molecular weight (SDS-PAGE). The actual situation is not that ideal, because the low-abundance protein cannot be successfully stained and seen, and the protein is deviated from the theoretical position after post-translational modification. A 2-DGE can identify a total of 1000–2000 proteins. Compared to electrophoresis-based techniques such as 2-DE and DIGE, iTRAQ/TMT has a high resolution. MtoZ Biolabs found 6,000 proteins at most in the cell samples it has treated, most of which have quantitative and qualitative information. Moreover, its iTRAQ has high flux and can complete up to 8 samples at a time. If TMT technology is used, it can complete up to 10 samples at a time, which is especially suitable for simultaneous comparison between multiple samples and dynamic detection of biological processes.


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ID large-thorned plant growing in Turkey
Can anyone identify this plant which is growing in a friend's garden in the Uzumlu area of Turkey. It has very large spikes/thorns. I'm told it doesn't have flowers or seeds so we are wondering how it propagates itself.

This is a palm (family Arecaceae). Many palms have spines; I'm no expert but it looks to me like it is a member of the Phoenix genus, perhaps a Cretan date palm (Phoenix theophrasti). Date palms do propagate themselves by seed (the pit of the date fruit). The palm in your picture, if a date palm, would be rather young, which could explain why it does not presently show flowers or fruits. Here is a photo of the spines and flowers of a Cretan date palm (by Wouter Hagens, from Wikimedia Commons):

It is very unlikely that this is Phoenix theophrasti, which has a very limited range. See, for example, the wikipedia link you posted: "with a very restricted distribution", giving quite specific info on where in Turkey the plant can be found.

@GeorgeWilliamRussel'spen, it may well be a different palm, but the natural range of P. theophrasti (or of other species) probably isn't all that relevant, as the OP's image suggests the palm was purposely planted as part of landscaping.

It's listed as NT by the IUCN, and as stated has a very limited range. It is very unlikely that P. theophrastii is planted as a part of landscaping or gardening. You would have to know about it in the first place, and then obtain a speciment. It's not a common plant, and to the best of my knowledge rarely planted.  P. dactylifera and P. canariensis are much more likely. And we can't tell from the picture.


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What is the name of this red and blue striped spider (?) - Brazil, Rio de Janeiro

Anyone knows the name of this thing? I found it in our bathroom. It is maybe 10-15 mm.
It looks like a spider but the colors left me puzzled

Definitely a spider (fused head+thorax, eight legs, jaws) but sheesh those colours :)

This appears to be some species of jumping spider (family Salticidae) in the genus Psecas.
For example, some red/blue striped species of Psecas:
]

 Sources: Top: Alchetron.com (image: Edwards, 2001)  |   Bottom: Tree of Life (image: Maddison 1994)
Wikipedia lists the following species from Brazil:

Psecas chapoda (Peckham & Peckham, 1894) – Brazil
Psecas chrysogrammus (Simon, 1901) – Peru, Brazil
Psecas viridipurpureus (Simon, 1901) – Brazil
Psecas zonatus (Galiano, 1963) – Brazil

Psecas chrysogrammus is my best guess given my limited knowledge of the specimen, this family, and arachnid literature.
We likely can rule out P. viridipurpureus (see here) and P. chapoda (see here) because of the longitudinal striping pattern of the dorsal abdomen of these two species.
I couldn't find any definitive or reputable sources regarding P. zonatus.
The sketch of P. chrysogrammus here seems to indicate that this specific species has the horizontal striping seen in the OP's specimen.
Salticidae.org provides these sources for P. chrysogrammus ID info:

M. E. Galiano 1963b. Las especies americanas de aranas de la familia Salticidae, descriptas por Eugene Simon. Redescripciones basadas en los ejemplares tipicos. Physis, Buenos Aires, 23 (66): 424, t. 32, f 14-18.
Simon E. 1901a. Histoire Naturelle des Araignees. 2(3-4) Paris: 460, f 528, 533(=H).


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Arsenic (V) Reduction to Arsenic (III) by Microorganisms
I am currently doing research on arsenic toxicity in microorganisms, and I learned about arsenic (V)/(III) cycling. Arsenic (III) (usually in the form of arsenite) is generally 50 times more toxic to biological life; however, most bacteria (or at least some) reduce the less toxic arsenate into arsenite. I just do not understand why these organisms would reduce arsenate into something more toxic. This doesn't seem to be an accidental reduction in which the microorganism mistook arsenate for phosphate, as there are plasmids specifically encoded with genes that reduce arsenate. Why is this happening? How would this be an advantage in these organisms and not a disadvantage?

Your confusion seems to hinge quite critically on the idea that Arsenic(III) is more toxic to biological life in general. Bacteria making effort to manufacture it would suggest that it's more toxic to other life than to the bacteria making it. Can you add a source for that statement?

https://www.sciencedirect.com/science/article/pii/S2319417016000159 states that bacteria encode arsenic resistance in the ars operon.

@Armatus — Excellent ref. Why not provide a summary and go for the bonus.

You can find a great and recent review on this topic, which is thankfully also free to access, here: https://www.sciencedirect.com/science/article/pii/S2319417016000159
Arsenic resistance is ubiquitous among bacteria, they virtually all maintain the ars operon. Among Arsenic-resistant bacteria, this is not an advantage, but Arsenic was and remains a ubiquituous substance and being resistant to it confers an advantage over those that aren't; which is why bacteria that save themselves the effort aren't abundant.
The core to your answer is in the very last summary paragraph:

ArsM transforms inorganic arsenic into a highly toxic organoarsenical species that kills off by competing the bacterial species and may also be responsible for carcinogenesis in animals. Competing microbial species have responded to this environmental pressure by evolving detoxification mechanisms for MAs(III). Some produces ArsI that demethylates MAs(III) to less toxic inorganic As(III) while other produces ArsH that oxidizes MAs(III) to nontoxic pentavalent MAs(V). It is likely that all of these processes are taking place in environmental microbial communities as bacteria, archaea, fungi, and protozoans constantly fight for dominance.

Summarised in Figure 5: https://ars.els-cdn.com/content/image/1-s2.0-S2319417016000159-gr5.jpg
The reason why ArsC and other arsenate reductases (reducing Ars(V) to the more toxic Ars(III)) evolved in the first place, setting off this whole Arsenic methylation cycle, is that

they are required for resistance to arsenate, which became the predominant arsenic species after oxygen appeared in the atmosphere.

Simply put: If I can make a poison that kills you but not me, why shouldn't I make it?


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Is it possible that there are two people in the world who belong to a different species?
There're over 7 billion people in the world and every one of them is different from everyone else. Is it possible that there are two people so different that they belong to different species (in the sense that they cannot reproduce to produce fertile offspring)?
This doesn't have to mean that there's someone in the world who's completely unable to reproduce with everyone else, just that these two individuals are so different that they can't reproduce with each other (they can still reproduce with other people who can reproduce with the other individual - a ring species system).
I'm particularly interested in an answer based on how much the genome varies between people vs. how much they vary against our closest relatives (such as Neanderthals). For example if humans and Neanderthals share 99% of their genes, and the largest variation among current humans is 0.001% of genes, then the answer to this question would be "no".

though not an answer, you might be interested in ring species

Yes, I was originally going to phrase the question in terms of that but then forget about it. Let me edit.

I have edited your question to change genetic code to genome. If you do not understand why, please read e.g. the Wikipedia entry on the genetic code.

Your question is basically interesting, although the idea that people can belong to a different species and that mere % difference in the genome will determine the fertility of offspring seems to me naive. I think a more scientifically productive approach would be to consider known examples of interspecies crosses like that between the horse and the donkey. Then you can ask how different the genomes have to be for viable offspring and what causes offspring to be sterile. I don't know the answer but would encourage anyone who does to respond.

At the beginning, the population of the parents who we are talking about should be made more specific. Let's limit it to adult, healthy individuals (let's skip pathologies, various kinds of random body injuries, personal sexual preferences and close relatives).
From the descendants group, let's also exclude children who would die from random causes, body injuries (unintentional :-( and intended :-((( ), genetic diseases, etc.In addition to the genetic variation (A global reference for human genetic variation), epigenetic variability (Worldwide patterns of human epigenetic variation) should also be taken into account.
If we give the most popular definition of a species (and there are very many of them), as individuals capable of giving fertile offspring, of course all humans belong to one species. Contrary to popular opinion, we are similar to one another like drops of water.

I'm not sure that I think the first two paragraphs of your answer are particularly pertinent, but at least you provide some sort of references. However your final sentence is obviously untrue: "Contrary to popular opinion, we are similar to one another like drops of water." Like it or not, some populations are very different from one another in appearance, a difference that has a genetic basis. Asserting otherwise betrays a political agenda and discredits your argument. In the context of the question all that is important is that different populations can mate and produce fertile offspring.

It is obvious that every population has a certain variation, but our impression of human diversity is illusory. It results from our perspective. Identical to us other individuals (eg penguins) are perfectly able to recognize each other. From their point of view, each penguin is different and unique. A similar situation occurs when a resident of Europe, Asia or Africa goes to another place where a different type of appearance prevails. At the beginning, everyone seems the same and only after some time begins to notice differences.

I happen to believe that we should live in racial harmony, but my points are (1) that this is a biology list, so that we should be careful to restrict ourselves to a discussion of biological facts in answer to a question that may or may not be loaded, (2) by making well-meaning but weak assertions you risk undermining the credibility of a position that may be correct/just. An example is the "like two drops of water". It would be easy for a racist to reply "No, like oil and water, which don't mix". So it is really best if social, religious and political opinions are kept off the list.

I assume that we are conducting a substantive discussion, not a worldview dispute. Hence the works cited earlier and now: How Humans Differ from Other Animals in Their Levels of Morphological Variation. I maintain my opinion: people are more similar to one another (less changeable) than most animals.

The question boils down to the following things:

Whether arbitrary mutations are possible. Yes, they are. (A simple proof: any rearrangements of matter that follow physical laws are possible - that's a direct consequence of physics and probability theory.) But most mutations have very low probability.
Whether further speciation is possible for humans. Yes, it is. (The proof is an unlikely and trivial example: mutating (see above) to become any other species that has existed, for example the ancestor species. We know that these species can exist. And probably an enormous number of new species are conceivable.)

From the above it follows that mutations towards speciation are possible (but improbable). So the answer is: yes, there is a very small statistical probability. (Even though some people like to claim that very small probability equals zero, but that is not correct.)
And by the way, we don't know what mutations are out there. Even if we would, we still wouldn't know much, because some speciation-relevant properties are not obvious just by looking at genotypes.

At SE we're looking for answers that provide some explanation and context. You need to explain why your answer is right, ideally with citations. Otherwise how can the poster or anyone else know whether or not you are correct? Assertions of the type you have made just don't cut it. See the Help for "how do I write a good answer?".

Edited to add proofs based on mathematics and physics.

OK. You support your premises now. I just do not agree that it boils down to the two things you mention. I think it boils down to the what determines separate species as defined by the poster "cannot reproduce to produce fertile offspring". It is my gut feeling that the variation in modern humans is less than that between humans and neanderthals or denisovians, and so the answer to his question is no. But I don't have the numbers. You might also argue that the neanderthals were different enough from us to be regarded as a separate species, but that's another question.

You are talking about how low the probability is. Yes, it is very low. But note that very low probability is not the same as zero probability. Poster asks "is it possible", i.e. is probability above zero. My proof works for any definition of "species".


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How does garlic preparation affect its active compounds or medicinal properties?
I read the following claims about how to consume garlic:

Consume immediately after crushing since the active compounds (allicin) is volatile and gets oxidized as soon as it's crushed
Allow to sit 10 minutes after crushing to allow time for allicin to form
Do not change the PH of garlic (i.e. mix with acid/lemon) in order not to disrupt the formation of allicin, during those 10 minutes
Allicin is completely lost within 20 minutes after crushing

If so:

Which of those claims is true? Is the wait-10-minutes practice is only recommended before heating the garlic? i.e. should you wait at all after crushing, when you consume it raw? (e.g. in a salad)
Given this is how I prepare a salad:
Cut vegetables and herbs
Crush garlic and mix in (no waiting)
Add lemon juice and vinegar and mix right away
Season with salt and pepper
Pour olive oil and mix right away
Let sit refrigerated in air-tight container 5-10 minutes
The salad is consumed at least 15 minutes after garlic is crushed, and it takes me another 15 minutes to finish eating the salad
By that time (30 min after crushing) are the active compounds in the garlic (particularly allicin) preserved or completely lost?
Will it make any difference if I mix the garlic in the oil first (to merely prevent oxidation), wait 10 minutes, mix in the acid, and pour everything over the salad right before serving?

This question has nothing to do with Biology in terms of SE Biology. You might try SE Nutrition as there doesn't appear to be a SE Quack Medicine.

@David I couldn't find SE Nutrition board, were you referring to SE Medical Sciences?

@David - that comment :D

Contrary to David's comment, there is no nutrition SE site. I inquired over at MedSci if this is ontopic there, but unfortunately not. Over here I see it as offtopic as it's more about the chemical properties of a compound. I've asked over at Chemistry. After that, I've ran out of ideas I'm afraid.

I doubt it would remain open on chemistry.se (I am a mod there, cc @AliceD). The question basically boils down to how is allicin formed when crushing garlic, and how stable is it after that, which is basically already answered on the Wikipedia page. (Questions about properties of compounds should be accompanied with the necessary literature research.) The other, principle, problem is that the conditions are probably producing a much larger uncertainty than you would be able to measure in the levels of Allicin, and all would not be reproducible.

I'm voting to close this question as off-topic because it's offtopic here as it's not a biological problem, but one of nutrition and chemical stability. I've inquired across the network, but unfortunately I can't find a suitable place, as mods of other sites have rejected it. Apologies.


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Gluconeogenesis in the liver
Glycolysis yields 2 net ATPs. However, gluconeogenesis (lactate->pyruvate->glucose) costs 6 ATP, with a total net loss of 4 ATP.
Does the body not care about the net loss because of the potential energy from glucose to yield up to 38 ATP?

Welcome to SE Biology. As a new contributor you should do some research before posting here, as outlined in the Help on Asking Questions. In this case you might like to ask yourself (1) Why do cells make ATP if not to use it? (2) What is the purpose of gluconeogenesis by the liver — what is the product, for what tissues is it destined, and what would happen if it did not occur? Even if you cannot answer the question for yourself completely it would allow you to construct a more focussed question.

The brain and also the erythrocytes need glucose to survive.
Gluconeogenesis is one of the possibilities of the body to keep the glucose levels stable and to avoid hypoglycemia. The precursors needed come from amino acid and lipid metabolism, and is turned on, when the body has no energy sources available which can release glucose, like carbohydrates in the food or the degradation of glycogen.
As you said, it comes at a price, making glucose itself costs a lot of energy. This process is available to maintain the level of glucose, which shows the importance of it.

One point worth mentioning. Lactate produced by anaerobic utilization of glucose in erythrocytes can be recycled so there is little or no net requirement for glucose. The need of the brain is for net glucose as this is completely oxidized and no lactate is excreted from the tissue.

On another note- you might wish to reference this answer, or I'll banner it ;-)


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How can we quantify the effect of pancreatin (biological enzyme) on the clarification of milk powder
Alright so I'm trying to quantify the rate at which casein (protein constituent of milk powder) is converted into a product (I am unaware of) by pancreatin (a biological enzyme that speeds up the reaction). I've attempted researching what the product of the reaction is erroneously given I couldn't quite determine the answer.
All I know is that this enzyme essentially allows casein to convert into whatever thus clarifying any water it would be poured into. Casein remains in suspension (opaque) and then progressively reacts and clarifies the water. How to quantify it on the other hand, I haven't merely got a conceivable clue.
Yes, this question is broad, perhaps you could inform me of any other notions that pertain to this experiment and thereby aid me in my pursuit of an answer.

Google immediately tells us that pancreatin is not an enzyme, but a mixture of enzymes.  Data on conversion rates, if it exists, would likely be reported for individual enzymes, not a mixture.


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Honeybee relatedness: workers and nephews
This is my first question on this site. If anyone could help me get to the bottom of it, I would be very grateful.
I am currently working on a lecture on kinship in animals. It goes without saying, it includes a part about the good old honeybee and its unusual relatedness coefficients. One of the interesting points I'd like to cover is worker policing, where workers remove eggs of other workers because they are more closely related to their brothers (the queen's sons) than their nephews. The resources I'm using state that this situation depends on whether the queen is monogamous or polygamous. When a queen mates with a single drone, workers are more closely related to their nephews (r=0.375) than their brothers (r=0.25). However, if a queen mates with more drones, the situation is flipped, workers are more closely related to their brothers and therefore eliminate unfertilized eggs laid by other workers.
The issue I'm having may seem silly and purely technical, but I can't for the life of me figure out how we arrive at a relatedness coefficient of 0.375 for worker and nephew when the queen is monogamous. I'd really like to understand this because I want to be able to answer as many potential questions students may have, and I can't do that if I'm not 100% sure about it. Any and all help is greatly appreciated. Thanks in advance!

Queens are generally not monogamous. Although they make just one mating flight, they store the sperm of multiple drones. Might your numbers work if you plugged in two, three, or four mates?

@KarlKjer Thank you for your reply. I'm aware that queens are generally not monogamous, and that the second situation is far more common than the first. My issue was in understanding how we calculate a relatedness od 0.375 for worker and nephew in the event when the queen mates with a single drone. I don't want to include this information in my lecture if I don't fully understand it myself.

Is this as simple as: Father of both workers is same, so are their paternal genes b/c he only had one set of chromosomes. The two workers are expected to share half of their maternal DNA. Both parents contributed equally, so the sisters are considered each related to each other at relatedness=0.75. The son of one is related to its mother by 0.5, as it only gets one set of her chromosomes. To determine the relatedness of the aunt to this son, multiply how related she is to her sister times how related he is to his mother: 0.75*0.5-0.375?