text:
How did Mendel know if a plant was a homozygous tall (TT), or a heterozygous tall (Tt)?
I had some issues while studying Mendel’s rules of inheritance.
How did Mendel, while running his test crosses, know if the plants in his F0 generation were TT (homozygous tall) or Tt (heterozygous tall)?
There seems no way to differentiate between them, and I do not know of any sophisticated tools which may do so, but surely they were not available to him?
There may be some flaws in my logic, as I am a beginner, but I am not able to find any sources which tackle this problem.
I am familiar with the basics of inheritance.

Pea plants naturally self-fertilize. So a pea plant that hasn't been manipulated will be "true breeding" that is, homozygous for the allele in question. You can therefore tell after you've let them self-fertilize.
Homozygous individuals have identical offspring for the trait when selfed, whereas selfing heterozygotes have a quarter of their offspring looking different for the trait.
In other words, you can't tell in the present generation who is heterozygous without molecular methods unavailable to Mendel. But if you are willing to self the individuals, save seeds, plant them, and track where they came from, you can figure out who was heterozygous/homozygous in the last generation.

So, does that mean that heterozygous pea plants (Tt) do not exist naturally? Again, I may be wrong.

Not for long.  Only half of the offspring of a heterogeneous organism will be heterozygotes if they self.

@swbarnes2 Heterogeneous plants will rapidly disappear when self-fertilization is the only reproductive path.  Crosses can happen in nature, though.


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Is it possible to live without iodine? (sea plants, seaweed or fish?)
I’ve come across a few other people asking this question on different forums such as on Quora, and Reddit…
With my current understanding, we evolved from sea creatures which is why we still need iodine in our system.
The RDA is 150 mcg, 220 for pregnant women.
Isn’t this amount of iodine something a person can get merely from sea plants and sea animals?
Do land animals need such a high amount of iodine as well, and are a majority of them iodine deficient? Unless there is some way for them to get iodine from land plants. Or are we supposed to eat iodine rich soil?
If sea plants and sea animals are a required for proper iodine RDA, this implies that they should be staple foods within our diets.
Sorry for all the questions.

Thyroid Hormone is needed by nearly every cell in our bodies, and without it, we would die. And, as @David said, Iodine is an integral part of the hormone. As a requirement for vertebrates, it is also found in vertebrates (whose products and flesh we consume) as well as in their diets. The majority of vertebrates today are not iodine deficient, but in the past, humans were moreso than they are today.

saying sorry does get around the one question per post policy, I suggest looking up the goiter line to get a lot of answers at once. Iodine is only limited in specific environments.

@John I lean towards a mostly vegan diet. So it interests me that unless a vegan eats seaweed, supposedly they aren’t getting enough iodine. But I can only assume that realistically if an environment has soil that is rich in iodine then sea plants wouldn’t be a requirement.

that's a problem with a vegan diet, IE without and meat, dairy or eggs. non-sea plants in general are low in iodine. most animals including most herbivores get them from the same places we do eating animals or eggs.. Or they are bulk plant feeders and make up for it with sheer volume and eating plants that would be toxic to us. keep in mind a 100lb deer will eat almost 10lb of vegetation a day plus the occasional bird or egg.

Iodine is a component of the thyroid hormones, thyroxine and triiodothyronine, so it is indeed a human nutritional requirement.
According to this Harvard University webpage, milk (especially), eggs and other dairy products are sources of iodine, as well as fish, mentioned by the original poster. In addition, in advanced countries iodine is added to table salt to help combat iodine deficiency.
Although iodine is also added to the diet of dairy cows, I have read that iodine is also present in their natural food. Iodine enters the soil from marine spray in coastal areas, and from rainfall further inland, and is retained by metals in the soil. It can therefore be taken up by plants. However I do not know which plants that would constitute a natural bovine diet are particularly rich in iodine or why that would be so.

I am not so sure that the cows that are being eaten regularly see any of their "natural food" ever, as they are not maintained on grass.

@CaroZ — It's their milk. You have to approach these things from a historical viewpoint — when dairy farming emerged originally the cattle would certainly have been maintained on grass. As for the contemporary situation in factory farms, iodine is actually added to animal feed, so supermarket milk in Britain and the US is, in fact, a good source of iodine.

Thanks for the answer! I lean towards a mostly vegan diet. So it interests me that unless a vegan eats seaweed, supposedly they aren’t getting enough iodine. But I can only assume that realistically if an environment has soil that is rich in iodine then sea plants wouldn’t be a requirement.

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text:
Initial population when I count backwards?
My question deals with the number of ancestors it took to produce me:

--> To produce me, it took 2 people (my parents) = ($2^1$) people = 2
--> One generation further included = ($2^1 + 2^2$) people = 6
--> In the past 500 years, my pedigree chart contains 15 generations, so $2^{16}$ people = 65.532 people to produce me (-2 to be completely correct)
--> When I calculate back to 35.000 year ago I get a larger number *)
--> When I calculate to all humans 2.400.000 ago I get a ridiculous large number *)
--> When I include up to all mammal grandfathers and grandmothers 60.000.000 years ago the total number takes pages to scroll *)

*) see: http://ed.je/2L6 for the actual numbers did not want to clutter here.
*) I took 3 generations per 100 years to let the numbers be small as possible.
So, I think I'm making a mistake somewhere. Only I don't know where: to create a child you need 2 parents. And to create a parent you need 2 further parents. But somehow calculating back to "all mammals" just related directly to me would mean $2^{1.800.001}$ mammals walking around 60 millions years ago being my direct predecessor back then.
So, where am I going wrong? Somehow, I can't figure out where my error lies (I've not studied Biology though).
I visualize a pedigree tree (reverse pyramid) starting with me and then logically each parent needs to be born out of 2 other parents just calculating my way up.

Your calculations are the following. Assuming non-overlapping generations, the number of ancestors you have in the last $t$ generation is given by:
$$\sum_{i=1}^t 2^t$$
This sounds correct. But there are some very strong assumptions:

Generations are non-overlapping. A more realistic model would need to consider $t$ as a continuous variable a give a probability of reproducing which depend on the age of the individual.
Never two related individuals mate together. Otherwise, you paternal grandfather might be your maternal grandfather. In reality we are all somehow related, we have a common ancestor (Hey Bro). For example if you consider that your parents are siblings and that their parents are siblings and so forth… then you don't need more than 2 great-great-great-great-grandparents. In order to keep track of such events (inbreeding), you need a stochastic model and you would need to know the population size $N(t)$ as a function of $t$.

Tracking the change of population size through time is part of a very big in biology which is called population biology. For example you will find in this post a model of population growth of two interacting species (prey-predator)

so the amount of non unique nodes in my pedigree chart will be this ridiculous large number. but the unique nodes will be less? (as the one i see in www.geni.com containing 65.532 people in 15 generations?)

@edelwater I didn't fully get your comment. What is (non-)unique node? Given that you checked the answer, I hope it means that you understood and agreed with my point Let me know if it is not the case.

if I draw a pedigree tree (genealogy) then i make a pyramid filling in the names of the grandparent etc... so each node in the tree is a uhm node. At some stage (probably longer than 500 years ago) some nodes will contain the same persons (or even mammels) as other nodes. So they are non unique nodes (and would have to draw a dotted line between the nodes). (while another representation would be a graph family tree where each unique individual occupies only one node).

thanks will dive more in population biology to make a follow-up. Will check population size as factor and other facors. Must have huge impact on the 2^1.800.001 direct forefathers I now have. Probably boils down to "the complete population" at a certain moment back in time.

@edelwater Ok, I understand the meaning of non-unique node. As I said, in order to compare the relative number of unique and non-unique nodes you need to know the population size. For example, if your population size is 2, then you are sure that you paternal grandparents are the same than your maternal grandparents. If the population size is very high, then you paternal grandmother is probably not the same person as your maternal grandfather. And if you want to assume different sexes, you will also need the sex-ratio

An easy way to visualize the mistake in your thought experiment is to consider a bottleneck event, when the ancestral population was very small, maybe just a few individuals. This would mean that the entire current population is descending from just a few individuals. Your thought experiment is assuming that the "pyramid" of your ancentors is expanding all the time, while the bottleneck event will essentially result in the opposite situation with an inversion of the pyramid, such as:
Your assumption:            Bottleneck:

 xx xx xx xx                     x
   xx xx                        x x
    x x                        xx xx
     x                      xx xx xx xx
           (present time)

The reason why the number of ancestors is smaller in the bottleneck event is naturally that the population is inbred (all individuals are related). In contrast, your thought experiment is assuming that all individuals forming the pyramid of your ancestors have completely unrelated ancestry. This is equivalent to assuming that the subpyramids for all ancestors never overlap.
Your assumption is unreasonable since human generations are overlapping, the fecundity distribution of individuals is skewed, inbreeding is common and reproduction between more distantly related individuals will happen by pure chance. We also know that humans have historically gone through several population bottlenecks, see e.g. Hawks et al. (2000) and Lui et al. (2006) for an overview. An realistic model of your ancestry is more likely to be (highly idealized and compacted):
       x
      x x
     xx xx
  xx xx xx xx
  xx xx xx xx
     xx xx
      x x
       x
     (you)

The issue we are discussing here is actually known as pedigree collapse, where you will eventually find overlap between your ancestors, which will mean that the pedigree collapses instead of growing exponentially.
Beside historical bottlenecks, there are also modern examples of extreme human inbreeding. Even if this is not directly related to your thought experiment, you might for instance want to look the pedigree of the Habsburg royal family. Here is the genealogy of Charles II - remember, narrow loops in pedigrees are seldom a good idea:

Here you can for instance see that Charles' father is also the uncle of his own wife. You can also see that only 5 persons enter in the family tree from the outside through marriages, which means that Charles only had 7 completely independent ancestors (ignoring relationships further back, outside of this tree). Going back 3 generations (sort of - hard to count with overlap), it is also apparent that Charles had a total of 8 ancestors instead of the 14 expected under your model. Another modern example of extreme human inbreeding is the Fundamentalist Church of Jesus Christ of Latter-Day Saints, where marriages between close relatives have been common along with high levels of rare birth defects. Both these examples definately show, in an extreme way, that you cannot assume that all your ancestors are unrelated.

Thanks, very interesting esp also the pedigree collapse. ALSO a great example since I'm in 19 steps related to Charles II of Spain :) (then again we are all related) : http://www.geni.com/path/Edward+de+Leau+is+related+to+Carlos+II+el+Hechizado+de+Habsburgo+rey+de+Espa%C3%B1a?from=6000000000569063853&to=6000000000840743803

Glad you found it useful, and cool that you have a Charles II connection  - hopefully with fewer loops in your part of the family tree thought ;)

Another way to demonstrate that the underlying reasoning in the calculation is not correct is to project into the future.
Given the assumptions, the approximately 7 billion people on Earth today could only produce 3.5 billion people (two parents per offspring). Projecting forward, after approximately 32 generations, there would be just one human in the world.
However, we know this is not accurate because a woman can have more than one offspring.

10 years later...

In addition: if you do not take into account uniqueness (of both individual and "2 individuals + unique child as unique) and draw a reverse pyramid starting from yourself it comes closer. But in that reverse pyramid the further you go upwards the more "patterns" you see of identical structures that you could replace with 1  reference block instead. This would however form the numbers above (if not unique). So if you would draw a genealogie tree of individuals but in that tree an individual can be represented more than once (e.g. by reference in the comments) then its a pyramid.

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What is the fundamental reason for death from too high or low internal temperature?
I have read something about why we die from too high or too low body temperature but have always found only general reasons. For example, that the liver fails. But why does the liver fail?
I would like to know the most fundamental reason why not possessing the appropriate body temperature can kill us. Ignoring the very extremes where it is I think obvious, such as temperatures below 0°C and above 100°C when water freezes and vaporizes.
I have supplied my reasonings below; if any reasoning here is wrong, please correct my thoughts.
As far as I understand, as the temperature changes, the speed of chemical reactions changes as well. As temperature goes up, the reactions occur faster and if the temperature decreases, the reactions slow down. So, if our body temperature changes, the speed of all reactions in our body change as well. Thus, with higher internal temperature we should just become more active, speedy and so, and with low temperature we should become slower. But that does not fit into the fact that we die from extremely high internal temperatures. So, is it that the speed of different reactions change with different rates, so the organism is not kept "in sync" and dies for that reason?
Or - as temperature changes, the volume of everything changes as well. I think that's called thermal expansion. But different materials have different rates of that process. So as our temperature changes, something inside us just literally breaks or deforms too much and we die?
So why do we (and other organisms) die from not having the right temperature?

Half of your question is answered here: https://biology.stackexchange.com/questions/36258/why-do-low-temperatures-kill?rq=1

Please be more specific about your question. SE is not a place for open discussion.

As mentioned in the comments, half of your question is answered elsewhere. Generally you are right, different processes change at different rates. Blood viscosity changes. Some complex systems, such as the heart, may completely fail to function. The other half of your question has a simpler answer. As heat increases, yes in theory so should enzyme performance. However enzymes have a tendency to denature if they get too hot. When heat is excessive, heat shock proteins are released which are naturally stable in hot conditions and which attempt to stabilize other proteins. This is only possible up to a limited extent, and sufficient heat will cause proteins to become entirely non-functional.

Does the downvoter care to explain what was the issue with this answer?

I am not the downvoter, but I would guess the downvote was for a lack of sources.


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Is continuous exposure to blue light lethal for mosquito larvae?
I have been observing developing mosquito larvae since 2 days and I saw, while exposing my laser light of blue colour to it, that it becomes unstable on exposure to blue light.
Thus, I wish to ask, will it die or whether it is fine? It has been one day since I shone the light on it, so please tell me: will it grow further or not?

There are lots of relevant results from Google Search for "blue light mosquito larvae". Here is just one of them:
https://www.nature.com/articles/s41598-022-14096-y
They are not all only mosquito related either, such as this one for insects in general:
https://www.nature.com/articles/srep07383
Or you could just find out for yourself. You are already set up for it. All you need is a control group, and preferably a third group that is exposed to high intensity laser light of a significantly different wavelength such as red or green in order to determine if it is just the intensity of the light or the wavelength.


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If race doesn’t exist; why do humans look so different?
I was talking about a speculative new race of humans that could be created with genetic engineering and several people told me that race does not exist and is a social construct. I get what they are saying but I also read many times over the years that different groups of humans all have slight genetic differences even though we are all the same species. Racism in the world usually relies on aesthetic traits, e.g. different skin color, facial features, hair. Those things seem trivial, but I would think that phenotypes would definitely be a big thing in our genomes. Therefore, why cannot race exist?
Also, while applying for jobs, hirers always ask for my ethnic background. The options are White/Caucasian, Black, Hispanic, Asian, Hawaiian, and Indigenous American or Alaska Native. First off, I think not separating Pacific Islanders with East Asian and South Asian is a big mistake. There is a huge difference in Asian and Indian culture, and I think they should have their own box. The same goes for Middle Eastern or Arabic, as I feel their culture is significantly unique as well.
Lastly, isn’t Hawaiian an ethnic background and determinate by geographical location not genetics?
This post is totally open-minded, and I have ZERO beliefs that any “race” is superior.

This here states that there is more variation within a "race" than there are between two different races. https://scienceandsociety.duke.edu/does-race-exist/ I'm guessing what it is referring to is that what we can see is only a very small contributor to the overall genetic variation. But what is specifically referred to in the article is there is a gradual spectrum between every "race" based on geographical proximity rather than clear delineations.  Sort of like colours. We say red and green are separate colours in regular speak, but if you look they are not distinct groupings.

It's not that race cannot exist theoretically, it's that is doesn't exist empirically among the lines drawn for humans as a socially-imposed phenotypic construct. In non-human animals and plants we might refer to "subspecies" as biologically legitimate groupings.

what makes you think a unique culture would be genetic and not say a unique combination of environment and history. Also cultures are not as different as you think, agricultural cultures are very similar compared to everything out there.

I think your friends are misunderstanding social constructionism and race theory. Countries are social constructs, but that doesn't mean that Italy doesn't exist. Money is a social construct, but good luck telling your landlord that it doesn't exist. Also, most US employers follow the federal government's five categories for data on race, so the one should read "Pacific islanders or Native Hawaiian." White and Asian folks living in Hawaii mostly know not to refer to themselves as Hawaiian in any context, even if they were born there and spent their whole lives there.

Definitions of race as we normally use it varies greatly from culture to culture, ones based on actual Biology don't match our preconceived ideas.
You could break humans into races, but if you do based on any kind of biological grounds, it can't be by the superficial things we traditionally use.
The biggest problem with race is if you split humans into races, everything 'not an African native' is one race. Or hundreds of native African races before the Norse and the Mayan are not the same race.
Almost all of human genetic diversity is inside Africa and that is for a species that has very little genetic diversity. one subspecies of chimp has more genetic diversity than all of humanity. A Norwegian native and an Australian native are more similar genetically than the Berber and Bantu two different native African lineages.
Source
On top of that there is more diversity within populations than between them because of how low the genetic diversity is. Only around 6% of human genetic diversity falls along classical racial lines, meaning they are superficial differences not representative of deep relationships. Humans almost went extinct at one point, and we are all the descendants of likely less than a thousand survivors, so we are all super related. and most of our differences are small changes since that point.

Skin color is useless, since it is a superficial adaptation to latitude. Native skin color correlates really well with yearly UV levels, and the adaptation happens fairly fast. thanks to 'Cheddar Man' we know the British people of 10000 years ago had black skin.
Skin Colour:

UV levels:

John's answer is the correct one about race, and this answer makes no attempt to address the biology.
However, to address why you only get those options in you questionnaires, it is because you are apparently in, or applying for jobs in, the USA, as that is really the only country that might be interested in Alaskan Natives  and Hawaiians.
There are reasons beyond race for such questions.
These groups are the ones specifically addressed in the law that was passed by executive order on the 25th of June 2021 in the USA, and are also ones included in things like Census questionnaires. You can read the full text of the executive order here. The order is titled

Executive Order on Diversity, Equity, Inclusion, and Accessibility in the Federal Workforce

and begins:

By the authority vested in me as President by the Constitution and the laws of the United States of America, including sections 1104, 3301, and 3302 of title 5, United States Code, and in order to strengthen the Federal workforce by promoting diversity, equity, inclusion, and accessibility, it is hereby ordered as follows:

The definitions section mentions the groups (note the similarity to your list), including whole groups whom you definitely couldn't term races. You should also note the wording - it specifically does not ask about race, rather about communities (emphasis in quote is mine), so this isn't a "race" driven question you are seeing in your applications, as you noted, but perhaps not realized, when you inquired about Hawaiian in the question:

In the context of the Federal workforce, this term includes individuals who belong to communities of color, such as Black and African American, Hispanic and Latino, Native American, Alaska Native and Indigenous, Asian American, Native Hawaiian and Pacific Islander, Middle Eastern, and North African persons. It also includes individuals who belong to communities that face discrimination based on sex, sexual orientation, and gender identity (including lesbian, gay, bisexual, transgender, queer, gender non-conforming, and non-binary (LGBTQ+) persons); persons who face discrimination based on pregnancy or pregnancy-related conditions; parents; and caregivers.  It also includes individuals who belong to communities that face discrimination based on their religion or disability; first-generation professionals or first-generation college students; individuals with limited English proficiency; immigrants; individuals who belong to communities that may face employment barriers based on older age or former incarceration; persons who live in rural areas; veterans and military spouses; and persons otherwise adversely affected by persistent poverty, discrimination, or inequality. Individuals may belong to more than one underserved community and face intersecting barriers.

Now, I am aware that this is titled for the "Federal Workplace" meaning that you might think it only applies to those organizations that are federal. In fact, I believe that this would apply to any organization that has federal funding, which includes a huge range of organizations, any of whom can get federal grants - all would need to comply with this law. This includes private businesses, research organizations, hospitals, charities; in fact just about any employer you can think of.

These categories were absolutely not laid out in an executive order in 2021

@BryanKrause See the large quote in the middle and reproduced here: Black and African American, Hispanic and Latino, Native American, Alaska Native and Indigenous, Asian American, Native Hawaiian and Pacific Islander, Middle Eastern, and North African persons That's pretty similar to the list in the question. The link provided is even whitehouse.gov...

These are standard US census categories.

@BryanKrause Yes, but they wouldn't be asked about in job questionnaires if there wasn't someone looking for them and having to fill diversity measures. The point of my answer (and perhaps I should make this more clear in there) that there are reasons besides race for asking these questions.'

@BryanKrause edited. I was unable to find any other law that specifically addressed these categories; even the civil rights laws don't go into them. By fill on my previous comment, I meant fill out as in report, not to imply that diversity needed to meet a quota of some sort, as the comment could be read.

Laws are rarely written that way. One law says you can't discriminate based on race; somewhere in administrative code they categorize race for some other purpose; someone collects information based on that definition to show they're in compliance with the law because they know it's something they can defend in court by pointing to the government document.

Also, Federal employees are only US Federal Government employees. Contractors aren't federal employees; my salary is paid by a federal grant but I'm a state employee in the state that my university is in, etc. This is all quite off-topic for Biology and perhaps belongs in Politics.

Let us continue this discussion in chat.


text:
Visual Quality Indicators for Soil and Plants
I would like to know what are the visual indicators that can be used to determining the quality of the soil and plants by looking at the in-situ photos?
Can the following quality indicators be determined by visual check such that a decision making can be done?

Approximate Soil Salinity
Soil pH
Soil Moisture
Soil Content (red indicates presence of iron etc)

For Plants

Presence of weeds
Presence of bug infestation (perhaps different visual patterns to
identify kind of infestation)
Plant Health (rigid looking vs hanging etc)

The above is whats there in the top of my head, can this list be expanded and upto what degree the quality indicators can be relied upon?

Note: Soil salinity might not be easily determined if the excess salt doesn't precipitate (visible white layer on the soil can help determine the excess of salt hence its not a good visual quality indicator for most of the time.

The type of plants, and their health helps decide what the soil is like, and whether overgrazing has occurred. Sorry no refs yet

@PolypipeWrangler Good point. But perhaps when we plant a seed, we might not have a visual evidence from the plant itself so a visual inspection of soil itself might be required. I am looking to see if algorithms for computer vision could be extended to assist and encourage planting.

There are numerous visual indicators for various type of plants that determine plant health. For example the rigidity of the leaves can help you determine that enough water is supplied to the plant (1). Now you can also determine the leaf shape and detect for presence of disease (2), pests (3), and plant health in general (4). This research however mentions no correlation between lamina shape and area so you would need wiser methods for your corrlelation methodology(5). Moreover, you can look at the fruit shape/sizes to determine if plants have been supplied enough nutrients(6). Another study which is worth mentioning is using chlorophyl to determine plant fitness but this cant be done insitu and you would need lab analysis (7)
All these are visual indicators for the plants itself. As far as soil is concerned is it more challenging because you can make soil and compost using various materials and methods so there is no general approach that can be used to determine the quality. So if soils is your primary concern then as @PolypipeWrangler mentioned looking at the plant fitness can help you determine soil quality.


text:
What percentage of the brain is memory | Storage of thoughts, episodes
I was reading the article, in which it is mentioned that human brain constitutes 2.5 petabytes of memory. This made me wonder how much of the brain is associated with memory itself. If we categorize brain by functionality, such as dedicated areas for visual processing, audible processing, logic processing, memory storage etc, what percentage of the brain is utilized for memory itself?
I speculate that the brain does more memory related tasks then any other. As a matter of fact, almost all tasks for humans requires memory, so perhaps 70-80% of brain might be just to store memory. Is this correct? If not then what percentage of the brain is used for storing memories?

All of it depending on how you define memory.

@John could you please elaborate. Memory is defined as "storage" of any abstract object such as past events, thoughts, dreams ..etc

everything you brain does is memory, learning how to interpret sense organ signals, muscle movement, etc is all memory.

@John, what about reasoning, cognition, they do indeed differ from memory, althought they utilize memory but I believe the part of the brain that deals with reasoning, cognition, emotions, are not memory themselves.

They are all memory, they learn patterns.

@John its quite hard for me to reason that how is cognition and emotion are memories. Cognition is related to attention and learning endavour, which utilizes memories to keep track of the learned stuff but how come they themselves are memories?

they are learned skills, thus memories. even emotions are plastic meaning their associations can be altered by learning.

@John alright i understood your point after reading the answer below :) so overtime memory shapes the 'function' that gives rises to emotion and it changes. So this function itself is plastic in nature. I somehow wanted to separate these so-called learned functions from 'data' and determine how much is function and how much is data so a function would be the brains 'capability' to recognize, and data is the specific object itself. So function is more or less genetically motivated "someone likes blue color while someone else likes red...". I wish I could have framed my question properly.

It's difficult to say a number because memory and activity are intermixed. Activity induces long-term modifications in the brain wiring which can be considered as memory, but at the same time, those connections play functional roles.
For example, in the retina, the codification of the visual stimuli that are going to be transmitted to the brain is done by a network wiring that is somehow shaped by previous activity.
At an ontogenic level, we could think that the brain architecture in any specie is shaped by a phylogenetic memory during evolution.
Because of that, I'm tempted to respond 100%, but no rigorous answer can be done as far as I know.

This is the answer I was looking for but I still need some clarification. I am interested in the reference for the codification of the visual stimuli that are going to be transmitted to the brain is done by a network wiring that is somehow shaped by previous activity Now I really want to separate out the evolutionary part from functionality part, the functionality of our brain is indeed encoded by external stimuli over the course of the evolution but "given the current state" of the encoded brain,  is there anyway to know how much of the brain is memory and how much function?

So for an analogy we can use evalutionary algorithms to shape hidden layers of artificial neural network, once we reach a satisfactory state, we get a function that although has been shaped by evolutionary algorithm (which relies on memory), is still a function and not memory, when this function is later used to train on some data, say image recognition, we acquire weights and biases which can be considered as memory as weights and biases may differ if one has to recognize certain person or a cat.

@gfdsal There is no difference between the memory and function. Memory is held in the synaptic weights in the connections between neurons; nervous system function involves patterns of activity which in turns are governed by those same weights.

@BryanKrause makes so much sense. Is there any mathematical model or even a general model of this. I want to see how exactly "pattern of activity" simulate a function and why our NN computational models are so bad and less robust against computational model of brain.

@gfdsal Neural networks and brains optimize completely different things, because things that are "easy" for biology to do are really hard to do in simulation, and some computations are really easy to do in silico but very expensive in real brains (for example, the distance between nodes matters in brains, it doesn't matter to any appreciable degree in silico). An adult human has almost 100 billion neurons each making thousands of synapses and trained over somewhere between 18 and 100 years.

@BryanKrause Do we know what exactly are these so-called things that brains optimize? Is there any model of such object. All I learned is that these synapse aggregate in similar fashion as neural nets, you are right that distance in hardware in silicon doesnt matter but we do utilize the notion of distance (more precisely inner product /norm) in the computational model which simulates the nearness of the entities/object being learn just like in the brain...so functionality is mimicked by computational model itself.

@gfdsal This is where I would stop and give the advice I have given numerous people trying to understand relationships between biological and artifical neural networks who are coming from the artificial side...If you want to compare them meaningfully, you need to be an expert in both. So, instead of starting with neural nets and looking for comparisons in biology, you need to start from the ground up in the biology and start learning the biology for its own sake. Then you can start to compare.

@BryanKrause acknowledge. Thanks for the advice.


text:
How reward / penalty is comprehended?
Technically brain is composed of billions of neurons for abstract computation of the world around us. I am bit confused that how does emotions such as fear/anger gets simulated by amygdala, which is nothing more then bunch of specialized neurons but we feel it as penalty. What part of the brain senses response from amygdala and determines ok, thats fear/penalty? What exactly is penalty?
How does human comprehend reward and penalty (fear/anger/sorrow)?

you might get a better response here https://psychology.stackexchange.com/

@user438383 but I am looking for associative answer, so psychology will only provide higher lever behavioral response instead of lower level response based on synaptic aggregation

The site is Psych & Neuroscience, not just psych, but the question you are asking doesn't have great neuroscientific/biological answers. I'd situate it as part of the "hard problem" of consciousness. There are several relevant Q&As at psych & neuro.

@BryanKrause I see, i thought there might be tangible answer for example, "fear causes incoherent/abnormal synaptic actuation patterns, which is anomaly and we sense anomaly as negative" just a speculation.  Well this also makes me hypothesize that signals firing that are coherent could be sensed as positivity/reward, we associate beauty with say symmetry face so signals are quite coherent when you experience symmetric face and we associate that to positive/reward. Again just a far fetched speculation.

@gfdsal There is no reason that "abnormal" or "coherent" patterns of activity are "good" or "bad" any more than activity in a particular brain area. If your speculations were true you'd still be left with the exact same question.

@BryanKrause allright makes sense, I just made a speculation based on lie detector test, where if one lies the body responses are different from nominal in-other words "abnormal"

@gfdsal Lie detector tests are pretty poor, but they work on the principle that people are more nervous when they lie, which increases their skin conductivity as they produce sweat. Not really an abnormal response, but a completely normal one in response to stress. One of the reasons they are so poor is because indeed, answering questions in a scary environment can also make people nervous.


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Parts of Brain Active for Dreams | Right Hemisphere or Cortex
I found a research that states cortex is responsible for the contents of the dream. Contents could be people, place, objects etc.

The cortex is responsible for the content of dreams, including the monsters we flee from, the people we meet, or the experience of flying. Since we are highly visual animals the visual cortex, right at the back of the brain, is especially active, but so are many other parts of the cortex.

While the other says right hemisphere is responsible  to create the dream.

The right hemisphere of the brain actually creates and displays the dream

And another source

the dream contents have their source in memories and impressions stored within the right half of the brain.

While there is another research that states posterior cortical hot zone that are responsible for our dreams.
Question: So what part of the brain is it? I know a coordination of various parts of the brain makes dreams possible but what part of the brain is responsible for main contents of the dream or major contributor to the dream?

Search this on google scholar- you will get a well sourced answer. Three of your sources are unreliable.


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Why is half dose of Oxford's vaccine of covid more effective than full dose?
I recently read in a newspaper that the half dose of the Oxford's vaccine is 90% effective while the full dose is only 62% effective.
Why is this the case ?

The true answer is nobody knows yet - even the developers of the vaccine have admitted they don't know the true reason yet. It may be the case that it is a statistical artifact of a reduced sample size in the group which was given the half dose. Either way, we need to wait at least until the paper is out until proper judgement can be made.

These explanations in nature magazine are very, very vague: https://www.nature.com/articles/d41586-020-03326-w If it's not an artefact of statistics, they say it could be because the larger dose caused the body to attack the associated adenovirus complex on which the vaccine is delivered into the body and blunt the immune reaction to the covid-19 complex,

There are also very recent news articles about manufacturing errors causing the wrong dosage, e.g. https://www.bloomberg.com/news/articles/2020-11-26/astra-faces-more-vaccine-questions-after-manufacturing-error  So perhaps the vials marked "half dose" were really full doses?  So the "answer" is that nobody knows yet.


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Is covid vaccine helpful for a covid patient?
I am not a biology student and this question came in my mind out of nowhere.
I read somewhere that the vaccines contain some denatured or almost dead corona viruses and when these are injected in our body , our immune system remembers them and if the actual (killer) corona virus enters our body , our body recognises it and quickly attacks it.
But if we have a  corona patient his body has already identified the corona virus and so if the vaccine is given the body will not have much changes to do and simply refuses it .
So is it okay to give the covid vaccines to a covid patient ? Can it make the infection even worse ?

This is a site about specific problems in biology, not one for general medical questions. Your question may be acceptable on SE Medical Sciences, but I regard it as off-topic here.

In short, no. It's not harmful but it won't do anything to prevent or mitigate the current infection.
How vaccines work in general is that they train the immune system to respond to an infection so that they are prepared for it. Generally protein component of the virus or an inactivated form of the pathogen is used as a vaccine. The immune system recognises the proteins as 'foreign' and develops anti-bodies to fight them. Then you are immunised to the virus without having to suffer the symptoms of infection. Vaccines work before you are infected as a preventative measure. Then when you are infected, the immune system is prepared and can fight of the virus with the antibodies already developed since the virus has the same "antigen" proteins as you immune cells have already been exposed to from the vaccine.
So what happens when you are vaccinated when you are already infected? Basically nothing.
The benefit of a vaccine is a head-start to train your immune system how to fight it to prepare for the early stages of infection. If you are vaccinated, your immune system will destroy the virus before the it multiplies or gives you symptoms. If you've already been infected then the active virus has already infected many of your cells and multiplied into many copies. Adding inactivated viral particles or spike protein antigen won't help your immune system, it's already been exposed to them by the ongoing infection. Your immune cells are just playing catch up to the infection that's already taken hold. The virus has already stormed the beaches and the immune cells were not prepared. Vaccination now is arguably pointless. They will eventually produce antibodies against the virus already in your system even if you weren't vaccinated.
Lasting immunity after recovering from infection is not guaranteed and a vaccine could give immunity to other strains. For these reasons, it could still be recommended by medical professionals if you've already been infected. However, you need to be vaccinated before exposure to the virus for it to be effective. A vaccine is not a treatment.
Note: the currently available AstraZeneca, Pfizer, Moderna, and Johnson & Johnson vaccines for SARS-CoV-2 do not contain live or inactivated coronavirus. They trick the host system into producing the spike protein from instructions carried by the vaccine.
Citation for clinical application: Jenner, E (1798) An Inquiry into the Causes and Effects of the Variolae Vaccinae.


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Is it true that recanalisation of the vas deferens, if any, tends to happen soon after a vasectomy (less than 1 year), and if so, why?
https://doi.org/10.1016/s0140-6736(00)02436-3 "How reliable is a vasectomy? Long-term follow-up of vasectomised men":

Most episodes of recanalisation are believed to happen soon
after vasectomy, and the pregnancy rate after vasectomy is
about 1 in 2000. Delayed recanalisation after the first year is
uncommon, only isolated cases are reported and its true
frequency is unknown.

https://www.medicalnewstoday.com/articles/326737#vasectomy-reversal:

Most cases of recanalization happen within 12 weeks of the procedure.

Is it true that recanalisation of the vas deferens, if any, tends to happen soon after a vasectomy (less than 1 year), and if so, why?

This is a medical rather than a biological question as it relates to a surgical procedure. Try SE Medical Sciences.

@David Thanks, the recanalisation process is biological.

But your question does not ask about the biology of the process, but asks if it is true that it happens a specific time after a surgical procedure. It's up to you, but if I wanted an answer to a question like this I know where the most likely place to get an answer is.

Is it true that recanalisation of the vas deferens, if any, tends to happen soon after a vasectomy

Yes. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7175481/:

Studies have shown that early recanalization usually occurs between 2 and 6 weeks post-vasectomy [9, 10].
Early failure, defined as a postoperative semen analysis showing persistent motile sperm, occurs in 1 in every 250 patients [6].
Late failure, defined as the rejoining of the severed ends of the vas deferens, occurs in 1 in every 2000 patients.

Note that the same article reports of a case of paternity that occurred seven years after a negative post-vasectomy semen analysis, which means that  recanalization can happen many years after a vasectomy, even though the odds are very low (<0.05% after 1 year).
Also, the risk of recanalization may depend on how the vasectomy was performed. For example, see:

How does the length of the vas deferens excised during vasectomy impact the risk of recanalization after a vasectomy?
Does the risk of recanalization increase if a person chooses an open-ended vasectomy (which closes only testicular end of the vas deferens)?


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Differentiating between hormones triggered on specific types of happiness?
Achievement:- Dopamine
Applause:- Seratonin
Discovering something new:-?
Remembering something after a long time/struggle:-?
Nostalgia:-?
Lust ;-Testosterone/Estrogen
Romantic Love:- Dopamine?
Attachment:- Oxytocin or Vasopressin?
Cuddling pets/babies:- Oxytocin or Vasopressin?
Motherhood:- Oxytocin & Vasopressin?
Also, is happiness in all cases equal? I mean that is happiness just differing in magnitude rather than type when comparing different activities? For eg, happiness on discovering something new is the same exact as happiness on kissing your crush, just differing magnitude and triggered by a different hormone?
Like in video games, we have damage versus status effect (losing hitpoints versus getting paralyzed or stunned), is that a better analogy to the various kinds of happiness or is it more like fire damage versus ice damage,

My apologies, but I'm having a bit of difficulty understanding your question. Can you try to edit it to focus more precisely on a specific aspect of what you are interested in?

which hormone is triggered when

How about Noradrenalin,  Melatonin, Tyramin & Tryptamin ? Not to forget the countermechanic, enzymatic groups that catalyze the oxidation of monoamines via monoamine-oxidases..

I think you need to narrow your question a bit, as right now it could be answered with several full textbooks. That said, a simple answer is that there is no such thing as a "happiness hormone" (despite some pop sci articles attributing this to one hormone or another), and all that you've listed are associated with far more than the pairings you've written here. You can give someone heroin and they experience happiness, but we don't call heroin a happiness drug.


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Does ATP production increase with oxygen availability?
I'm not a biologist so pardon any ignorance on my part. I'm working on a speculative evolution project and I'm looking to understand how the partial pressure of oxygen effects the maximum aerobic performance of muscle. This paper gives the maximum aerobic performance of 100 Watts per KG of muscle. This limit is stated to be observed for both insects and vertebrate fliers and is in turn used to calculate the aerobic flight capacities of various animals. The paper also mentions that squamate muscle tissue can achieve 450 W/kg anaerobically.
I have used the equations listed in the linked paper to calculate the size limits of my speculative world's fauna. The only problem is that this assumes an aerobic power output of 100W/kg of muscle. It is my understanding that aerobic respiration in muscle cells is driven by ATP production and that ATP production is dependant on a constant supply of oxygen. It seems logical that the maximum aerobic power output should be higher if there is more oxygen available.
For context, the atmosphere of this speculative world contains 13.5% O2 at a pressure of 12atm. This equates to a partial pressure of oxygen of 1.62 - approximately ~8x higher than our current atmosphere. In these conditions, there is 8 times the amount of oxygen available for respiration. If oxygen availability is the sole factor in ATP production (thus aerobic muscle power), then this means the aerobic power output would net 800W/kg of muscle (assuming the biology of these creatures are the same as known animals). This is almost double what lizards can produce anaerobically which doesn't seem likely.
My question is how would ATP production scale with available oxygen? I assume there comes a point where mitochondria simply cannot process ATP any faster, which would imply a maximum aerobic power output. I have read that some athletes breathe canned air to reduce fatigue. Does more oxygen equate to more power or does it simply mean that muscle cells would not fatigue as quickly? If I've made any mistakes in my reasoning then please correct them. Thanks.

Welcome to Biology.SE! Please take the [tour] and then go through the help pages starting with [Ask] questions effectively on this site and [edit] your question accordingly. Your "atmospheric composition" isn't for any planet I've ever lived on — please [edit] your post to use the correct values for Earth or clarify where the values you are using come from and why you are choosing to use them. ——— In addition, each question should be posted separately — this improves the chances that you will get answers for each question and makes the answers more accessible for future users. Thanks!

Thanks, I thought the description would be sufficient to explain the purpose but I'll restructure it so it's more concise. I don't think the other questions would serve much purpose individually since I don't think you could answer the title question without them. They're more like parameters wthin the overall question. I'll see if I can condense it a bit further though so thanks.

I've reduced the scope of the question. Hope this makes it clearer.

Carbon dioxide removal may be the limiting factor more than oxygen supply, even on Earth.

@PolypipeWrangler Do you have any links available? I'd be interested in reading about this.

The factors limiting ATP production are the rate of fuel (glucose, fats, amino acids, etc.) metabolism and its efficiency (ATP molecules per fuel molecule).
It is possible to produce ATP with zero oxygen by the glycolytic pathway; if this were not true, there would be no anaerobic organisms on Earth (which there clearly are). Muscle can do this too for short periods of time, producing lactic acid. In fact, many researchers believe that this pathway can produce ATP the fastest of any route of glucose consumption, even though it is least efficient. In other words, the number of ATP per glucose is small (only 2), but glucose "flows" through this pathway so fast that it is still generated faster than by respiration, which produces 30-32 ATP per glucose, but can process far fewer molecules of glucose per second. The actual rate of ATP generation by mitchondria is only limited by O2 concentration, in a chemical kinetics sense, in hypoxia, i.e. when a tissue does not have adequate blood supply, as in certain tumors.
The main effect of oxygen availability is likely size scaling--if you have more O2, you can get it through a larger body more easily. It's not that the muscle cells themselves generate more energy, it's that you can supply more muscle fibers that are farther from the lungs/gills/whatever. That's why in the carboniferous period on Earth, where there was considerably more O2, many animals (particularly invertebrates) were much larger than they are today.

Thank you so much! This makes a lot of sense. Just one follow up-question: You said metabolism is a limiting factor, does this mean that metabolic rate effects how quickly ATP can be produced aerobically? I'm using flying organisms as a case study as powered flight can only be sustained aerobically (otherwise it would transition to gliding/soaring). This is why I'm looking specifically at aerobic respiration, if that makes sense. Without throwing too much in the way of speculation, the speculative animals have photosynthetic capabilities so gluscose may also be more abundant.

Numbers of mitochondria per cell change in response to conditions also.

"Metabolic rate" usually refers to the rate of nutrient consumption in an organism as a whole, i.e. how much of the tissues (particularly muscle) are active vs. resting. The bottleneck I'm referring to concerns the rates of the enzymes themselves--no matter how much glucose (or oxygen) is available to a cell, there are only so many molecules the enzymes in a given mitchondrion can react with per second. The enzymes that break down glucose without oxygen are faster in this regard, considering how many can fit in the same volume.


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Common House Spider got shrunked and appeared lifeless when touched by water
I was trying to save a house spider which was on my water tub, it was desperately trying to move out of the tub but due to the smooth surface couldnt manage, the tub was wet but not filled with water so I tried to assist it with a net, but it end up slipping into tiny puddle of water (like a drop or two) and it got shrunked (the water probably made its legs closed due to surface tension of the droplet)
I then managed to gently soak the water with paper towels but the spider appears lifeless.
Is it dead? The whole process of getting soaked in water and being dryed up with paper towels was less then a minute.
Now I saw some reference where it says that it takes hours for spider to drown. So is it likely that the lifeless spider on my paper towel is most probably still alive?

Update (1 hours passed) I notice some twitching of one of its legs, very subtle though. Not sure if it is still alive or just muscular spasm.
Update (2 hours passed) 3 of its legs seems to be oriented in a way that they are touching the base of paper towel. Maybe the twitching action was to fix its legs? The spider still appear lifeless though :(
Update (2 days later) no movement as the spider appears lifeless. Most likely died but I want to know why? how can a drop of water kill a spider, when ants and other insects survive. Is it the crushing force of water droplet tension that cramped its legs? I could see very subtle adjustments of its legs after I dried it. The final form it took is in the picture is below. Looks like it managed to re-orient its legs but in the process didnt survive.

Was the "wetness" in the tub hot, or in any way soapy?

your link shows a giant house spider - was it one of those, or a common house spider (a cobweb weaver)? If it was juvenile, like a recently hatchling or maybe past one molt phase, it can drown in a drop of water. Alternately, if the spider was old and near the end of its life, the trauma of getting pushed around and into water. It's hard to fully grasp in what way "it got shrunked". If it remains still, you can probably get a very clear picture to share

@JiminyCricket. the tub was cold, I am not sure about the soapy

@JimN the spider was common house spider about the size of a pea. But I dried it up quickly with paper towel. It seems lifeless in day 2 so I am certain its dead. Its quite delicate creature and I felt quite sad when it shrunked because of mere drop of water. Its still on my paper towel and I shall share picture once i am back.

@JimN eventhought it somehow managed to get all its legs on the paper towel to orient itself upright, it looks lifeless to me now :(

@JimN I have shared the picture.

@user0193 thanks for the update and photo. A spider that size should not drown that quickly upon contact with water. Where are you geographically located? This is not any 'house spider' I'm familiar with (not parasteatoda sp, not Eratigena sp like you linked). It is coloured like dysdera crocata, but I would need a look at its face/jaws to be sure. Not that its identification will lead to any answer on how it died, but for completeness' sake, a correct ID would improve the question quality.

@JimN, Ok I tried to open up its legs using cotton buds and since I am no expert it may appear botch job. I am currently in Dubai, does that narrow it down? I tried searching if the spider is in dormant state / hibernation because it did managed to fix the orientation of its legs rather slowly (over few hours) but under observation for 2days didnt come back to life.

Perhaps the reason it could not climb out of the tub was because it got soap residue on itself, and then when it fell into the drop of water that residue was able to cover the spider's body.

It seems like [Brown Recluse Spider[https://en.m.wikipedia.org/wiki/Brown_recluse_spider]], also that twitching was from changing cephalothorax pressure which they do to to extend their legs (she was alive at that moment) unlike other insects spiders have muscle only to flex their legs not to extend so in order to extend their legs they use their body pressure/ hydrostatic pressure for hydraulic legs they do this by changing heart rate. Also when they die they curl up for the same reason(heart stops hence no hydrostatic pressure to extend the legs)

@daemon looking at your link, it does appear that it was indeed Brown Recluse, so looks like it could be combination of factors that could have killed her, soapy water, drying action, lack of energy, potential damage during picking up with paper towels (even-though I was very careful and held paper towels from the further ends so as not to have any hand pressure applied). Also with your Iink realized that they are one of the species whose venom do require medical attention.

@DKNguyen so a soapy water can kill a spider if it is covered with it?

@user0193 Soapy water is used by exterminators on wasps. It coats them in a suffocating film.

This is not a brown recluse. The carapace is too shiny (like a Cicurina) and unmarked (unlike the brown recluse, which would have the notorious fiddle mark). Also, there are no brown recluses in that area. This looks like a Sahastata  https://inaturalist.org/observations/124127 (which does exist in that area).


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Does GABA enhance or inhibit negative effects of glutamate?
A study on NCBI studied the correlation between a depressive mood and chronic pain. I researched this because today I noticed unusual emotional volatility as a result of 2 days of acute back pain combined with acute muscle soreness (DOMS).
I am certain that the pain and difficulty sleeping (although I slept in on both days), and challenges with finding a sleeping position without pain, and continuous pain on most moving, standing, and sitting, that this has caused some emotional volatility on a physiological level. (Psychological effects as a direct result of temporary chemical changes in the body/brain due to acute pain; not due to neural pathways causing depression, of which I do not have, and I am a joyful person normally).
This question is not about alleviating pain, as it will go away on its own soon. The back is getting near healed by end of week and the sore muscles which have DOMS due to intense workout will also resolve on its own in a few days to a week.
Rather, my question is specifically concerning a particular phrase which I am unclear about:

Glutamatergic activity can be promoted through the breakdown of efficient inhibition of the actions of glutamate by GABA

I am unclear if this is stating that GABA reduces the effects of glutamate or if it enhances the effects.
There is no clear answer to my full [temporary] issue, since the study itself states that neither the corresponding pathophysiological mechanisms of chronic pain and depression nor their mutual correlation has been identified, so there is no pathophysiological scientific answer to the chemical workings, so I can only speculate.
The end result is I wanted to discover whether increasing or lowering GABA could have any effect on my mood as a result of my pain in the short term, which is easily experimented rather safely by either taking GABA or taking a supplement that inhibits GABA. It could have no beneficial effect - no problem. It's worth a try though. I've taken GABA before BTW.
To reiterate the particular question: With regards to the statement:

Glutamatergic activity can be promoted through the breakdown of efficient inhibition of the actions of glutamate by GABA

Does this imply that GABA enhances or reduces glutamatergic activity?
Note:
I think it's saying that GABA creates glutamatergic activity which inhibits the neuroexcitatory effects of glutamate. That is, taking GABA would decrease effects of glutamate. Let me know if this is correct or not.

It would be possible to rewrite this question without the personal medical details, but please don't use such an answer to do anything besides understand biology. In any event, it certainly is not as simple as eating GABA increases GABA in the nervous system (no matter what someone trying to sell you a bottle of GABA might say).

Glutamate causes an EPSP (Excitatory Post Synaptic Potential,) thereby making the neuron less negative depolarize) and closer to voltage required to cause an Action Potential (AP)  and thus fire.  GABA causes an IPSP (Inhibitory Post Synaptic Potential) making the neuron more negative (hyperpolarize) and further away from the voltage required to fire and cause an AP.  GABA & Glutamate receptors  are generally on different neurons that synapse with other interneurons & oppose each other, although neither one is generally the end neurotransmitter of the locus,  nor the only neurotransmitter of the neuron, so basically act as neuromodulators on the post-synaptic neuron. Glutamatergic receptors generally affect Sodium Channels &  GABA-ergic neurons generally  affect Chloride Channels. In theory, inhibiting an inhibitory neuron would be the equivalent of exciting an excitatory neuron, but since they primarily affect  post-synaptic neurons, the effect is cumulative, so the post-synaptic interneuron is basically adding up all the EPSPs & IPSPs to get a RMP (Resting Membrane Potential) & some additional stimulus must occur to get the neuron to fire (AP)

You might recheck what you've written here because a lot of this answer is incorrect or at least mis-written.


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Inhibitory effect of GABA through GABA(A) receptors
Over at Wikipedia, the following is written in the article about GABA(A) receptors:

"Upon activation, the GABA(A) receptor selectively conducts Cl− through its pore. Cl- will flow out of the cell if the internal voltage is less than resting potential and Cl- will flow in if it is more than resting potential. This causes an inhibitory effect on neurotransmission by diminishing the chance of a successful action potential occurring." (https://en.wikipedia.org/wiki/GABAA_receptor, Accessed: 22 May 2018)

Based on my understanding, if an action potential is to be inhibited, the internal voltage of the neuron needs to be decreased further away from the voltage at which the neuron's voltage-gated sodium channels open up.
With this in mind, I take issue with the statement Cl- will flow out of the cell if the internal voltage is less than resting potential.... If the internal voltage is less than the resting potential, and the Cl- flows out from the cell, then the internal voltage will increase, hence coming closer to the action potential.
This would increase the probability of reaching an action potential, not decrease it, wouldn't it?
My Question: Does Wikipedia have it wrong, or is there something I haven't understood?

Great question! This apparent contradiction has puzzled many neuroscience students before you.
Short Answer:
This is often called "shunting inhibition," in particular when excitatory and inhibitory conductances are out on dendrites.
Longer Answer:
The part that is wrong is this (emphasis mine):

the internal voltage will increase, hence coming closer to the action potential. This would increase the probability of reaching an action potential, not decrease it, wouldn't it?

The idea that "hyperpolarization is inhibitory, depolarization is excitatory" is only partly true. It is very important to also consider what the spike threshold is, and to think in terms of reversal potential for a given ion channel (or more generically we can just call it a 'conductance'), and then you can revise the statement to say this:

Conductances with reversal potential greater than spike threshold are excitatory, conductances with reversal potential less than spike threshold are inhibitory.

Most often, chloride-based channels fit into the second statement: their reversal potential is less than the spike threshold.
How Shunting Inhibition Works:
Any time you open a channel, you will shift the membrane potential towards the reversal potential for that channel. The amount of current that flows through a channel depends on the 'driving force': the difference in voltage from the reversal potential.
Let's consider a fairly typical textbook cell, with a spike threshold at -50mV, a resting potential of -65mV, and a chloride reversal at -60mV.
If the cell is at rest, and you open chloride channels (such as with GABA via GABA-A receptors), the resulting flow of current will tend to push the membrane potential towards -60mV, so the cell 'depolarizes'. However, no matter how big of a chloride conductance you open, you will never pass -60mV, so you will never reach spike threshold.
If, in that same cell, you instead opened AMPA channels, with a reversal of around 0mV, you also get depolarization, but in this case as you open more AMPA channels you can potentially depolarize the cell all the way to 0mV. Of course, unless you have blocked sodium channels you will get an action potential before you reach that point, but that's the key: you will cross threshold, therefore we call it excitatory.
Now let's consider a third case where we open both AMPA channels and GABA-A channels. As long as the membrane potential is <-60mV, both channels contribute to depolarization. However, as soon as the membrane potential is >-60mV, chloride ions will start flowing into the cell. We call this "shunting" inhibition because if you look at the sum current flow in the cell, it will look small, because you have chloride ions coming in at the same time as sodium ions, resulting in little change of the membrane potential despite lots of ions moving.
The result is that GABA-A channels, even if they can depolarize a cell that is at rest, will act to prevent the cell from depolarizing far enough to reach threshold. It's important to consider the dynamics of the membrane potential, rather than thinking of the membrane potential as something that is simply added or subtracted to instantaneously.
Important Caveats:
Ion concentrations matter! If chloride concentrations are not 'typical' or if the spike threshold is more negative than in a 'typical' textbook cell, then chloride conductances can indeed be excitatory! In fact, excitatory GABAergic transmission is important are certain stages of development. If cells have too much chloride in them, this can also cause GABAergic transmission to become excitatory (or at least limit the efficacy of the inhibition), and this can lead to epilepsy (see Cohen et al. 2002).
There can also be a time window where GABAergic transmission is excitatory even in a typical cell: this is the period where the GABA-A channels have closed, but the membrane remains slightly depolarized and has not returned to rest. Excitation that arrives during this time will sum with the residual depolarization, and there are no open GABA-A channels to 'shunt' the current.

Alger, B. E., & Nicoll, R. A. (1979). GABA-mediated biphasic inhibitory responses in hippocampus. Nature, 281(5729), 315.
Cohen, I., Navarro, V., Clemenceau, S., Baulac, M., & Miles, R. (2002). On the origin of interictal activity in human temporal lobe epilepsy in vitro. Science, 298(5597), 1418-1421.
Purves, D., Augustine, G. J., Fitzpatrick, D., Hall, W. C., LaMantia, A. S., McNamara, J. O., & White, L. E. (2014). Neuroscience, 2008. De Boeck, Sinauer, Sunderland, Mass.


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What degree of influence do SNPs have on activity of ligands at receptors?
I know that generally, evolution tends to evolve towards having some wiggle room in respect to effect of polymorphisms on binding of endogenous ligands, but with synthetic ligands, especially modern structurally-unrelated molecules, does the same continue to hold true?
I've been particularly wondering about this in respect to biased agonists with selective functionality for some pathways activated by a receptor over others - wouldn't activity of that degree of selectivity be particularly vulnerable to disruptions by SNPs?
Hypothetically, would a ligand preferentially activating therapeutic pathway A but not a highly hazardous pathway B of an ABC receptor be a viable drug at all? Or would it be prime "expect it to kill somebody sooner or later" material?

Can you please define what you mean by "effector"? It's not standard terminology. At first I thought you meant receptors, but you mention receptors in your last paragraph, so I have no idea what you're talking about.

@MattDMo Sorry, I'm still catching up to speed on biology - I'm thinking about the components of the signaling cascade that are responsible for activating the different separate effects that a receptor's activation induces with e.g. functionally selective ligands. I must have misinterpreted something along the way, as I thought the component was called an effector.

So basically, effector == signaling pathway?

@MattDMo Is that the proper term, then? If so then yes.


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By what means do "nerve agent" compounds like VX spread through the human body so quickly?
It has been demonstrated that so-called nerve agents are able to incapacitate and kill a human in only minutes after exposure. One such substance, VX, only requires a few milligrams to contact the skin of a human in order to trigger such a reaction.
I understand that many nerve agents are acetylcholinesterase inhibitors, so they promote a surplus of acetylcholine which causes loss of muscle control due to the inability to "rest."
What I totally fail to understand (or find in my searches), is how such a small drop of e.g. VX is able to cause full-body symptoms. In other words, if a drop of this substance gets on a person's hand, how is it that in 1-2 minutes, they begin to have full-body convulsions, defecate uncontrollably, etc...? I would understand this if the substance was sprayed all over someone, but having a drop in the order of milligrams on an extremity, it's not clear how this triggers such a severe reaction all over the body. I am aware that it gets absorbed through the skin, but otherwise I have no idea what happens after that.
My lack of understanding is partially due to:

(A) Neurotransmitter (acetylcholine, ACh) released from nerve endings binds to receptors (AChRs) on the muscle surface.

Kuo IY, Ehrlich BE. Signaling in muscle contraction. Cold Spring Harb Perspect Biol. 2015;7(2):a006023. Published 2015 Feb 2. doi:10.1101/cshperspect.a006023
How does VX so quickly get to the surfaces and inhibit acetylcholinesterase all over the body? Is it a matter of simple blood circulation after the agent makes its way through the skin and into the blood stream?

Welcome to Biology.SE. Please [edit] your post to clarify your question. As written you seem to be asking about the circulatory system, but since that is common knowledge I'm guessing you have a more sophisticated question that isn't clear.

hi @tyersome thanks for explaining that. So I made a minor edit to clarify the final question. After doing a bit of research on that subject, I found that the circulatory system can indeed push blood in full circulation from heart and back in a matter of sub minute. But I'm still only speculating here.

You're welcome! It seems to me that all of the symptoms you describe could occur due to effects on the CNS, so a nerve agent doesn't even need to get to the whole body. I'm doubtful that anyone on this stack has the kind of background to answer this with any specificity — you could try [MedicalSciences.SE], but be aware they may expect more prior research. Also, please do not crosspost, instead request migration after consulting that sites help.


text:
Growing Penicillium Digitatum Mold
I left a cup of tea with Lemmon on my desk and after a while green mold start growing on the water. From my understating this is Penicillium digitatum. I gave it some sugar and after one day black spots appeared. I read that it can be little bit dangerous to inhale mold so I wrapped the cup with saran wrap and make some holes in it in order to give the mold oxygen.

What do I need to do in order to give the mold better condition to grow?
Can it be dangerous growing it?

What's your goal with this project? You don't really know what you've got in that tea-cup, and DIY dirty dish biology doesn't sound like a great idea in general...

What makes you think it's specifically P. digitatum? Penicillium molds are very widespread in the environment, and can be almost impossible to differentiate based on visual appearances alone. That being said, I echo @jakebeal - what is your ultimate purpose in this experiment?

You could place part of the mould into a cut in a piece of citrus fruit to continue its growth. Citrus can also host P. italicum, the below website is one mentioning how to differentiate between them.
http://www.pestnet.org/fact_sheets/citrus_storage_moulds_197.html
Hazards.
Aspergillosis: (fungal spores growing in the lungs) which is uncommon.
Asthma: penicillium spores have been associated with increased chance of onset of asthma, and problems with breathing in people with asthma.
There may be other hazards.
I just cite one paper below, but a search using terms of penicillium and asthma shows lots more.
"Household airborne Penicillium associated with peak expiratory flow variability in asthmatic children"
published in :
Annals of allergy, asthma & immunology : official publication of the American College of Allergy, Asthma, & Immunology
by:
Kemp W. Bundy, MD, MBA, Janneane F. Gent, PhD, [...], and Brian P. Leaderer, PhD
doi: 10.1016/S1081-1206(10)60139-1

thanks. It seems too dangerous to keep growing it. Should I worry that it was in my room for a few days?

@ziv as long as you're not immune compromised and you haven't been purposely inhaling the fungus, you should be fine.


text:
Determining net charge of amino acid at given pH
I am trying to calculate the net charge on an amino acid, but I seem to be doing it wrong. The question I am trying to answer is "In a pH 7.0 buffer, what will be the charge of Methionine?" We are referred to a table that gives us the following information:
$$\pu{p}K{_\pu{a\mathrm{1},\ce{COO-}}}=2.28$$
$$\pu{p}K{_\pu{a\mathrm{2},\ce{NH3+}}} = 9.21$$
$$\pu{pI = 5.74}$$
From what I understand, if pH > pI, (which it is here), the amino acid should have a negative charge because even though the pH is high enough to deprotonate all the carboxyl ends and not enough to deprotonate all the amino ends, since it is higher than the pI some of the amino ends have been deprotonated (in addition to all the carboxyl ends).
Yet my answer book says that the net charge would be zero! Are 5.74 and 7.0 "close enough" that we can consider net charge to be zero still? If so, what is the standard permissible 'fuzzy' range? If not, then what is going on here?

You are right in your reasoning: at any pH for any titratable group, there is a distribution between the protonated and deprotonated species. We can calculate this distribution and therefore the average charge of the species with the Henderson-Hasselbalch equation:
$$\mathrm{pH = pKa + log\left(\frac{[B]}{[A]}\right)}$$
Or, rearranged:
$$\mathrm{\frac{[B]}{[A]} = 10^{pH - pKa}}$$
Where A is the conjugate acid and B is the conjugate base. For carboxyls and primary amines, this can also be written as $\ce{\frac{[COO-]}{[COOH]}}$ and $\ce{\frac{[NH2]}{[NH3+]}}$, respectively. As a simple example, if the pH was 2.28, the ratio between the protonated and deprotonated form of the carboxyl group (pKa = 2.28) would be $\ce{\frac{COO-}{COOH} = 10^0 = 1}$. This means $\ce{[COO-] = [COOH]}$ and the average charge of the carboxyl is thus -0.5.
Now, for cases where $\mathrm{pH \neq pKa}$, we need to determine the mole fraction, $\chi$, for each charged species. Given that $\mathrm{\frac{[B]}{[A]} = \frac{\chi_B}{\chi_A}}$ and $\ce{\chi_A + \chi_B = 1}$, we can derive these equations:
$$\mathrm{\chi_{COO^-} = \frac{1}{1 + 10^{pKa - pH}}}$$
$$\mathrm{\chi_{NH_3^+} = \frac{1}{1 + 10^{pH - pKa}}}$$
Plugging in the numbers, we get:
$$\mathrm{\chi_{COO^-} \approx 0.999981}$$
$$\mathrm{\chi_{NH_3^+} \approx 0.993872}$$
To state it another way, ~99.9981% of the carboxyl groups are in the deprotonated (negative) state and ~99.3872% of the amino groups are in the protonated (positive) state. The average charge of methionine at pH 7 is simply the sum of these mole fractions, accounting for the charge of each species, and is approximately equal to -0.006109. I assume your textbook is rounding.

You can plot these functions to see how charge varies with pH:

Your answer is very detailed and interesting. However, I thinks it raises an additionnal question: if the amino acid's charge is around 0 for a wide range of pH (approx. between 4 et 8 here), why bother defining a pHi?

@Flo The pI will tell you where the transition from net negative to net positive charge occurs. Depending on your application, that information may or may not be useful. I work with proteins, and the pI of a single amino acid has never been crucial information for me. However, knowing the pI (usually estimated) of an entire protein is important for applications such as gel electrophoresis and chromatography. Because proteins contain many titratable side chains, their charge can vary more significantly around the pI.

Thanks for this great answer! Are there any guiding rules by which to determine/estimate when it could be rounded, or would I need to use these equations to see how close to each other the values are?

@Jo.P For your case, the rules would be dictated by the instructor and you should ask them for clarification. A rule of thumb that I've heard is that when the pH is >2 units away from the pKa, you can treat the species as either protonated or deprotonated. At |pH-pkA|=2, the ratio of acid to base will be 100:1 (or vice versa).

Oh the horrors of Schiff bases and pHs..... +1

IMO the inclusion of a chart like the one you provided turns a good answer into a great one. +1 and more if I had them.

@BryanKrause I always appreciate pictures in answers. Thank you and AliceD

@canadianer-Tnx!


text:
Sensitivity vs. Limit of Detection of rapid antigen tests
I'm comparing a bunch of SARS-CoV2 rapid antigen tests:

Source
Columns 4 and 6 list the values for sensitivity and limit of detection (LOD). How come that a test with a several times lower limit of detection can have a worse sensitivity?
As an example, consider tests #2 and #4:
#2 - Sensitivity: 97.7% - Limit of detection: 2.0*10^2.4 = 502 TCID50/ml
#4 - Sensitivity: 91.4% - Limit of detection: 2.5*10^1.8 = 158 TCID50/ml
Shouldn't these values correlate, i.e. the more sensitive a test is the smaller the amount it is still able to detect?

Not necessarily. Sensitivity and specificity are decision criterion-based measures. They are not actually separable from another, they are a consequence of choosing a threshold at which to say "the test reports positive" or "the test reports negative", a consequence of this binary result. As such they are weighed against each other. You can always make a test with 100% sensitivity as long as you always report "Yes". You can always make a test with 100% specificity as long as you always report "No".
Similarly, you can define what it means to have reached a limit of detection, but this need not be the same trade-off as the one you use for sensitivity and specificity. For example, you might declare this as the point where your readout is "significantly greater"  than baseline in a collection of known positives vs known negatives. But if you set your decision threshold right at that level of detection, you may still have, let's say, only 50% specificity at that level and accept too many false-positives, so you set a different decision criteria.
They are apples and oranges, there is no reason they need to correspond.

Thanks for your answer! So which value is more indicative for the quality of the test? Say, I have two tests with the same sensitivity, but one has a much lower LOD - or - two tests with similar LOD, but one has a higher sensitivity (all other parameters being similar, incl. specificity). How to make a decision?

@david There isn't enough information to make that decision. Probably all of the tests on your list are statistically equivalent, unless there are substantial discrepancies in how they were evaluated. For example, you could get an artificially high sensitivity if you tested only very saturated target samples. You would need much more extensive real-world evaluation than I am aware of anyone having on hand as of yet.

Also, making a test report always "Yes" doesn't make it 100% sensitive if it gives false positives most of the time, does it? Sensitivity measures the true positives, so one cannot simply "tweak" the reported sensitivity by relaxing specificity, right? Example: If my test reports "Yes" every time it encounters aqueous oxygen, this doesn't make it 100% sensitive (it could very well be 0% sensitive by completely failing to detect the antigen in a deoxygenated solution).

@david Sensitivity is "true positives"/"actual positives". If you always report Yes, you will have 100% sensitivity: you report every actual positive as true positive. You will also report a lot of Yes when it is an "actual negative", but this doesn't hurt your sensitivity, it hurts your specificity. A test that always says "Yes" has 100% sensitivity and 0% specificity. You're right that this isn't a very good test, but just knowing sensitivity doesn't help much with that.

Are you using "true" and "actual" as synonyms or are you saying that sensitivity = true pos./actual pos.?

@david A "true positive" is a positive your test says is positive that is truly positive. This is standard terminology. "Actual positive" isn't standard terminology, usually people just say "positives", but I'm using it to indicate the number of positives in the sample. So it's the latter equation you write. In this terminology you could also write "actual pos = true pos + false neg", since false negatives are the positive cases that are falsely marked negative.


text:
In which reactions of glycolysis is magnesium involved?
I am currently studying the metabolic pathways for biochemistry and I am not quite clear in which reactions of glycolysis magnesium is involved.
So I have now found out that magnesium is present in the three ATP-dependent reactions (1st, 3rd and 10th reactions), but also in the 2nd, 7th, 8th and 9th steps.
According to this diagram:

In our university we have been tought, that Magnesium is present in all ATP reactions, but also in Step 2... this is what causes confusion for me:

Ok, have you found out what purpose magnesium can have in molecular reactions?

@Chris ok thank you for the hint, i should and will do that now.

@Chris I know that magnesium is used to regulate the movement of minerals across cell membranes. But what does it specifically in glycosis?

The general answer to this question is "all reactions involving ATP". This is covered in answers to another question.

please check my edit, why is it involved in Step 2

What is the source of your figure with magnesium ions required for the PGI reaction? The paper reporting the crystal structure of PGI and the protopedia page have no involvement of magnesium ions in the mechanism of the reaction. I have no reason, therefore to believe this is true. Furthermore, you should ask your University why they are filling your head with miscellaneous facts (or fictions) instead of teaching you to understand the principles of glycolysis.

In the 1st step where glucose is converted to glucose-6- phosphate by the enzyme hexokinase, in the 3rd step where fructose-6-phosphate is converted to fructose-1,6-bisphosphate by the enzyme fructose-1,6-bisphosphatase and in the last reaction where 2 phosphoenolpyruvate is converted to pyruvate by the enzyme pyruvate kinase.. In this 3 reaction Magnesium is needed as they are ATP dependent reaction and Magnesium stabilises the ATP in this reaction and help the reactions to proceed faster.


text:
Do partial (nighttime) curfews curb the spread of epidemics (and via which mechanisms)?

Do partial (e.g., nighttime) curfews curb the spread of epidemics?
What is the (epidemiological) mechanism by which partial curfews curb the spread of epidemics?
Is there evidence from past or present pandemics that this works?

Related questions

This question in SE:MedicalSciences asked about nightly curfews 8 months ago, but with a focus on economic and other effects. It cited evidence that curfews failed for economic reasons during Ebola outbreaks. It did not elaborate why limiting the time everyone can go to a shop would magically lead to less many people being in the shop at the same time. The only (non-accepted) answer to the question is speculative and concludes that the author is not sure if curfews are effective.
The same question was cross-posted here in SE:Biology and closed for that reason (cross-posting). There appear to have been some comments but these were deleted when the question was closed.

Related Research
The only papers on the topic i could find are two papers in the context of the Ebola epidemic in Liberia in 2014/2015. Both papers unfortunately focus on public health policy and not on the epidemiological merits of the measure:

Kirsch et al. 2017 (mentioned above)
Blair et al. 2017

The standard SIR- (and SIS-, SEIR-, ...)-Models predict a reduction of the infection rates when social interactions are reduced. This is obvious and not in doubt. Some common infection prevention measures (working from home, suspension of inter-regional travel, social distancing, restriction of contacts between households, closure of social gathering places) are designed to do this. In the case of partial curfews, it is not clear to me, if this (reduction of social interactions) is the objective and by what epidemiological mechanism that objective (reduction of social interactions) is meant to be achieved with partial curfews.
Why would a nighttime curfew not curb (possibly increase) the spread of the epidemic
People are still allowed (and will still) go to shops, do exercise etc., but if they have to do it at specific times, they are more likely to bump into each other. Human nature may even cause people to congregate in shops just before the curfew time (because you realized that you're out of pasta or so). So this might actually make it easier for the virus to spread.
Why would a nighttime curfew curb the spread of an epidemic
I am not sure; this is why I'm asking.
Some very far-fetched possibilities I could think of:

Making illegal gatherings inconvenient while being easy to enforce?
Reducing service personnel working away from home?
Forcing people to stick to the regular workday sleep cycle even while staying at home to prevent mental health issues which would lead to more people attending hospitals?

Context (Why is this relevant?)
Several countries have declared night-time curfews or are considering these to tackle the current wave of Covid-19 outbreaks. This includes, among many other countries, France, Germany, Spain, Hungary, Tunisia, South Africa.
For some measures, the objectives are clear and obvious: social distancing, closure of restaurants, bars, workplaces, schools etc., self-isolation of infected people and their contacts, face masks, vaccination, etc. Last year Spain took this policy to the extreme by assigning specific time slots to specific demographic groups.
However, I do not understand what good nighttime curfews would do - or other part-time curfews for that matter - unless the curfew is complete, 24 hours a day every day (i.e., everyone except for essential personnel locked in their homes, like in Hubei in early 2020).
To be clear:

I do not dispute that limiting social interactions helps.
It is easy to see that a full (24 hour every day) curfew should effectively halt the spread.
I am not asking about effects on mental health or on the economy.
I am specifically asking about the epidemiological rationale behind imposing nighttime curfews.

Edit (Jan 29 2021), note regarding the Covid-19 curfew in the Netherlands in on January 23 2021.: The Dutch government claims "Research has shown that night-time curfews help to reduce the spread of the virus." This suggests that there is scientific evidence, but they do not detail what evidence that is, what the underlying epidemiological mechanism is, or where it can be found and reviewed. They only add that the Dutch curfew between 9pm and 4.30am "will prevent people from visiting each other and gathering in groups". At the same time, "visiting each other" remains explicitly permitted in the Netherlands during day-time, although for only one visitor at a time. (Yes, the Dutch curfew is the one to which some violent Neonazis and Antisemites in the Netherlands responded by rioting and looting. I would like to point out that the Dutch curfew and the riots etc happened only after I asked this question and that I have no sympathy for those responsible, although I would still like to understand how exactly night-time curfews are supposed to help.)

@David This answer on SE:Biology Meta suggests that epidemiology is on topic here. While you may argue that restrictions such as curfews are unrelated to epidemiology, I specifically asked about the merits of a specific policy from an epidemiological perspective. Also, there was a similar question earlier (linked in the OP) that was closed not for being off-topic but for being cross-posted. If everyone agrees with David, please go ahead and close or delete. But I have to admit, I am a bit shocked by the level of anger in David's comment.

I don't speak for David, but do share his frustration that many of the posts in this site are completely inappropriate and often seem to involve no thought on the part of the poster. He may seem harsh, but he is not attacking you personally. Your post does have on-topic parts. but you've buried them in questions about intentions (e.g. the title). I encourage you to rewrite to focus on a single concise biological question. The [tour], [ask], and other [help] pages for more details on what is expected.

@tyersome Thank you. I tried to rewrite the question to focus it on the epidemiological question. I am sorry that people are frustrated about many off-topic and inappropriate posts. But may I just reiterate (MattDMo said that yesterday) that the tour and how-to-ask do not state to a lot of detail what is or isn't on topic. I looked it up on SE: Biology Meta (see link above) and posted believing that what I was asking was actually on topic.

I think Skeptics.SE would likely take up the specific claim by the Dutch government. I think the biology side of the epidemiological question here is pretty superficial. The intent of the curfew is to reduce contacts between people, particularly contacts between people who are not already in contact at other times of the day (like family members). This is pretty obvious and has little to do with any underlying biology. The extent to which it is truly effective seems like a different question that isn't itself related to biology.

I'd add that I don't think the rationale for the specific policy is epidemiological, but that the policy makers agree: "limiting social interactions helps." Their goal is to make this happen with as little impact as possible, which is a political and economic calculation.