text:
Is the flesh of a fruit selected for the benefit of the sprouting seed or to attract the frugivorous seed disperser animal?
In a question about the low protein content in fruits, one answer suggests the energy, carbohydrate, and protein content in a fruit evolved to entice animal seed dispersers, not foster the sprouting seed.
Another answer suggests plants are made mostly of cellulose, hence why the fruit has more carbohydrates than protein. The implication here is that the content of the fruit is optimized for the benefit of the sprouting seed, which is constructing a plant, not an animal.
Both of the answers to this other question: Plant a whole fruit or only seeds? suggest fruit is all about dispersal.
Which is the correct explanation?
It seems like it would be an easy answer to prove experimentally: plant two seeds in nutrient-poor soil, one with its fruit whole, another with its fruit mostly eaten (or even entirely passed through an animal's digestive tract). Then see which seeds thrive better.
Obviously fruits cultivated for human consumption have had their evolutionary course commandeered for benefit of the frugivore. And to a lesser extent probably many plants have a symbiotic relationship with their seed dispersers. But is that relationship an enhancement of the primary evolutionary purpose, or an suppression?

worth noting it is a lot easier for a plant to make carbohydrates than proteins, that alone should make it mostly made of carbohydrates.

While I know you didn't mean this, it's worth clarifying there is no purpose in evolution, the fruit is what it is because that's how the various evolutionary processes such as natural selection and random drift have shaped it.
That said there isn't a known evolutionary mechanism for a fruit evolving in any other way than to benefit itself.  The only way I can think of in which the second option you suggest, that the plant does it explicitly to help the animal survive could be true, is if the animal surviving helps the plant in some way.  For example it is well known that some trees produce sugar water for ants to eat, and in exchange, the ants will attack herbivores that try to eat the plant.
Otherwise, the sugar is there to help the tree's offspring, but not how you think.  The plant's baby doesn't literally use the sugar in the fruit for itself.  Instead the plant offers the sugar to entice an animal to eat the seed.  The seed will then be deposited by the animal in pile of undigested nutrients in a place far away from the parent plant.  If the plant just dropped the seed below itself, it would have to compete with it's own child for sunlight, water, etc.  So instead the fruit offers the sugar to an animal to get the seed dispersed.  In this way, the plant must offer a benefit to an animal for it's own selfish interest.  But the seed itself will only use the nutrients on the inside of the shell casing, even if the fruit is never eaten and still surrounds the seed.

OP already understands all this (besides some imprecise terminology they could improve about "purpose"): they clearly are not suggesting that the fruit is anything but selfish, they're asking about whether the selection is for attracting distributors or feeding the new plant.

oh. lol. well, it's to attract pollinators, I've never heard it suggested anywhere the fruit is for the plant's offspring to use, that's typically considered the part only inside the protective shell.  It's called the endosperm: https://en.wikipedia.org/wiki/Endosperm


text:
Why don't electric eels shock themselves?
Why do electric eels not stun or pain themselves when they discharge their high voltage shocks? While it is known that they use those high voltage shocks to track their prey (as discovered by my professor Kenneth Catania [1]), and there is most likely some form of cage effect provided by the water (until they come out for a more powerful sting to scare predators), and that when curled less current might return through their own bodies [3], it is not clear why there discharges do not interfere with their own central nervous system (cage effect) or peripheral nervous system (through which current would flow in parallel to the water and target)?
[1] https://www.nature.com/articles/ncomms9638
[2] http://www.pnas.org/content/113/25/6979.full
[3] http://www.cell.com/current-biology/fulltext/S0960-9822(15)01147-1

My information isn't very reliable but I saw in a non-documental serie that eels are inmune to their electrical current because the have a thick layer of fat in their skin.

Short answer, no one knows, there is some minor evidence they are do shock themselves but are resistant to it, (they react far stronger in air than in water to their own discharge), but it is not a high priority for research so no one has really tested it.

source: Stack Exchange

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

sort: votes


text:
Can neurons become cancerous?
I've been reading about brain cancer lately, and something I've noticed is that the tumors seem to start in all tissues, except neural tissue. Am I missing something, or is there an explanation?

Short answer
Neuronal tumors are rare, but they do exist. These cancers develop from neuroblast cells, a population of undifferentiated, dividing precursor cells that will eventually fully differentiate into functional neuronal cells.
Background
Most neuronal cell types have lost their ability to divide, because of their progressed state of differentiation. There are but a few regions in the brains that generate new nerve cells in adulthood, for example in the hippocampus where neuro-regeneration is believed to be involved in memory formation. Because of the rarity of cell division of neuronal cells in adulthood, neural cancers are rare.
The point where neuronal cells actively divide is during development. These cells are basically still stem cells. A prime example here are retinoblastomas. These are tumors in the photosensitive part of the eye, namely the retina. During early development stem cells actively divide to lay down a layered structure in the back of the eye eventually forming the rods and cones and other visual cells. If this division process goes out of control, tumors can develop. Retinoblasomas can now be diagnosed in utero (Paquette et al., 2012).
Tumors with a neuronal origin developing post natally are rare, but do exist. Neuroblastoma being a prime example. This is a rare cancer (prevalence of 1:100,000) most commonly found in children younger than age 5. It affects the sympathetic nervous system, which regulates involuntary bodily functions such as heart rate, blood pressure, breathing, and digestion. Neuroblastoma typically begins in the nerve tissues of the adrenal glands but may also begin in the nerves that are located anywhere along the spinal cord, including the neck, chest, or abdomen. The cancer can metastasize (spread) to other organs.
Note that both examples here are called blastomas, those are tumors caused by malignancies in precursor cells, often called blasts, these cells are dividing cells that will develop into a neuron often after a migration phase. Neuroblasts differentiate from neural stem cells and are committed to the neuronal fate. Hence, although these tumors are from a neuronal origin, they are technically not derived from (fully differentiated) neurons.
Reference
- Paquette et al., AJP Rep (2012); 2(1): 55–62

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


text:
Is mate choice in non-human primates MHC-dependent?
Whether the major histocompatibility complex (MHC) affects or not mate choice in humans seems mired in controversy at the moment. Without implying that looking at non-human primates would solve this controversy, I'm still curious if some sort of scientific consensus could be reached in non-human primates regarding MHC and mate selection.

tl;dr It's messy for non-human primates too. Winternitz et al. (2017) ("Patterns of MHC‐dependent mate selection in humans and nonhuman primates: a meta‐analysis", Molecular Ecology 26(2)) review studies of MHC-based mate choice in human and non-human primates. Some of the take-home messages, mostly from the abstract:

[abstract] the overall effect sizes of primate MHC-based mating preferences
  are relatively weak ... calling for careful sampling design in future studies.

There is a

"systematic trend" for primates preferring MHC diversity (p. 679)

(I think this means "not significant" ...)

(p. 680) Nonhuman primates tend to consistently prefer MHC-dissimilar mates (Fig. 4a), but our power to detect a significant average effect is limited by our small sample size (N=6) and by the addition of random effects to control for pseudoreplication.

For MHC-diversity preferences:

Examined separately ...  nonhuman primates had a non-significant trend for mate choice for diversity (primates = 0.110 (-0.207 to 0.456), N=7, Fig. 1b)

Here are some of the key figures (these figures also include data for humans, omitted here). However, note that the overall estimates in this figure do not account for the effects of study ID and phylogenetic relatedness (see Figure 1 in the paper), which tend to make the confidence intervals wider/weaken the statistical significance.

Figure 4a, preference for MHC-dissimilar mates [disassortativity] (overall CI is [-0.01, 0.18], consistent with the "almost significant" comment referenced above)

Figure 4b, preference for MHC-similar mates [assortativity]:

For reference, the species included here are: Rhinopithecus roxellana (golden/Sichuan snub-nosed monkey); Cheirogaleus medius (fat-tailed dwarf lemur); Papio ursinus (Chacma/Cape baboon); Microcebus murinus (gray mouse lemur); Mandrillus sphinx (mandrill); Macaca mulatta (Rhesus macaque).


text:
Is it the theory of the 5 senses obsolete?
An enigmatic topic in traditional science was labelled as the mystery of the 5 senses, and how to best group senses by type.
Is that theory now meaningless?
Do Scientists still agree that that there are 5 types of sense, and no salient new 6th sense which can't be classed with the others?
There was widely accepted merit for that summary classification, because it was the best logical process to approach a complex subject.
The theory questioned the controversial logic of these groups: Soundwaves, Photons, Chemical scent of the air, chemical scent of taste and touch which represents any nerves found in the rest of the body.

This is a question and answer site about specific biological facts and concepts. If your question is whether there is a sense other than the five you fail even to mention, please give some reference to sources in support of it as a basis of discussion of the evidence for or against it. Your question is wrapped up in references to teaching, relevance, monikers, enigmatic topics, clades and the like, but their seems little of substance inside.

A knowledgable man commented:...[ "We have only 5 senses, a 6th sense has been controversial" - This is meaningless. There are well over 5 senses. The 5 senses thing is a biology myth taught to children. – ]... Sorry, I have some wrong words due to not being English. The question is: whether the 5 sense theory is today inaccurate?

I don't think there is any non-trivial biological content in this question, and there is no "mystery." I don't know what knowledgeable man you are referring to but it is trivial to list more than 5 senses - the idea of there being 5 senses goes back to Aristotelian views of the world. This question really just seems like an opinion-based question of whether it makes sense to teach about 5 particular senses.

Your comment is in conflict with David's so apparently there is a question to be resolved. If your own view has a factual basis, you can briefly quote the scientific terms for those facts via an answer post?

No, because your question isn't about biology - it isn't good to answer bad questions here. If you want to ask "are there more than 5 senses" then ask that. And I don't think my comment differs much from David's in this occasion, as rare as agreement between us can sometimes be ;)

Regarding your English, my criticism was that you were using empty flowery language of the type one might expect from undergraduate philosophy students. Just get to the point if you have a question and state it clearly and simply, providing sources for any contentious point of view you wish information on. But make sure you are talking about science, not metaphysics.

It depends who's counting and according to what criteria.
Some neuroscientists argue that smell and taste are one sense because altering one produces substantial changes in the other.
Conversely, if you break down the senses to receptors, you get at least 5 different for taste and 1000 or more for smell.

Apparently one should not trust psychologists to count receptors. That 1,000 figure for olfactory receptors probably comes from adding both genes and pseudogenes. Counting only the former gives around only around 400: https://www.ncbi.nlm.nih.gov/pubmed/23585039


text:
What made this small light weight bee hive-like structure?
This structure was photographed in mid December in Eastern Iowa, USA along a path within a public use area with tall grasses framed by small to medium trees.  It is approximately 5 cm (2 inches) long and 10 cm (4 inches) in diameter.  It had the light airy appearance of honeycomb but was one solid ribbed structure attached to a small branch.  I'm not sure if this was something used over the summer by an insect or if something will come out of it in the spring - winter temperatures often go below -18 degrees C (0 degrees F) in this area of the country.  Any help would be appreciated.

This is a mantis (Mantodea) egg sack, or ootheca. The female mantis makes it in the fall and it will remain over winter until (juvenile) nymph mantises emerge from it in the spring.
The following site introduces how to raise mantises from eggs but also has some general background information including on how seasonal temperature changes can affect the ootheca:
https://www.keepinginsects.com/praying-mantis/caring-for-mantis-eggs/


text:
What is known and what can be measured of biofilms?
Context for the question
I am a mathematics researcher working on the mathematics of imaging and parameter estimation (inverse problems). I found an interesting diffusion equation that models the growth of biofilms. A question I am interested in: Given some measurements of the biofilm, and assuming the mathematical model is accurate, can we deduce the coefficients in the model? This, however, is not the question I want to ask here.
Please pardon nonstandard use and misuse of biological terminology and gaps in knowledge; this is by no means my field. I have never done biological experiments in a laboratory, for example, or studied any university-level biology.
The model
Let us assume a simple scenario where we have a biofilm and some substrate it consumes to grow. We consider a surface where the model should tell how fast and to where the biofilm grows. The parameters in the model are:

$d_1$ substrate diffusion coefficient;
$d_2$ biomass diffusion coefficient;
$K_1$ maximum specific consumption rate;
$K_2$ biomass decay rate;
$K_3$ maximum specific growth rate;
$K_4$ Monod half saturation constant (relative to initial data $S_0$);
$a$, $b$ biomass spreading parameters.

The quantities that are solved from the equations are the following, both of them scaled so that $0 \le M, S \le 1$. Both of them are functions of space $x$ and time $t$, which I omit from the notation.

$S$ is the concentration of the substrate that the biofilm feeds on
$M$ is the biomass density

The governing equations are the following, with some boundary conditions I will not specify here:
$$
\begin{cases}
\partial_t S = d_1 \Delta_x S - K_1 \frac{SM}{K_4+S} \\
\partial_t M = d_2 \nabla_x \cdot \left( \frac{M^b}{(1-M)^a} \nabla_x M \right) - K_2 M + K_3 \frac{SM}{K_4+S}
\end{cases}
$$
The questions
Can both $M$ and $S$ be measured with fair accuracy in laboratory conditions? How is it done and how reliable is it? Can the experiments continue afterwards, or does the measurement significantly alter the experimental set-up in some way (by for example destroying the biofilm or mixing the entire thing etc.)?
Of the parameters in the model, which are well-known?
I suppose the answer to last question depends on whether the biofilm is of known or unknown nature, and in the case of an unknown substance, only $d_1$ might be known. What about a known kind of biofilm?


text:
How does the brain’s limbic system work together to form a working memory, short-term memory, and long-term memory?
In the past few days, I was reading about the limbic system and how its components (hippocampus, hypothalamus, thalamus, etc.) cooperate.
Among papers and forum posts I read about how those components interact and how each of them plays a vital role in the memory formation.
But, is there someone who can give me an abstract view of how the limbic system components form the cycle that results in the formation of memory?
Something like:

The sensory signal comes through the Temporal lobe.
Goes to Thalamus where it is classified as new, existing or similar to already existing memory.( maybe somewhere between this or maybe after the next step the working and short-term memory should be involved?)
Goes to Hypothalamus to be classified as good or bad experience.
Goes to Hippocampus so it can be saved the neocortex at some point (while sleeping for example).

and so on...
Thanks!


text:
What are limitations of giving birth to a baby from a frozen embryo?
Recently the story of a woman giving birth to baby girl from an embryo frozen 24 years ago hit the news. After an in vitro fertilization the embryo was frozen on 14 October 1992(
Article in the Guardian)
So I wonder about the limitations concerning freezing embryos. Especially the following questions came to my mind:

How much time after the embryo has been fertilized has passed before
he was frozen?
How much more time after fertilization could pass before the embryo
has to be frozen?

There are a lot of questions here. Can you narrow things down some?

As suggested by @kmm I deleted two questions.


text:
What happens to the language processing brain part if no language is ever learned?
Language is processed in the human brain in multiple regions.
Some of them seem to be used exclusively or mainly for language processing,
other regions are distributed overlapping with other functions.
If a feral child is never exposed to any language, and therefore never
learns one: What happens to the language related parts of the brain,
like the ones exclusively used for language?
The language processing is not the central point - so feel free to use analogous examples of brain regions that are unused based on exceptional circumstances. Blindness from birth on comes to mind. Also, no need to base examples on homo sapiens.

Although this specific experiment wouldn't be done, similar experiments have been done in experiments in animal models where a sensory input is removed/altered. These experiments show that if you remove some sort of sensory input, the parts of the brain originally responding to that input will take on other tasks. There have been many studies that show this, but the canonical reference is often this one, where the part of the brain previously responding to sensory input to a finger instead responds to stimulation of another finger after the original finger is amputated:
Merzenich, M. M., Nelson, R. J., Stryker, M. P., Cynader, M. S., Schoppmann, A., & Zook, J. M. (1984). Somatosensory cortical map changes following digit amputation in adult monkeys. Journal of comparative neurology, 224(4), 591-605.
There have also been studies of humans with sensory deficits like blindness or deafness that show similar reorganization, depending on the age the deficit is acquired. For examples, see:
Finney, E. M., Fine, I., & Dobkins, K. R. (2001). Visual stimuli activate auditory cortex in the deaf. Nature neuroscience, 4(12), 1171-1173.
Kujala, T., Huotilainen, M., Sinkkonen, J., Ahonen, A. I., Alho, K., Hämälä, M. S., ... & Salonen, O. (1995). Visual cortex activation in blind humans during sound discrimination. Neuroscience letters, 183(1), 143-146.
In summary, the result is that the neocortex is a very flexible, adaptable structure, and if inputs of a certain type are impoverished, that region of the cortex is used for other purposes. Essentially, neighboring functions creep in to that space.
Language processing in humans includes both auditory areas that respond to the sounds made by language, and premotor processing areas that seem to be important both for understanding the semantic content of language and for producing verbal output. None of these areas are truly language-unique, though, they are just regions that are active more than other areas when language-based tasks are occurring. In a person not exposed to a language, it's likely they would develop some rudimentary language-based skills anyways unless they were truly raised in some sort of sensory deprivation context - at this point an answer would get too far into speculation. Besides that, those areas would probably be re-purposed for other types of sensory processing and other types of motor planning.

Using these analogous examples is perfectly fine. Interesting...


text:
Are there official criteria for an experiment to be considered statistically robust for publication in a decent scientific journal?
For a high school project, I investigated the effect of breathing meditation on teenagers. 15 students were asked to follow specific directions and meditate for 10 minutes a day for 8 weeks. Each week, their heart rate, ventilation rate, maximum lung capacity and blood pressure were measured with 5 trials. These measurements were also done prior to the meditation regimen.
My question is, to publish an experiment in a scientific paper, must there be a specific number of participants, trials, or time-length of the experiment?
This is to talk about in the discussion part of my report.
Please let me know what you know!

Based on the complaints that have been made on my questions, this question might get attacked as being off topic.

@DanielGoldman — "attacked"? I think you should choose your words a little more carefully. The SE system allows users with a certain ‘reputation’ to review questions and vote to close them if they are regard them as off-topic in the terms defined by SE Biology. This is not ‘attacking’ but is performing a public duty to help maintain the standards of the site (you can get badges for it). So, yes, I do consider this probably off topic, but no, I haven‘t voted to close as I thought it wouldn‘t hurt for someone to answer this young person.

one important thing to consider would be to compute the statistical power of your experiment. There are online calculators, e.g. here, but it does sometimes take some creativity/adjustment to match your experimental design with the numbers the calculator is expecting. The most important thing is that you need to pick an effect size that you are expecting. (This is arguably more of a statistical question, e.g. for Cross Validated rather than Biology SE)

There is no single measure for "robustness" and a lot of it boils down to the field. Usually physics has a very high degree of precision: p value close to 0. For instance, the Higgs boson was a confidence level of 5 sigma, while biology or psychology is going to usually have more leeway: maybe 2 sigma (Sigma).
However, there should be no (statistical significance) criterion to publish. The idea that only positive studies should be published has led to biases in available data in a number of fields (Fighting publication bias: introducing the Negative Results section). Negative results are very useful to us as robustness of a theory is often evaluated using meta-analyses. If a person fails to publish their results because it does not robustly justify their theory, then the data available to perform a meta-analysis is diminished.
Clearly, you want the study to be properly run and you want the method to be reasonable. A garbage study, regardless of the statistical significance measured, is going to be looked upon negatively.
That being said, if your topic is something that has been researched a number of times, a small study is not going to be looked at very well, as there is already "better" information available. The study should provide some kind of new insight into the topic.

“p values close to 1”? I think there is at least a 0.00 missing from your answer.

Yeah; should be really close to 0, not 1. Sorry. Corrected.


text:
Why do zoologists classify sponges as animals rather than plants?
Sponges are fixed, do not move settle at one place, do not have a reproductive apparatus, respiratory apparatus, or organs, and live in marine environments. Why then zoologists consider that sponges are animals? In the past, zoologists considered them as plants and then considered them animals. What is the principe that zoologists have adopted to classify sponges are animals rather than plants?

Organisms are classified, not by their behavior, but by their phylogeny (evolutionary relationships). Sponges have unique and complex molecules in their intracellular matrix that developed in a common ancestor of sponges, and are shared with sponges and all other animals. These molecules include collagen, proteoglycans, integrin, and adhesive glycoproteins. These molecules are made by the cells, exist outside the cells, and fill the space between them.

@Ναείστεαισιόδοξοι If you think Karl's answer answered your question, you can click on the check mark next to his answer.


text:
What medium is the bacteria used to synthesize B12 sourced from?
Would that be from water, soil, plants, funguses,...?
I asked the question in Quora but that, at the time of posting in this forum, haven't been very helpful. I also have searched for the information, but I haven't been able to find it. In Vegan Health it says that

"The vitamin B12 component in B12 supplements and fortified foods is
  made by bacteria and sourced from bacteria cultures; it is not taken
  from animal products"

But I wonder where did those cultures come from. One day someone had to collect the bacteria from somewhere in order to start the cultures.

What exactly are you asking? The geographical location from which the bacteria were originally obtained from?

@canadianer I'm asking what medium is the bacteria used to synthesize B12 sourced from -water, animal intestines, plants, soil, feces.


text:
What British bat is this?
What kind of bat is this? I saw it flying quickly between trees in Buckinghamshire, UK, at about 4pm in September (so about three hours before sunset). I think it might be a common noctule but I was surprised to see that there are something like fourteen other British species to choose from.

Sorry the photo quality isn't amazing but it was hard to capture anything at all!

I would guess that it's a noctule (Nyctalus noctula) also.  The Bat Conservation Trust has a nice UK section with fact sheets for the 18 different species of bats found there.  It seems you can rule out the long eared bats by the photo and the pipistrelle because you didn't mention it flying eratically.  The fact that it was out so early seems to narrow it down to either the noctule, which is usually the first to appear, or the leislers (Nyctalus leisleri) which appears shortly after the noctule.  A distinguishing feature of the noctule is a mushroom shaped tragus, and for the leislers is long fur around the shoulder and back.  Although this is a great photo, it's going to be hard to make a definitive determination without knowing size and some of the other finer details.  Photos of the noctule and leislers can be found on the linked data sheets and the link to the UK section can help you determine if there are any other possible candidates I missed.

Thanks -- that's all useful information. I doubt I could have spotted the size difference between a noctule and a Lieser's. The relative abundance makes the noctule quite a bit more likely but I agree that a definitive identification seems impossible.

It is a Big Brown Bat (Eptesicus fuscus).
From Wikipedia:
The big brown bat (Eptesicus fuscus) is a widespread species of bat found throughout North America, Central America, the Caribbean, and extreme northern South America.
It is a relatively large microbat, weighing 15–26 g (0.53–0.92 oz).
Adult body length is 110–130 mm (4.3–5.1 in). Its forearm is usually longer than 48 mm (1.9 in). Its wingspan is 32.5–35 cm (12.8–13.8 in). Its dorsal fur is reddish brown and glossy in appearance; ventral fur is lighter brown. Its snout, uropatagium, and wing membranes are black and hairless. Its ears are also black; they are relatively short with rounded tips. The tragi also have rounded tips. Its dental formula is
2.1.1.3
3.1.2.3
, for a total of 32 teeth.
One study of a population in Colorado found that their average life expectancy was a little over 6.5 years; the oldest known big brown bat was 19 years of age (!) and documented in Canada.

This bat doesn't live in the UK so this can't be correct.


text:
DNA of cellular organelle
Why do some cellular organelles like mitochondria and plastids have their own DNA. And what is the basic difference between the DNA of the nucleus and these organelles?

Mitochondria and plastids are the result of two ancient mergers. A kind of symbiotic relationship where one cell phogocytized another. Rather than being digested, the phagocytized cell, complete with its own DNA cooperated with the cell that "ate" it. This was part of the evolution of eukaryotes. This idea is called endosymbiosis, and was championed by Lynn Margulis in the late 1960s. Mitochondria and plastids come from Bacteria, and carry the traces of their original DNA. However, a complete genome was no longer required for the new function, so mitochondria lost many redundant genes. Mitochondrial genomes are much smaller. Plastid genomes are larger than mitochondrial genomes, but smaller than the genomes from which they originated.


text:
Vitamins — how did they get their names?
There are several types of vitamins. A,B,C,D,E,H,K,P, etc. How did they get their names?

I'm voting to close this question as off-topic because it is about the history of what is obviously an arbitrary nomenclature rather than biology.

http://www.chm.bris.ac.uk/webprojects2001/harvey/namingvitamins.htm

Here's a very comprehensive guide to the first person to propose alphabetical vitamines and the renaming to vitamin: https://gizmodo.com/why-are-vitamins-named-using-the-alphabet-1555934736 There used to be vitamine B1, B2, B3, B4, B5, B6...

I’m voting to close this question because it was poor when it was posted and it is being used as evidence for continued posting of a new inappropriate question.

They were more or less named in the order that they were found.  Letters F-J are skipped because many of those were reclassified or later found not to be vitamins.  The K comes from the German word for Koagulation because the vitamin is involved in the coagulation of blood.
The discovery dates of the vitamins and their sources /
Year of discovery   /Vitamin    Food source

1913 Vitamin A (Retinol) Cod liver oil
1910 Vitamin B1 (Thiamine)   Rice bran
1920 Vitamin C (Ascorbic acid)   Citrus, most fresh foods
1920 Vitamin D (Calciferol)  Cod liver oil
1920 Vitamin B2 (Riboflavin) Meat, dairy products, eggs
1922 Vitamin E (Tocopherol)  Wheat germ oil, unrefined vegetable oils
1929 Vitamin K1 (Phylloquinone)  Leaf vegetables
1931 Vitamin B5 (Pantothenic acid)   Meat, whole grains, in many foods
1931 Vitamin B7 (Biotin) Meat, dairy products, eggs
1934 Vitamin B6 (Pyridoxine) Meat, dairy products
1936 Vitamin B3 (Niacin) Meat, grains
1941 Vitamin B9 (Folic acid) Leaf vegetables
1948[42] Vitamin B12 (Cobalamins)    Liver, eggs, animal products

There are many different B vitamins, water soluble, because many vitamins previously given different letters where later found to be part of the B complex. For example H is now B7.  Additionally, many letters, such as P, are no longer classified as vitamins.
More information can be found on this Wikipedia page.

ascorbic acid is water soluble

1 * Vitamin A:
Name: Retinol. It was discovered in 1909
Function: Carotene compound responsible for transferring light to the retina.
The most common sources: whale liver oil, meat, eggs, liver, kidney, cheese.
Diseases resulting from deficiency: lack of it leads to night blindness.
2 * Vitamin C:
Name: Ascorbic acid. It was discovered in 1912.
Function: Important in the synthesis of collagen, the protein component of the body's tissue frame.
The most common sources: fruits, vegetables, oranges, lemons.
Diseases associated with deficiency: Lack of it leads to scurvy (weakness of the capillaries), which is characterized by the presence of fragile capillaries, poor healing wounds, and deformity in children.
3 * Vitamin B1 B1:
Name: Thiamine. It was discovered in 1912.
Function: Acts as a catalyst in the metabolic process of the body.
The most common sources are: whole grains, rice, legumes, wheat germ.
Diseases resulting from deficiency: the most important disease Berri, a disease of the nervous system and heart.
4 * Vitamin D:
Name: A group of vehicles with multiple names. It was discovered in 1918.
Function: It is with calcium helps to promote bone health.
The most common sources: sunlight promotes the manufacture of sufficient amount of vitamin D in the skin.
Deficient diseases: Deficiency can lead to osteoporosis in adults and bone rickets in children.
5 * Vitamin B2 B2:
Name: riboflavin. It was discovered in 1920.
Function: As a catalyst for enzymes that stimulate chemical reactions in the body.
The most common sources: dairy products, eggs, green leafy vegetables.
Diseases resulting from deficiency: Lack of inflammation causes inflammation of the lining of the mouth and skin.
6 * Vitamin E (E):
Name: A group of vehicles with multiple names. It was discovered in 1922.
Function: Antioxidants, protect the body cells from destruction.
The most common sources: spinach, broccoli, wheat germ.
Diseases associated with deficiency: deficiency can lead to anemia.
7 * Vitamin B12 B12:
Name: Cobalamin. It was discovered in 1926.
Function: One of the fundamental factors in the synthesis of DNA (genetic material of cells).
The most common sources: meat, fish, eggs, dairy products.
Diseases related to deficiency: deficiency leads to anemia (anemia), also called sober anemia.
8 * Vitamin (K K):
Name: Generally known as vitamin clotting, it includes a group of compounds with multiple names. It was discovered in 1929.
Function: A key factor in the formation of coagulation factors.
The most common sources: spinach, leafy vegetables, broccoli, cabbage, fish, liver, meat, eggs.
Diseases associated with deficiency: lack of it can lead to abnormal bleeding.
9 * Vitamin B5 B5:
Name: Bentothenic acid. It was discovered in 1931.
Function: Incorporates some important compounds that help to decompose fatty acids and manufacture cholesterol in the body. It is used in natural medicine as an alternative to creatinine, and its presence is required for healthy and natural growth of hair.
Most common sources: Most foods especially in legumes, vegetables, eggs, red meat, whole grains, and royal jelly.
Diseases resulting from deficiency: burning foot syndrome, allergies, adrenal insufficiency, adison disease, and rheumatoid joints.
10 * Vitamin (H or B7):
Name: Biotin. It was discovered in 1931.
Function: It is necessary for the manufacture of insulin, antibodies, and some enzymes, and helps in metabolism.
The most common sources: Available in almost all natural foods, found in liver and yeast.
Diseases resulting from deficiency: deficiency is often the result of defects in its use (feeding on white eggs), not the lack of food because it is made by intestinal bacteria. The lack of biotin is rare because a large quantity of it is reused several times before being taken out in urine. Symptoms of the deficiency are on the body of skin peeling, hair loss, loss of appetite, nerve fiber damage.
11 * Vitamin B6 B6:
Name: pyridoxine. It was discovered in 1934.
Function: A catalyst for enzymes.
The most common sources: whole grains, vegetables, liver, beans, fish.
Diseases resulting from deficiency: lack of it leads to inflammation of the skin and mouth, nausea, vomiting, weakness, dizziness and anemia.
12 * Vitamin B3 B3:
Name: Niacin. It was discovered in 1936.
Function: plays an essential role in the enzymes involved in the metabolism of the body.
The most common sources: dairy products, eggs, fish, legumes.
Diseases resulting from deficiency: Lack of inflammation causes inflammation of the skin, rectum, vagina and mouth, as well as delayed mental development.
13 * Vitamin B9 B9:
Name: Folic acid. It was discovered in 1941.
Function: It is an important factor in the synthesis of DNA (genetic material of cells).
The most common sources: leafy vegetables, fruits, dried legumes, peas.
Diseases associated with deficiency: Folic acid deficiency leads to anemia (megaloblastic anemia).
Vitamins are divided into two parts:

Vitamins that dissolve in the water is vitamin C and B complex (C, B complex).
Fat-soluble vitamins A, D, E, K (A, D, E and K).

Fat-soluble vitamins are stored in the tissues of the body. Vitamins that dissolve in water (except vitamin B12) can not be stored in the body, and should therefore be constantly replenished.
After discovering vitamin A, vitamin B was detected and thought to be just one vitamin, but later it was discovered that vitamin B is a group of vitamins that dissolve in water. To differentiate between these vitamins were added numbers of their names, and resulted in vitamins B1, B 2 ... Today there are 8 vitamins in group B. One of which is called B12, which indicates that several substances from this group have been eliminated that have been shown to be non-B vitamins.

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


text:
Theoretical question: Would immune cells that produce blue light be an effective and better alternative to inflammation?
It's well known that blue light is effective against a wide range of bacteria (type "antibacterial blue light" into Google for starters). This article (https://www.ncbi.nlm.nih.gov/pubmed/23009190) claims that blue light also works on some fungi.
With that in mind, would it be advantageous to have immune cells that produce localized blue light when they detect a bacterial infection? In particular, instead of producing inflammatory chemicals, reprogram white blood cells to produce bioluminescent compounds rigged in the 400-470 nm range when they detect bacteria.

I guess no. Afaik an essential part of inflammation is to prepare the tissue so that leukocytes can more easily penetrate it, irrespectively on what they will do when in place. Another thing is that light would not be really as local as oxygenizing radicals.

The difference in light intensity between known bioluminescent samples and the blue light used as an antibacterial is huge. There is simply no known biological mechanism that would produce the intensity of light required.
If you could somehow make an immune cell produce high intensity blue light to damage bacteria, you would find that it would also damage surrounding cells - the chemical products released to destroy bacteria are much more short-ranged.


text:
Fossil record of previously thought extinct animals
I was watching this video from the Youtubers SciShow titled "7 Animals We Used to Think Were Extinct (But Aren't!)." Some of the extinct animals, were suspected to have gone extinct close to half a billion years ago, which leads me to believe that their fossils were obviously found in layers corresponding to those time periods and not in newer layers; however, since these animals are known to be still present today, I was wondering how it is possible that they do not have fossils in newer layers of the earth. Similarly, What caused the sudden stoppage of fossils?
I know very little about evolution, biology, and fossil records except from what is taught in high-school, and haven't taken a biology course in a few years, so if it is possible to get a simple answer that a biology ignorant person could understand I would greatly appreciate it! Thank you!
https://www.youtube.com/watch?v=e_TjrqWTV5s&t=187s

The formation of fossils is exceedingly rare. A number of unlikely events must all line up for us to find one. So there would be no reason to expect that we would find a fossil of anything but the most common and easily fossilized organisms. The probability of NOT finding a fossil is much greater than finding one.


text:
How did biologists find out that bacterial plasmids were circular?
I was always curious how it was determined that bacterial plasmids were circular, since there isn't an obvious way to find this out. I heard somewhere that there was a difference when gel electrophoresis was conducted. Could anyone give an explanation?

Where did you hear this? Having a reference would help.

i searched google that exact question and the first few pages talked about gel electrophoresis but sadly none of them gave a clear explanation


text:
Human spine: Is the coccyx really fused?
Prologue: This post is about the adult (say, a 20 year old) human skeleton; I'm not particularly interested in infant skeletons.
The human spine has is composed of cervical, thoracic, lumbar, sacral and coccygeal vertebrae

 Image source

My school textbook (which has a history of possessing erroneous/outdated information) states:

The coccyx consists of 4 coccygeal vertebrae that are fused to become a single bone.

However, this Wikipedia article states:

Most anatomy books incorrectly state that the coccyx is normally fused in adults. In fact it has been shown that the coccyx may consist of up to five separate bony segments, the most common configuration being two or three segments.

Is Wikipedia correct?
If so, what is the (most common) number of bones that constitute the spine? Is the number of vertebrae that constitute the spine going to be different?

This other Wiki article appears to be particularly contentious:

A fully grown adult features 30 bones in the spine, whereas a child can have 33.

The cervical vertebrae (7)

The thoracic vertebrae (12)

The lumbar vertebrae (5)

The sacral vertebrae (5 at birth, later fused into one)

The coccygeal vertebrae (5 at birth, some or all of the bones fuse together but there seems to be a disagreement between researchers as to what the most common number should be. Some say the most common is 1, others say 2 or 3, with 4 being the least likely. It is counted as 1 in this article.)

I understand that there is little to no variation in the number of cervical, thoracic and lumbar vertebrae among humans, so they altogether constitute $\mathrm{7+12+5 = 24}$ vertebrae/bones (in this case, I believe "vertebrae" and "bones" are synonymous).
Assuming that the sacrum really is one fused bone (my question's regarding the coccyx, so I'm not going to question the anatomy of the sacrum in this post) consisting of five vertebrae (I think there's a bone-vertebra distinction here, so they aren't the same thing)
In that case, the cervical, thoracic, lumbar and sacral contributions are $\mathrm{ 24 + 1 = 25}$ bones, or  $\mathrm{ 24 + 5 = 29}$ vertebrae. (Right?)
According to the Wikipedia article I cited above (the second one), the adult human spine has 30 bones.
So the coccyx contributes $\mathrm{30 - 29 = 1}$ bone to the spine, or $\mathrm{30 - 25 = 5}$ vertebrae to the spine.
In other words, the second Wiki article implies that the coccyx is a single (fused) bone. However, the first article states that the coccyx is really composed of 3-5 (say, 4 on an average) bones.
This is horribly contradictory.

If the finer points of my question was lost, I'll restate them here:
1) Is the coccyx a single bone or multiple bones?
2) How many bones are there in the adult human spine?
3) How many vertebrae are there in the adult human spine?

Although from an academic standpoint these are critically important questions, the variability in human anatomy unfortunately renders the academic answers reasonably meaningless regarding the coccyx in any clinical circumstances. Although variability is much less, higher in the spine it is common to see a sacralized L5 or an S1 that failed to properly fuse, even more rare are the cervical ribs. Clinically, some of these items actually mean something, yet I have never seen a clinically significant issue related to coccygeal fusion.

@RudyB And that was the point I was making (with a different emphasis) in my comment below. Academically, the fusion (or lack thereof) of the coccygeal segments matters. Clinically (meaning practically), it really doesn't in most cases.

The wikipedia article links to two papers. The first article has data for 120 pain-free and 51 affected patients with data on the number of coccygeal segments in each. We can back-calculate a reasonable approximation of segment distributions from their percentages:

1 Segment: 7%
2 Segments: 51%
3 Segments: 38%
4 segments: 4%

So 2 or 3 segments makes up almost 90% of the population. Given that only 7% of the subjects had single element coccyxes, I think it's safe to call the coccyx usually made of multiple elements.
Whether you refer to those multiple elements a single bone if largely a semantic argument. Since there is variation, it seems reasonable to call the collection 5 of variably fused terminal vertebrae the "coccyx".
As a practicing anatomist, I would say that there are 29 vertebrae, as in 29 vertebral elements (but you can't say 29 ossification centers, because each is made of multiple centers). These fuse into 24 free vertebrae, the sacrum (5 fused vertebrae) and one coccyx, which is variably fused.

It is odd that you say you don’t trust Wikipedia for anything, but then base your entire answer on a paper that Wikipedia cites without analysis on whether that paper is accurate and up-to-date, which was really the question. Wikipedia can usually (though definitely not always) be trusted to accurately report the sources it cites, but whether or not it has the best source available is a much more difficult question—the kind of question you would bring to experts to get their opinion on.

@KRyan -- kmm's Bona Fides and profile/activity/awards rather makes this answer an "expert" opinion. -- Wikipedia can be edited by anyone and the "peer review" quality varies widely, as anyone with expert knowledge in a field who has used Wikipedia knows. -- I've had my own edits rolled back when I not only cited sources but cited the legally documented source that defined the very answer I gave. i.e. I literally proved my answer right outside of any matter of opinion and still my answer was rolled back. That was the last time I contributed to Wikipedia.

@user23715 I’m not doubting them, I’m saying that his answer does not so much as even assert that this is the right article to be looking at. “I am an expert and this paper is up-to-date and correct,” would be fine. But instead the answer is more like “the paper says this, which Wikipedia accurately reports,” which even I (who cannot name all of the major bones of the arms and legs) could have determined myself.

@KRyan -- I think he has that covered with, "As a practicing anatomist, I would say...", no? -- His disparagement of Wikipedia is founded IMO. Besides, if one has to "trust but verify" every time one uses Wikipedia why not bypass it to begin with and go straight to the sources? -- Something like Wikipedia made more sense when a search engine like Google did not exist. Now, failure to find appropriate sources is one's own fault. Using a squiffy source like Wikipedia as a first pass is rather redundant and their difficulties in getting funded lately means many others have figured this out.

To be fair, I do think it's incongruous that it wouldn't matter to you as a "practising anatomist". Anatomy is all about definining body structure. That includes variations, both common and less common. As a practising doctor, I've studied Anatomy in med school, and I know how important minutiae about spatial relations and variations are in the subject - I mean, that's the whole point of the subject! I bet this sort of thing is even more important to academic practitioners of Anatomy. What you said may have made more sense if you'd said "physician" (or even "surgeon") instead of anatomist.

lets answer in order.

Is the coccyx a single bone or multiple bones?

answer yes, A bone is not a concrete definition and can be used to describe the number of elements or the number of contributing elements. Bone is more a definition of material than object. My favorite example is the fused mammalian jaw which can be one or two bones (two fused dentaries one mandible) or two bones (two fused dentaries). Even using the word elements can get confusing. Like many things in biology nature doesn't care about our attempts to define and categorize.

How many bones are there in the adult human spine?

26 -35 depending on the individual and how you use the term.

How many vertebrae are there in the adult human spine?

this one is easy, 34-35 for most people. The variation is becasue not everyone develops all the coccyx vertebrae. Fused vertebrae are still counted as several individual vertebrae. This is why we have a seperate term for the fused element, the sacrum or attach the descriptor "fused".  This comes up a lot in paleontology since animals change the number of vertebrae they have and how they are distributed as they evolve.  Sauropods are particularly known for swapping vertebrae across segments.

I made a mistake on my math on question 3, I have fixed it, no stunning revelation I just added wrong. .

I suggest using >  instead of four spaces. It's HTML5-ly better, and looks nicer.

It isn’t just nicer looking—proper quote boxes are also vastly better for accessibility. Which is to say, they aren’t actively terrible for accessibility, which codeboxes can be. Please never use code formatting for non-code: quote boxes, or simple quotation marks, work quite well for quotation. When you use code boxes, you may see a gray box with monospace font, but others—say, those listening to the page because they are blind—may get something very different, which may be hard to understand. Reading letter-by-letter is not unheard of! So please, format properly.


text:
What is the expected amount of DNA shared by first cousins and the people between them in a family tree?
What is the expected amount of DNA that is shared by all of the people between first cousins, including the first cousins, in a family tree?

To simplify your problem, let's just consider autosomal DNA. In this case,  your expected amount of shared DNA should be synonymous with genetic consanguinity, which can be conveniently checked from this image.
Thus, you share approximately 1/8 of DNA(I know saying so is not scientifically strict as there are recombinations and mutations that prevent the DNA to be exactly the same.) with your first cousins. Same is true between first cousins.
Source: Wikipedia image gallery.

How much of the 12.5% shared DNA between first cousins is also shared by, say, their parents who are siblings?  Is it a lower expected percentage which is common to all four people?

@michaelc35 Their parents who are siblings should share more DNA in common, 25% in fact. You can think it in this way. Your first cousins' DNA is diluted by other people who married into your family, each of your first cousins only carry a half of DNA from their parents who are siblings, so they just have 12.5% in common.

@michaelc35 If you are satisfied with the answer, please accept it manually. It will encourage me to produce more quality answers in the future, thanks! :D

I'm interested in what the expected amount of DNA that all four people have in common - the two first cousins and their parents who are siblings.  It seems that the expected percentage of DNA shared by all four would be lower than 12.5%.

@michaelc35 Yes, definitely it would be lower. But there is no precise value in this case. An averaged estimate will put it at a half of 12.5% considering the amount of DNA shared between a first cousin and the sibling of his/her parents.

@michaelc35 There's no precise value because you are cross comparing different people in different generations. In this case, there might be no direct genetic relationship between particular members besides the fact they all inherited something from their common ancestors.


text:
What is the "male gender rudiment" that women allegedly have?
In The Man without Qualities Robert Musil wrote (my emphasis):

"But the nature," he thought, "gives the man nipples and the woman
  a male gender rudiment. We cannot conclude from this, however,
  that our ancestors were hermaphrodites."

What male gender rudiment does he mean? It must be some "useless" body part in female body (like man's nipples).

Original German text:

"Aber die Natur" dachte er "gibt dem Mann Saugwarzen und der Frau
  ein männliches Geschlectsrudiment, ohne dass daraus zu
  schliessen wäre, unsere Vorfahren seien Hermaphroditen gewesen.

First, let's briefly discuss the development of the the male and female internal genitalia and sex glands:
These include the ejaculatory duct, prostate and seminal vesicles for males, and uterus, uterine tubes and the proximal part of the vagina for females.
They all develop from two tube-like structures called mesonephric and paramsonephric ducts.
These ducts initially exist in both males and females, but normally, only one develops while the other degenerates, depending on the presence of sex-determining factors and hormonal activity.
The mesonephric ducts will develop to the male internal genitalia (the organs are mentioned above), while the paramesonephric duct will develop to the female internal genitalia (also mentioned above).
Now, to your question:
A male rudiment that exists in females is the non-fully degenerated mesonephric duct, named the Epoophoron and Paroophoron in adults, which later in life may form the Gartner’s cyst.


text:
Which kind of mushroom is this?

I'm in Western Arkansas, and these are red, hollow mushrooms with a brown slimy coating that popped up in our mulch, roughly a half an inch in diameter and they have grown several inches tall. Is there anything specific that I can/should do to these things? I have young kids and pets that I assume I don't want eating these things.

This looks like a type of stinkhorn fungus.  They commonly pop up in urban settings, including mulched areas, and can come in many different appearances.  The slime on these mushrooms is used to attract insects and flies which will disperse their spores. They are found in North America including in temperate and north-temperate climates.  According to MushroomExpert.Com these mushrooms will not hurt you, your children or pets.
Specifically, the stinkhorns in your photo look like Mutinus elegans to me.

Source: http://www.projectnoah.org/spottings/635556012


text:
What happens to neutrophils in whole blood stored for transfusion?
The lifetime of neutrophils is normally quite short, 3-5 days in vivo (link).  On the other hand, whole blood can be stored for a fairly long time, up to 35 days (link).
What happens to neutrophils in whole blood for transfusion that was stored for more than 5 days?

I have not worked in a shop that has whole blood available for transfusion in a while (typically only very large trauma centers use whole blood, everyone else uses individual components), but most packed cells for transfusion are given as leukocyte reduced with those neutrophils being filtered out prior to transfusion.

@RudyB Thanks!  I know whole blood is not common nowadays, it used to be standard in the past.  I'm just curious whether the neutrophils  stay alive longer, or apoptose, or get eaten by macrophages, or something else, in that situation.

There is actually a resurgence of whole blood usage due to trauma studies showing that it is the best resuscitation fluid, but storage, cost, usage, etc. mean that only few places keep it. Outside of trauma, component transfusions predominate (PRBCs/ FFP/ platelets). However, using it is much easier (minutes) relative to thawing FFP (an hour) or trying to get emergent pheresis platelets from Red Cross (multiple hours in the best case).
The neutrophils are the part of blood that clinically nobody wants due to things like graft versus host disease, so I honestly do not know what happens.


text:
Why don't chilli peppers taste as hot in space?
The following commentator writes:

Chili peppers don’t taste as hot in space as they do on Earth. Nobody knows why.

We know that the 'hot' feeling of chilli peppers is caused by Capsaicin. We read:

Capsaicin inside the pepper activates a protein in people’s cells called TRPV1. This protein’s job is to sense heat

There appears to be some question about the cause of the 'spicy' taste of chilli peppers.
My question is: What is the reason that chilli peppers don't taste as hot in space?

What atmosphere pressure is used in an orbital space craft?  How does that compare to the pressure in an aeroplane cabin, where food is also comparatively tasteless?   Hypothesis, taste bud efficiency drops with air pressure.  So, how does food taste in a diving bell, or other pressurised vessel ?

@Criggie the pressure at ISS is 101.3 kPa, the same pressure of sea level and higher than an airplane cabin. So, that doesn't seem to be the cause.

TL;DR
All food taste bland in space, not only chilli.

The claim in that tweet ("Chili peppers don’t taste as hot in space as they do on Earth") is not exactly correct because, the way it's worded, it gives the impression that only chilli peppers have a different taste. In fact, astronauts/cosmonauts use more chili and other spices than they regularly do on Earth, for a reason: they say that food in space (microgravity) taste bland. All food, not only chili.
Since the beginning of space flight, astronauts report that food taste different in microgravity. According to the Scientific American article When It Comes to Living in Space, It's a Matter of Taste (Romanoff and Romanoff, 2017):

Many said that flavors are dulled and they crave fare that is spicier and considerably more tart than they would prefer on Earth.

So, due to the food tasting so bland, astronauts in fact use more chili and other spices than they normally do on Earth:

It's possible that hot sauce and salsa could be key ingredients to the success of a manned mission to Mars. The kicked-up condiments already came close to causing a mutiny on the International Space Station (ISS) in 2002 when astronaut Peggy Whitson threatened to bar entry to the crew of the visiting shuttle Atlantis unless they came bearing a promised resupply of the spicy stuff. Only when shuttle commander Jeff Ashby announced that he had the goods did Whitson say, "Okay, we'll let you in then." Whitson was joking, but the need for astronauts to be able to  spice up their food while in orbit is no laughing matter.

However, it's still unknown why food taste bland in microgravity. Also, there is no consensus about that fact, to start with:

There's little scientific data to back up astronauts' claims that taste changes in space, despite a number of studies since the 1970s on the effect of microgravity on the sense of taste and smell. In essence [...] study participants were split on the matter.

For those that report a change in the taste, some hypothesis were proposed:

One of the most prominent physiological changes associated with spaceflight has to do with fluid shifting from the lower to the upper parts of the body because of weightlessness. This facial and upper-body swelling also creates significant nasal congestion, and because odor is essential to the sense of taste, a decrease in the perception of flavors would occur.

And also:

The shuttle has a "sterile" smell, which when combined with other odors, such as the scent of their rinse-free shampoo, can be somewhat distracting.

However, there is little scientific evidence supporting this fluid-shifting hypothesis. According to Vickers et al. (2001), reproducing that fluid-shift in a simulated microgravity, where people had a head-down bed rest, has no effect on the threshold sensitivity of tastants. The same lack of changes in the taste and smell sensitivity under simulated microgravity was found by Olabi et al. (2002).
Despite that, this fluid-shifting hypothesis is supported by NASA (Nasa.gov, 2017) in an educational resource for kids:

From the early 1960s, astronauts found that their taste buds did not seem to be as effective when they were in space. Why does this happen in space? This is because fluids in the body get affected by the reduced gravity conditions (also called fluid shift). On Earth, gravity acts on the fluid in our bodies and pulls it into our legs. In space, this fluid is distributed equally in the body. This change can be seen in the first few days of arriving in space when astronauts have a puffy face as fluid blocks the nasal passages. The puffy face feels like a heavy cold and this can cause taste to be affected in the short term by reducing their ability to smell.

The same source says:

When food seems to lose its flavor, astronauts usually ask for condiments, such as hot sauces, to give food some intensity of taste. A variety of condiments are available for the crewmembers to add  to their food such as honey, and sauces like soy sauce, BBQ, and taco. (emphasis mine)

Conclusion
For reasons yet unknown, it seems that all food (not only chilli peppers) taste bland in microgravity. To cope with that, astronauts rely on chili and other hot spices.

Sources:

Romanoff, J. and Romanoff, J. (2017). When It Comes to Living in Space, It's a Matter of Taste. [online] Scientific American. Available at: https://www.scientificamerican.com/article/taste-changes-in-space/ [Accessed 26 Dec. 2017].
Nasa.gov. (2017) [online] Available at: https://www.nasa.gov/sites/default/files/files/Taste-in-space-TLA-FINAL.pdf [Accessed 26 Dec. 2017].
VICKERS, Z., RICE, B., ROSE, M. and LANE, H. (2001). SIMULATED MICROGRAVITY [BED REST] HAS LITTLE INFLUENCE ON TASTE, ODOR OR TRIGEMINAL SENSITIVITY. Journal of Sensory Studies, 16(1), pp.23-32.
Olabi, A., Lawless, H., Hunter, J., Levitsky, D. and Halpern, B. (2002). The Effect of Microgravity and Space Flight on the Chemical Senses. Journal of Food Science, 67(2), pp.468-478.

The lecture on skepticism seems misplaced since the claim in the question is accurate (although narrower than the whole truth).

Odd that this answer spends a lot of time concentrating on fluid-shifting and doesn't note that taste is strongly dependent on smell and that odor particles diffuse differently in microgravity.

@CarlKevinson fair enough, lecture removed.

@chrylis there are several other hypotheses and possible explanations. However, I normally write about what I can reference. And, in this case, most papers and NASA support the fluid-shifting hypothesis. So, nothing odd here. However, if you found a peer-reviewed paper explaining the role of the particles diffusion in changing the taste in microgravity, feel free to add your answer, I'll certainly upvote it.

Is it possible that it is not the taste of food which is different but that individuals in space have a desire for different nutrition ? What if microgravity was affection the creation for a specific protein, so the body change it's biological desire for the precursor nutrients of that protein. If that makes sense...

@Shodan even if that were possible (which is extremely unlikely) it doesn't match the speed of the changes: astronauts report a change in the taste after few hours/days in space, and that's another thing to support the fluid-shifting hypothesis.

None of this supports the claim that chilli peppers taste less hot in space. It only says that astronauts eat them more often. Nasal congestion wouldn't affect chilli hotness the way it affects other flavors.

Could just a more mundane answer about chilli tasting bland in space...because astronauts are using it all the time?
As an avid chilli eater, I can report that the more you eat, the less sensitive you are to it, and if you are having it all the time in prolonged period of times, you will feel less effects.
As an example, I recently eat raw two of the reportedly stronger chilli of the Philippines without needing drink or food (in Earth), and without it bothering me. I just got a slightly runny nose.


text:
Endogenous retroviral insertions as evidence for evolutionary relationships among primates
A synopsis of a 2005 paper in PlosBiology by Yohn et al. states that:

Searching the genomes of a subset of apes and monkeys revealed that
  the retrovirus had integrated into the germline of African great apes
  and Old World monkeys—but did not infect humans and Asian apes
  (orangutan, siamang, and gibbon). This undermines the notion that an
  ancient infection invaded an ancestral primate lineage, since great
  apes (including humans) share a common ancestor with Old World
  monkeys.

Also, Micheal Lynch writes :

"Remarkably, we have found many cases of parallel intron gains at
  essentially the same sites in independent genotypes," Lynch said.
  "This strongly argues against the common assumption that when two
  species share introns at the same site, it is always due to
  inheritance from a common ancestor."

Since shared ERVs in humans and chimps is touted as one of the proofs of humans and chimps sharing ancestry (like by Ken Miller here), does the above paper (and quote) undermine this line of reasoning?
Is there any good (recent) source which discusses proof of common descent using ERVs?

I have changed the first sentence of the question so as to provide a reference to the actual paper, rather than just the synopsis. I have changed the title so that it indicates the area of biology the question is about and spells out endogenous retroviral for general comprehensibility and indexing. In relation to the original title ("Does this paper show…") would point out that it is scientific facts established by observation or analysis that may or may not show something, not the papers.

The Yohn et. al. (2005) paper (from Evan Eichler's lab) is describing a single type of endogenous retroviral element (loosely think of it as a 'species'), called PTERV1. They show that there were multiple independent infection events that resulted in permanent integrations in the ancestors of modern species (~3-4 MYA in the ancestors of gorillas and chimps, ~1.5 MYA in the ancestors of baboons and macaques). This in no way contradicts the notion of common ancestors among the apes/monkeys; indeed, they state this as a given in their analysis (emphasis mine):

A total of 275 of the insertion sites mapped unambiguously to
non-orthologous locations (Table 2), indicating that the vast majority
of elements were lineage-specific (i.e., they emerged after the
divergence of gorilla/chimpanzee and macaque/baboon from their common
ancestor).

The presence of an ERV (or intron, or any general genomic synteny), can be used as evidence to support a particular model of common decent. Changes in genomic architecture are stochastic processes, and the work you cite by Li et. al. (Lynch lab) is showing us that ERV placement can occur at a similar, or nearly identical, location at a much higher rate than previously thought. We therefore need to take this into account when calculating how strongly a shared ERV increases our confidence in a given phylogenetic model.
The video you linked to uses a completely random (i.e., very simple) model of ERV integration, setting the chance of an insertion at a given location at 3.3e-10. The findings by Li tell us that this is incorrect. In daphnia, at least, ‘hotspots’ may account for nearly 25% of new intron gain. The video also failed to include all of the instances of ERVs that are not shared between humans and chimp (back-of-napkin, this could account for differences of ~0.3% between their genomes, see Mun et al. 2014). This will increase the probability of an exact match occurring by chance (e.g., put two people in a room, what’s the chance of them having the same birthday? Put 100 people in a room, what’s the chance of any of them having the same birthday?).
So, let’s be extremely conservative and say that the chance of the same insertion at a given location in both chimps and humans is one in one thousand (1e-3, seven orders of magnitude more probable than in the original model). Sixteen shared ERVs are identified in the video; if each is considered an independent event because of no shared decent, we are still looking at odds around 1e-48 (1e-3 ^ 16). An alternative could be that they are derived from insertions that predate the split from a common ancestor. Given Li et. al., maybe each event should be given a probability of only 0.75 instead of 1.0 (as per the video) because up to 25% of them could be from hotspots. In this scenario, the probability is 0.01 (0.75 ^ 16). Therefore, the second hypothesis is 46 orders of magnitude more probable than the first. In my mind, this is extremely compelling evidence that humans and chimps share a common ancestor, using only ERV data.
I want to be clear, I am fudging these numbers extensively towards not supporting common descent. The real odds will be much higher in favour of common descent.
For further reading, Welkin Johnson wrote a comprehensive review on ERVs in 2015 (paywalled, so you may need to search for Alexandra Elbakyan's scientific literature retrieval method if you don't have institutional access).

References
Johnson WE. (2015). Endogenous Retroviruses in the Genomics Era. Ann. Rev. Virology. doi: 10.1146/annurev-virology-100114-054945
Li W. et al. (2009) Extensive, Recent Intron Gains in Daphnia Populations. Science. doi: 10.1126/science.1179302
Mun S. et at. (2014) Chimpanzee-Specific Endogenous Retrovirus Generates Genomic Variations in the Chimpanzee Genome. PLoS One. doi:  10.1371/journal.pone.0101195
Yohn et. al. (2005). Lineage-Specific Expansions of Retroviral Insertions within the Genomes of African Great Apes but Not Humans and Orangutans. PLoS Biol. doi: 10.1371/journal.pbio.0030110

I wasn't saying that these quotes contradict common descent. I was asking if, in the light of the quotes I mentioned above, ERVs can be presented as evidence of common descent of man and chimp (as many, like Ken Miller, have done).

Yes, they absolutely can be used as evidence. This is just one class of ERV, and the authors clearly explain why this class presents as non-orthologous copies in different taxa.

Ok. I got that this paper was talking of only one type of ERVs, but Michael Lynch's statement above says that even if we find ERVs (or generally, introns) at the same site in multiple lineages, it doesn't serve as proofs of common descent. If this is the case, then how can ERVs be used to prove common descent (especially, human/ape common descent)?

I've modified my answer to better address our discussion.

@Bond....SteveBond You have a cool name. And on top of that you write good answers +1. Good to have you active on Biology.SE!

Thanks a lot. Have marked the answer as accepted. Just one more point. How many ERVs are found among humans and chimps at the same location? Different sites seem to be giving different answers. This one says there are 40 such ERV families : https://genomebiology.biomedcentral.com/articles/10.1186/gb-2006-7-6-r51
This one says there are 14 shared ERVs : http://scienceblogs.com/erv/2009/06/19/charles-jackson-expert-on-ervs/

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


text:
Recession of skin tan
In early October I was on a holiday near the equator and got tanned. Now, roughly 3 months later, the tan on my face and arms has gone almost entirely where my belly, chest and legs are still moderately tanned. It seems that body parts that are exposed (to light) more than others seem to loose the tanning effect more quickly. Why is this? Or is there another reason?
I am not a biologist so I would appreciate an answer that is articulated in a way non-biologists can understand it.


text:
Humans have tails?
Today in biology class, my teacher said that all chordates have all the necessary traits, at least during the embryo stage, and we humans are chordates. So, one of these necessary traits was that they should have tails. My question is, humans don't seem to have tails, so how can they be chordates?

Oops.... I am always surprised when my vote to close alone is enough to actually close a question. I think @kmm answer is good (+1), I just wanted to highlight that the question can be though as a duplicate of another one.

What is meant by a "necessary trait"?

@MamaTank what I meant is that, a species can be called a chordate only if it has all the traits a chordate is supposed to have.

The chordate trait you are describing is more precisely termed post-anal tail. It is one of the basic characteristics of all chordates, along with, among others, pharyngeal pouches, a hollow dorsal nerve tube, and a notochord. Two other traits are less commonly considered chordate traits: segmented body musculature and a thyroid gland or endostyle (the latter particularly controversial).
These characteristics are present in all chordates at some point during their ontogeny. These traits are shown below.
We can see these most clearly in embryonic forms. For the post-anal tail: in humans, there is a short "tail" that extends past the anus (end of the yellow tube). This tail does not typically persist for very long. Similarly, the notochord is absorbed into the vertebral column, and remnants of the pharyngeal pouches are not externally visible.
The key phrase is "at some point during development." Non-embryonic humans don't have a tail, but that doesn't mean humans are not chordates.

What do you mean "non-embryonic humans"?


text:
Biological EM emissions
What sorts of EM frequencies are emitted by the human body?
Are there any processes in the human body that produce Radio/Microwaves or uv/x-rays/gamma rays?

have you googled this at all?

I agree with @aaaaaa's comment but the downvote is a bit much in light of the user's newness to the site, IMO.

i will upvote when @bobiscool add  results of some research and mention may name in comment (so i can see).

https://io9.gizmodo.com/how-much-radiation-does-the-human-body-emit-1719085023
This confirms part of my question, radioactive isotopes can be mistaken for needed materials in the body.

@bobiscool: aaaaaa would not get your comment unless you use his username. I added your link to my answer and found a paper and discussion that also support the premise of your question.

According to this author (1) the human body emits radiation, mostly in the infared region. Human body temperature generally exceeds that of its surroundings and so there is a net flow of heat from the body into the environment, some due to convection and some due to thermal radiation.
This Czech paper suggests (2) human EM emission in a particular low-frequency band (0.5 - 30 Hz), but the writing is awkward and I do not think this is peer-reviewed.
A more comprehensive Russian paper (3) discusses, among other things, emission of photons (light!) from human skin. The energy of this light is not very high (1-3eV, which is 1-3 times $1.602~ \text{x}~ 10^{-19}$ Joules), but it's not nil.
This interesting topic has been studied extensively and this is a quick glance. Am adding the link furnished in a comment by OP above which does suggest that the body can emit energy via radioactive decay.
Also, this link (4) based on the paper by Toohey below discusses radioactive emission by humans in some detail, including radioactive decay of potassium-40. There is apparently a mechanism by which ambient gamma radiation can interact with atoms in cells (photoelectric effect) to produce x-rays, which are emitted from the body.
(1) Olivia Lee, Hong Kong Observatory, Sept. 2010
(2) Lipkove, Cechak, Human Electromagnetic Emission in the ELF Band,Measurement Science Rev. vol. 5 sec. 2, 2005
(3) Ignativ et al., Fields in the Electromagnetic Spectrum Emitted From the Human Body..., J. Health, Medicine and Nursing, vol. 7, 2014
(4) Toohey RE, Keane AT, Rundo J. Measurement techniques for radium and the actinides in man at the Center for Human Radiobiology. Health Phys. 44(1):323–341; 1983.

Do the neural processes which produce electrical "noise", such as that detected by ECGs and EEGs, produce any EM radiation at all, or are they not coherent enough for that?

@Watercleave: The short answer is, only locally (doesn't radiate). See, for example, https://www.quora.com/At-what-distance-can-brain-waves-be-detected.

1-3eV light sounds like infra-red radiation (heat dissipation basically). Not sure about photons of visible part of the spectrum though. However, there is intrinsic fluorescence so that photons get emitted when tissue is being hit by photon of shorter wavelength

@aaaaaa: visible spectrum emission was news to me and was surprised that reliable measurements could even be made of energies this small (on a human--vs. some purely mechanical system).


text:
Why does deamination in the lagging strand lead to an increase in the relative number of guanine and thymine to cytosine and adenine?
My question arose from this article on Wikipedia on the GC-skew in bacterial genomes: https://en.wikipedia.org/wiki/GC_skew
As far as I understood, the lagging strand (the template strand), during replication, is more often single stranded than the leading strand (template), so it is more prone to mutations like deamination. Therefore, on the lagging strand (here, the one being the template to the strand formed by Okazaki fragments), one should expect more Ts and fewer Cs. Conversely, the strand synthesised by Okazaki fragments should have an enrichment of As and a depletion of Gs. Why does the Wikipedia article mention a increase in the ratio of (G+T)/(C+A)? I would expect an increase in the ratio of (T)/(C). I don't get the link with Gs and As.

Please cite as a quotation the actual sentence(s) that mentions the (G+T)/(C+A) ratio. I cannot find it and without it your question is unclear. The article you mention is very dense — I have not been able to understand it merely by skimming it — and the impression I get is that it is not mainstream, but represents opinion rather than fact. You may be unaware that anyone can write articles for Wikipedia — the only quality control is readers.) I think your question would be better as “What causes the GC skew between strands” and cite this article as one explanation (which you don’t understand).

I'm voting to close this question as off-topic because the purpose of this list is to answer questions about biology, not to clarify the reasoning of scientific authors. In this case rephrasing the question so that it is focused on the possible causes of GC skew would be valid but not one in which the answer is assumed in the question.

wikipedia article has it exactly wrong. For reasons beyond comprehension people responsible for this article refuse attempts to correct this very confusing error. Lagging strand, not the leading strand, has the excess of Gs and shortage of Cs.
I'll use the occasion to edit it again, let's see how long this edit stands.

You may or may not be right but your answer is inadequate here because it is merely an assertion without argument or external support. You are wasting your time just editing a Wikipedia article when your edit is reverted. You need to engage in a discussion notifying others of your intended change and your arguments for it and asking why it was previously reverted. If you fail to get agreement, then I believe there are adjudication procedures. As here, you may be e convinced you are right but you have to convince others.

I think you are referring to this sentence from your wikipedia link:

There is a richness of guanine over cytosine and thymine over adenine in the leading strand and vice versa for the lagging strand.

Note that this is not saying (G+T) > (C+A). It is instead saying (G)>(C) and (T)>(A). I think that those are not the same as saying (G+T) > (C+A), though that is also true, probably?
So I think that there is no contradiction there- it is just, as you say, more Ts (relative to expected equality with As) and fewer Cs (relative to expected equality with Gs).
If I understand correctly, the importance of the GC skew, and the reason that it is interesting, is that it acts as a deviation from Chargaff's parity rules (as explained in the article). These rules state that for any given hunk of DNA, (G)~(C) and (T)~(A), which is the expected composition for (for example) double-stranded DNA, because of base-pairing.
Edit: for more information on Chargaff's rules, see this other question which I have (through pure coincidence) answered here. Note that the second parity "rule" is a statistical phenomenon, rather than a logically required rule. The wikipedia page on Chargaff's rules is also informative.
Hope that helps.

I don't understand the second parity rule of Chargaff: 'In other words, in each DNA strand the frequency of occurrence of T is equal to A and the frequency of occurrence of G is equal to C because the substitution rate is presumably equal.' Why should the numbers of Cs and Gs be equal on one strand? "It is instead saying (G)>(C) and (T)>(A)." Is that true in a single strand? In the template strand of the lagging strand?

see edit to answer linking to answer to question about parity rule.

Both of Chargaff’s rules were based on observation rather than logic. Indeed, it was because he was unable to rationalize his first ‘rule’ that Watson and Crick got the Nobel Prize for the structure of DNA and not him. It is also the reason to regard these ‘rules’ as no more than history.

@David is correct about Chargaff making descriptive observations, as is also stated in the linked answer. I'm not sure that I understand why these rules should be purely regarded as history when they remain a highly accurate (though merely statistical) portrait of DNA composition. I think there are a lot of arguments about why that Nobel happened the way it did, I'm not sure that I agree with that characterization but going into it would be rather off-topic here.

but isn't the second parity rule of Chargaff broken in bacteria? How could he analyse the nucleotide composition of a single strand?

Let me put it differently. I dislike the word ‘rule’ in this context because it implies some fundamental understood physical ‘law‘, and I dislike the two being associated as they are distinct in time and importance. A better word would be ‘observations’. The first set of observations were made on a limited subset of genomes and were not understood until the double-helical nature of DNA was established. They then became history — observations that were now explicable. The second set of observations are distinct and obscure. Associating them with the first set as another ‘rule‘ is unjustified.

@David- I can agree with that interpretation of 'rule', hence scare quotes. I think that further work has come closer to putting the second 'rule' on the same footing as the first, but it is fairly unintuitive.

The second parity rule is still holding in bacteria, in that the frequency of complementary nucleotide on a strand are highly correlated. I would say that deviations from the rule are larger in bacteria, for a variety of reasons (including the increased prevalence of GC skew). Note that in strict terms (e.g. A nts == T nts on a strand) probably no genome exactly matches Chargaff's second rule, due to sampling error etc. The wikipedia page on the rules has a lot more information if you are interested. But as David said we are getting quite off-topic relative to original question.

The problem with Chargaff's so-called second rule is that almost nobody has heard of it (that included me, who's been around a long time) and almost nobody seems interested in it (it is barely mentioned in the literature). I suspect that there must be a trivial explanation for the observation, such as recombination randomizing the position and direction of genes, which is what you find if you compare different bacterial genomes. So ultimately I cannot see that any deviation from this 'second rule' to be either interesting or important.


text:
Negative Oxygen Consumption Rate
Oxygen consumption rate (OCR) is defined as the rate at which cells consume oxygen. I reason that for cells not capable of photosynthesis, OCR is strictly non-negative.
That was until I read this article which provides a graph with negative OCR values. Could someone enlighten me as to how this might be possible? If the cells are consuming no oxygen, I would expect OCR to be zero, not negative.

Scientific Paper:
http://www.pnas.org/content/108/33/13829.full

Start by asking if the zero in the scale actually zero, an arbitrary baseline, or a proxy measurement? in this case it appears to be a proxy so zero might not represent actual zero.

The diagram is not clear. They should write "change of oxygen consumption rate".
The caption of the diagram makes it clearer what they are describing:
" In A, a time course for measurement of oxygen consumption rate (OCR) and extracellular acidification rate (ECAR) is shown under basal conditions, [...] ".

So basically they are measuring oxygen consumption rate under basal conditions and apply some chemicals and depict the change in oxygen consumption rate in a diagram, given in percentage.

Hi there, thank you for your answer. Will your answer still hold if the OCR was measured in units of pmol/min? (i.e. moles of oxygen per unit time)


text:
what is the exact definition of entdothelial cell fenestrae?
In fact, I want to know that are fenestrae 1.holes which exist between cells or 2.they are holes in a cell( for example, a cell is like a paper we have punched it and the holes are called fenestrae). which one is true?

Fenestrae are basically holes within the cytoplasm of the squamous cell, that allow the transmission of macromolecules, therefore, according to the two options you've provided, your second example is the correct one.


text:
Recommended reading to quickly get up to speed on infectious diseases
I am in the beginning stages of a capstone project for my master's in Data Science. For various reasons, I have landed on the subject of Clostridium difficile infection. My background is in Computer Science, Mathematics, and Statistics, but biology is way outside of my wheelhouse. While most of my project will focus on the statistical modelling aspect, I would like to be able to speak intelligently on the subject itself and be able to read through journal articles without getting tripped up on some of the terminology.
I'm not trying to cut corners, but I'm on a tight timeline (about 4 months). What resources - books, references, online courses - would you recommend to bootstrap me into the field of infectious diseases?

Welcome to Biology.SE! Is it an intro book to epidemiology that you're looking for?

I think that could be helpful. Something to get me started with basic concepts or to use as a reference maybe.

Since I didn't get an answer, I'll mention what I did.
My goal was to understand a particular disease well enough to talk intelligently about it while focusing mostly on the statistics. So learning Epidemiology from the ground up wouldn't have been practical in the 4-5 months I had.
I started with a high level patient-oriented book, C. diff in 30 Minutes. That gave me a general understanding of the disease. Then I began reading academic articles. Not only were these useful for citations in my paper, but it also helped expand my understanding. I would notice common terms that kept popping up. Gram-positive, rod shaped, anaerobic, endospore-forming is intimidating at first, but each of these modifiers can be googled individually to build an understanding.
Finally, it was necessary to know how much I needed to know. I began reading about the hypervirulent strain, ribotype 027 with its binary toxin yadda yadda. None of that was actually important for my paper because that level of detail wasn't in the data.
So while knowing the general landscape was important, knowing each and every detail, for my purposes, wasn't.


text:
Do You Need Vitamin B12 To Utilize Folate
Just wondering if Vitamin B12 is necessary for the body to utitlize folate. My husband is on Methotrexate for rheumatoid arthritis, a medicine which is known to destroy folate. The doctors therefore prescribe high dose folic acid. He also, however, has a geographic tongue which is supposedly due to B12 defiency. If he is deficient in B12, and yet if B12 is necessary for folate absorption, the extra folic acid is presumably doing no good. Whether the two vitamins are essential co-factors is interesting to know because I've just read that folic acid deficiency gives people a 69% higher risk of heart disease. And he's just had a massive heart attack.
I can't seem to find the answer on standard search engines, would be grateful to know whether B12 is needed to utilize folate. Many thanks.

From Wikipedia: "In the form of a series of tetrahydrofolate (THF) compounds, folate derivatives are substrates in a number of single-carbon-transfer reactions, [...] It is a substrate for an important reaction that involves vitamin B12 and it is necessary for the synthesis of DNA, ...".

B12 deficiency is not the cause of benign migratory glossitis. It is the cause of pernicious anemia, though.

B12 is not necessary to utilize folate but it is necessary to replace B12 before repleting folate as otherwise you can induce subacute combined degeneration of the cord.  There are multiple mechanisms of folate absorption from the small bowel and large bowel which don't require B12.
Geographic tongue is not caused by B12 deficiency, and the actual cause is not known.  It does cause raw beef tongue.
You don't normally need to prescribe mega doses of folic acid with methotrexate.  Common doses are 5 mg per week, and 0.8 mg daily, though some physicians don't bother using folic acid at all.  Although folic acid was commonly prescribed because it was believed that methotrexate works by virtue of its ability to antagonize folic acid, it is now known that this is not true. It works as an adenosine antagonist, and so you can take the folic acid on the same day as the methotrexate if you wish.


text:
Why Goldman Equation cannot be used to calculate dynamic changes of membrane potential
I'm reading about Goldman Equation and I've seen in some resources that it calculates the resting potential (not membrane potential in general) and that this equation cannot be used when membrane potential is changing. One example is in Kandel textbook:

This equation applies only when Vm is not changing. Principles of Neural Science. Eric Kandel, Fifth edition. p. 135.

I don't really understand why this equation cannot apply when Vm is changing. Precisely, I understand that this equation defines how membrane potential changes taking into account permeability and concentration of ions. If you "give" to it the concentration-permeability changes for each moment, it'll show the Vm for each of these moments.
Could someone explain that to me?
Thank you very much!

What's the purpose of the Goldman equation?
I think that statement you posted from Kandel is a bit misleading, though not incorrect - I think he's just warning against a pitfall he's seen students make.
The Goldman Equation is an equation for steady-state voltage or in other words the reversal potential, not for Vm. It will only give you Vm in a (mostly) steady-state condition, like in the context of a resting membrane potential. However, that doesn't mean it isn't useful to calculate the Goldman equation voltage when Vm is changing or that it doesn't apply, but rather that it is not sufficient to use. It will still accurately tell you what the reversal potential is at any moment in time, but it can't tell you what Vm is at that moment.
How the Goldman equation can be helpful in understanding dynamic voltage changes:
Importantly, the rate of change of the voltage of the cell is going to be proportional to the difference between the reversal potential (from the Goldman equation) and the current voltage Vm, and after a long time the voltage will eventually asymptote to the Goldman voltage.
Therefore, if you know the current Vm, and you calculate the reversal potential with the Goldman equation, you can make some inference about what will happen to the voltage at the next moment in time: it will change in the direction of the reversal potential by a magnitude proportional to
Vm - Ereversal
Why the Goldman equation is not sufficient while Vm is changing:
I suspect what Kandel and others are warning about is that this isn't quite enough information to know what happens in the next moment of time:
It takes time to reach a steady voltage, and you need to know the membrane capacitance, which isn't represented in the Goldman equation, to know what the actual change in voltage is after $\delta$t, or how long it will take to reach a particular voltage.
Also, because of voltage-dependent conductances in a neuron, the permeabilities to different ions are also changing as a function of Vm, so the reversal potential is also changing constantly.
Furthermore, simulations of Vm sometimes need to consider the changing concentrations of individual ions, because the reversal potential will change as ion concentrations change. Therefore, it typically makes more sense to think about the driving force of individual ions given by the Nernst equation rather than the Goldman equation which gives you the net reversal potential across all ions.
Summary
In summary, authors that warn against using the Goldman equation when Vm is changing are reminding you that voltage changes take time and depend on membrane capacitance as well as changes in conductance from voltage-gated channels. However, the Goldman equation is still a correct way to calculate the instantaneous reversal potential at any moment in time (but not Vm), even if Vm is dynamic.
You could edit Kandel to say:

The Goldman equation only outputs the present Vm when Vm is not changing; also, when Vm is changing, the output of the Goldman equation is also changing due to changing conductances and ion concentrations.

..but you can see this is a bit verbose.

Thank you Bryan for your very complete response.
Do we have an equation that permits us calculate Vm when the cell is not at resting levels?

@Alexei You need to use differential equations, because the Vm will always be a function of itself as well as other parameters. There are lots of different ways to express these equations, you can find some of them here: http://www.cns.nyu.edu/~david/handouts/membrane.pdf In practice, though, changing voltage-dependent conductances mean that a lot of the quantities that seem to be constants in these equations are also functions of time and the other parameters, so in that context you need a model like the https://en.wikipedia.org/wiki/Hodgkin%E2%80%93Huxley_model

I've found this resource http://www.physiologyweb.com/lecture_notes/resting_membrane_potential/resting_membrane_potential_in_real_cells_multiple_ions_contribute_to_the_membrane_potential.html
Focusing in the text that refers to Figure 1, would you say that this part is wrong or, at least, not totally correct?
Reading this resource I thought I've understood the lesson, but your responses have made me see that it's no so easy :(

@Alexei Without going into it line by line, that figure seems fine, but what is important to realize is that this is a toy example showing you how relative permeabilities influence the membrane potential if one sets them magically in a model. It's really important to understand how this works, because it's an important building block to understanding the rest. Then, when you move on to real cells, it's important to recognize that the permeabilities are all changing dynamically because they are driven by physical channels rather than experimenter-set variables.

Then I understand that de GHK equation can serve as an introduction to the "picture" but isn't the whole picture at all. Thank you Bryan for your kind responses :) You've been very helpful.

@Alexei Glad to help. If this answer was useful it's appropriate to vote it up; if you think this answer fit everything you needed then it's appropriate to accept it, otherwise the community bot will keep bumping the question occasionally, assuming it doesn't have an answer yet.

Nicely answered