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If the flu vaccine is the exact same as last year, would it still offer protection this year?
I understand why the flu shot changes and that's why we get an annual vaccine; however, if the vaccine is the same as last year, wouldn't people theoretically still have the same antibodies this year? Do antibodies disappear after a year?

If one flu strain wouldn't change between the years (meaning there wouldn't be any new mutations in it) and the same strain would circulate again in the following year, the "old" vaccination would protect people. This is the same as with other viruses which do not change, once you reached a protection (usually one basic immunization and one booster), this protects for a long time (see measles vaccination as an example here).
There are surprisingly little articles available on how long the immune response after a vaccination lasts. There is a difference between the livettenuated influenza vaccine (LAIV) and the inactivated influenza virus (IIV), with the former giving a less good protection (see reference 1).
Data for the LAIV suggests that there is protection for at least one year after the vaccination (see reference 2).
However, there is evidence that the immunity against the flu after an infection against this specific strain might last life-long, as a paper demonstrated on survivors of the 1918 flu epidemic (see reference 3).
Having the flu against being vaccinated against it is a complete different thing (higher exposure, probably more antigens), but the question is if the immune response against vaccinations may also for a longer time.
The problem with the flu vaccination are:

The strain circulating in a year is changing.
The stains are mutating, making them different from the virus used for vaccine production. Depending on how different these mutations make the circulating strain, it can render the vaccine more or less useless. This is something what happened this flu season.
The flu vaccine is prepared from different flu strains to cover a broader range. In a tri-valent vaccine these are typically 2 Influenza A and one Influenza B virus strains, in tetra-valent vaccines 2 A and 2 B strains. The composition is based on a prediction (from epidimiologic data) which strains are likely to circulate in the next season and is done early in the year for the following season (production takes time, etc.).

Because of these problems, researchers are working on a universal flu vaccine; which is based on virus parts which do not change and should protect against all virus strains. Then only the basic vaccination would be necessary as with other vaccinations.
With all these limitations, it is still advisable to get a flu vaccination, as it is a pretty severe infection.
When not challenged (i.e. upon infections) antibodies are cleared from the blood within a few weeks, but there are low amounts produced (which are enough for detection). The immunologic memory is maintained by memory B cells which can ramp up production of the highly specific antibodies in a very short time - this is the reason for the protection by immunizations.
References:

Modest Waning of Influenza Vaccine Efficacy and Antibody Titers
During the 2007-2008 Influenza Season.
Longevity of B-cell and T-cell responses after live attenuated
influenza vaccination in children.
Neutralizing antibodies derived from the B cells of 1918 influenza
pandemic survivors

Thank you very much. It is concerning as there have been many children dying from the B strain, that experts are claiming is the one covered in the vaccine. The vaccine is exactly the same as last year, so wondering if those who received the vaccine last year would have some protection, obviously taking into account changes and mutations

The majority of deaths usually occurs in the non vaccinated.

Chris, can you support your claim of prolonged immunity against influenza vaccine (i.e. antibody persistence)? Some viruses do have astounding antibody persistence. Others have little.

@anongoodnurse Yes, there are some papers, I will dig them out. There was especially one paper on survivors of the 1918 flu. It has to wait, until I have paper access again at work.

So in saying this. Antibodies that have developed after receiving the flu vaccine does not wear off after a year, correct? So someone that received the shot in Canada last year but not this year, would have the same level of antibodies, as someone who received it this year. As the vaccine has the exact same strains included in the shot as last year. Is this correct


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Reusing pipette tip
I'm new to research and one of the things I'm learning is pipetting. I've got the basics down but say I'm reusing a pipette tip because the solution I'm using is the same. So first I depress to the first stop, aspirate liquid, then release the liquid to the second stop. However after this, do I take the pipette out and release to the very top then back down to the first stop to gather more liquid or do I take the pipette out and raise it to the first stop and gather more liquid?

Once you've depressed to the second stop, you need to remove it from the liquid, else you're re-aspirate OVER the defined amount. You also won't then be able to eject it all fully. If your pipette is set to 1000 uL, for instance, the tip volume will be 1000 uL from first stop to first stop. The second stop depression is purely there to ensure all the liquid is expelled from the tip.

Once you dispense the liquid after the first shot, you raise the plunger back all the way to the top, and start the whole process over, as if you had a fresh tip. (the first of your two options)

One thing you should do if you are new to pipetting is to pipette water into a weigh boat on a precise scale. Pipette 100 microliters, 10 times in a row, tare, and repeat. Make sure each shot weighs 100 milligrams, just to test yourself.

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when does osmosis stop
I have a question about osmosis that goes a bit deeper than most basic textbooks so I cannot find the answer.Here's the problem:
Imagine an animal cell, say a red blood cell, in a slightly hypotonic solution.
The water starts to flow in osmotically.
The concentration of solute in the cell decreases.
The cell slowly starts to swell but does not burst.
The question is:
Does this water entering increases the pressure on the membrane (similar to turgor in plant cells only less, because the cell can increase in volume - comparable to elastic energy that must be overcome when blowing a baloon...) and does this cause osmosis to stop BEFORE the concentrations come to equilibrum (meaning that cytoplasm still has a bit more solute concentration than outside of cell) or do the concentrations perfectly match?
Thanx in advance.

It doesn't
As long as liquid water is present osmosis will never stop, the closest you can get is a point at which it happens at equal rates in both directions, called equilibrium.
Plant cells will help you understand as osmosis will create immense internal pressure as water enters the cell even though the cell cannot expand thanks to the cell wall. the amount of water inside the cell will keep rising until it reaches equilibrium, this also makes the cell more rigid.

If animal cells are incubated in pure (or v. Low solute conc.) water, they will swell until they burst.
So in that respect, I think osmosis doesn't stop for animal cells. At least not until either equilibrium has been reached, or the cell has burst.

Equilibrium must be reached for osmosis to stop, but what equilibrium? Look at this example: http://canacopegdl.com/images/osmosis/osmosis-14.jpg    Here, as water level rises in one side and falls in the other, hydrostatic pressure builds up. When hydrostatic pressure equals osmotic, net water flow into the STILL HYPERTONIC solution stops from the STILL HYPOTONIC one. My assumption is that something similar (just to a lesser extent) exists in the case of animal cell swelling so osmosis stops when the pressure buildup in the cell equals osmotic pressure.

Hydrostatic pressure won't effect cells in the same way as that scenario. As the cells are surrounded by the solution, the pressure against the cell wall can lead to the cell bursting, if the osmotic potential of the solution is off. For mammalian cells, it's typically around 300 milliosmolar. Similar to tissue fluid.

Anyway, not really. Either the cell will swell and burst, or shrivel and die. In both scenarios the membrane disintegrates, so the cells contents mix with the solution. Now for an artificial membrane that cannot burst. That's a different question.

I found this, which I think proves my point, but I cannot say I really understand all the math behind it.
https://i.stack.imgur.com/GgO01.jpg
http://www.princeton.edu/~akosmrlj/MAE545_S2017/lecture13-14_slides.pdf

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fermentation in soil bacteria
I am doing a project on microbial fuel cell. For the purpose of the efficiency of the question, MFCs can be summarized to:

Devices that use anaerobic bacteria as the catalysts to oxidize organic and inorganic matter and generate current. I referenced this article

While writing the analysis I was quite confused about the fermentation process in which anaerobic bacteria in soil undergo. Usually the fermentation process and its byproduct would be specified, however, in this case there are numerous bacteria that the soil contains.
I want to ask if there is a specified fermentation process that the soil bacteria undergo (which is probably not the case), or is it unknown so I should just talk about fermentation in general.
Thanks in advance!
ps. it would be greatly appreciated if a link to some websites or articles that would possibly help me is included :)


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What is the relationship between snails/slugs and clams/mussels?
Slugs and clams are both phyla in mollusca, but how can I tell which features they inherited from an ancestor? Basically, I'm curious about how excatly these organisms are related but can't find any information and do not know where to look.

The Tree of Life web Mollusc page  shows that gastropods (snails/slugs/etc.) and bivalves (clams/mussels) are two of the major groups within Mollusca:

You can click through to get more detail on the individual groups (but there isn't much more information about the defining characters, date of divergence, etc.). At the very least, these technical names for the taxa (and of the Conchifera, their parent taxon) should help you search for more information, e.g. a Google scholar search on "bivalvia gastropoda divergence", which gets to Investigation of molluscan phylogeny using large-subunit and small-subunit nuclear rRNA sequences ("scaphopods are more closely related to gastropods and cephalopods than to bivalves") or Phylogenetic relationships of annelids, molluscs, and arthropods evidenced from molecules and morphology. (You do have to be careful in reading the phylogenetic literature, as it's rapidly evolving; the latter paper is from 1996 and may well be superseded.)

There isn't that much easy information for snails and clams, They diverged 550 million years ago, and their anatomies are well studied. If it wasn't for genetic evidence perhaps not all scientists would agree that they are monophyletic.
The shell is the most obvious common feature, made of silicon (nacre/pearl) and calcium, and the next nearest animal to have a similar growing shell is which animal? a wormy thing with a shell doesnt exist AFAIK. Even the shell is different:
nacre layers in gastropods and cephalods (Nautilus) are formed by the
progressive nucleation of crystals at the top of conical stacks of
aragonite platelets and the lateral thickening and eventual coalescing
of older crystals at the base (Mutvei 1970. Wise 1970a. Wise
1970b, Erben 1972, Mutvei 1978, Nakahara et al. 1982, Wilbur
and Saleuddin 1983). In contrast, in bivalves. growing sheet nacre
has a steplike structure, and at each step, there is a gradient of
maturing crystals overlying fully formed layers (Wise 1970a. Wise
1970b).

Snails and Clams have nearly no articulations, only one major muscle as a result, the grinding and filter apparatus in both is very different, so that only leaves simple things like the heart and circulations and shell and muscle anatomy in common.
https://en.wikipedia.org/wiki/Evolution_of_molluscs
https://www.researchgate.net/publication/259355769_The_Continuing_Debate_on_Deep_Molluscan_Phylogeny_Evidence_for_Serialia_Mollusca_Monoplacophora_Polyplacophora
perhaps someone can tell you from this image of genetic distance the percentage of the genome they have in common.
https://www.researchgate.net/profile/Julia_Sigwart/publication/259355769/figure/fig2/AS:213874457485316@1428003052255/Preferred-molluscan-tree-Maximum-Likelihood-analysis-RAxML-28-hardway-of-pruned.png


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What percentage of genome do slugs and scallops have in common?
We can know genetic distance of thousands of species. The OTT tree of life gives genetic distance for nearly all species. Is there a resource to compare the genomes of any sequenced animals to know the percentage of DNA they have in common? I wanted to know for slugs and scallops.

The question is actually not that easy. Many parts of the genome will fail to align and many aligned part will differ in length. So the question "What percentage of the genome species A and species B have in common?" is actually quite undefined.


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Why do humans retain two kidneys?
If one kidney can function just as well as two, why do humans have two kidneys? The cost of growing two kidneys must surely be quite high, especially since one kidney is all that is really needed.

Perhaps because humans are pretty much bilaterally symmetric, and have two of almost everything: arms, legs, eyes, lungs... even two brain lobes.  A better question might be why we don't have two hearts or livers...

All vertebrates have two kidneys. There's no selection pressure to reduce to one.

@james the answer to that is kinda cool you might want to ask it, it has to do with the fact the ancestral circulatory system is not paired but one way with a single central vessel going in each direction, and the heart evolved from a portion of the vessel. the liver as part of the digestive system has a similar reason.

One of the easiest answers to the question; "Why do we have ____?" is "Because our ancestors did". This is not trivial or flippant, as it is a significantly important answer that is so often overlooked. Humans are members of Bilataria; a deep branch of the animal tree that is characterized by bilateral symmetry. Humans are typical of other vertebrates in having two kidneys. Selective pressure to reduce to one of two organs is typical in snakes, whose body form favors reduction. But even snakes have two kidneys. Natural selection does not reduce features we don't need unless such a reduction would increase fitness.

So are you saying it would cost more energy-wise to evolve to one kidney and possibly restructure the body than it would save to only have to grow and maintain one?

Its about dying before you can produce all the offspring possible. So if the second kidney does not kill you, there would be no need to optimize the numbers. How would a single kidney result in more offspring? "Energy savings" would be pretty slim.


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Identification of Unknown Insects found in landfill (tiny, full of hair on body)
Could someone help me to identify the following insect with full hair on body? They are very small, so I use macro lens to capture them. I have tried to capture them as clearly as possible.

They were collected from a closed section of Tseung Kwan O Landfill and Clear Water Bay Country Park of Hong Kong. This area is revegetated so the ecology is much like a country park just nearby the landfill.

Were they found in landfill debris or in a natural setting? They are very similar to the larvae of beetles in the Dermestidae family (carpet beetles),  which are known to feed on decaying organic matter. Adults are easier to identify. If you can keep them alive in a warm, moist environment and feed them until they form adults, then you can post photos of the adults.

They were found in natural setting, the site that is similar to forest with tree planted. While there are decaying matters deep down in the soil as the site was used as landfill previously, because the gas analysis shows that there is no gas leaking from decayed matter (methane, CO, H2S etc.) I am not sure if the environment flavour the growth of Dermestidae.

Can you explain why you need to identify these insects? For example, do you need to understand their ecosystem function with respect to landfill processes? Are they very abundant in the collection location?

I agree with @prefectionist , they look like carpet beetle larve


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Have some humans evolved to be less attractive to mosquitoes?
https://www.youtube.com/watch?v=38gVZgE39K8 at 10:10 minutes in the video.
It has been found out that single letter differences in people's genomes at specific locations have affected their attractiveness towards mosquitoes. This means there might be a possibility that some humans might have evolved to be less attractive to mosquitoes. Does any proof exist regarding that?

We now know based on a twin study that attractiveness to mosquitos is heritable (with a fairly high heritability of 0.62). Based on a genome-wide association study (GWAS) [which is probably the study referenced in the youtube video] we have found some of the genetic loci that control attractiveness; in particular, 15 single-nucleotide polymorphisms (SNPs) relating to (self-reported) attractiveness, were discovered in the latter study. These SNPs were in regions of the genome related to the immune system (which isn't surprising since immune system genes are closely linked to human odor profiles).
However, figuring out (a) whether these genes have been under selection (by looking for signs of genetic hitchhiking or unusual ratios of synonymous to non-synonymous substitutions) and (b) whether that selection is due to mosquito avoidance will probably a great deal more work - and may be very difficult given that the immune system is under selection for many different characteristics simultaneously ... the GWAS study says its results

illustrate the complex genetic and immunological landscapes underpinning human interactions with mosquitoes ...


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Tumour cell injection into a mice
I am going to inject mice tumour cells into mice to create them tumours and I am wondering if I need to have special precautions for that, even they are cells from mice tumour I am afraid what can happen if I inject myself by accident, I guess is not necessary to do it a hood either?

I hope you understand from the answers and comments that injecting mice (or any other thing) with live tumor cells is not without serious risks.

You should not be asking random people on the internet about this. Talk to your lab safety people. Get detailed instructions on handling requirements. As for the hood, again, do not ask here, ask your animal care people (IACUC or equivalent).  If you don't have both lab safety people and animal care people immediately available and involved before the experiment begins, you should not be doing this experiment.

And you will most likely need a permission by an ethics comission.

IACUC is an ethics commission. If humans are not being experimented on, there probably won't be a need for a second ethics review.

Ah, I didn't knew this abbreviation. But since I have seen people who wanted to start immediately, I thought I mention it briefly...

+1 This is occupational safety and health for labs 101: If you develop a procedure, it needs to be reviewed to ensure the proper personnel, training, controls and PPE are available. Before you perform the procedure!


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In what does Genetic clustering and Cline sharpness differ?
They are  both ways to measure divergence in species but I'm not understanding in what exactly the differ if both use hybrid zones and gene frequencies in the study.

The concept of cline sharpness is not a common one to my knowledge. I suspect you encountered this concept in a hybrid zone literature. Can you please link to the paper where you found those two concepts.

I am voting to close as unclear because we would need the original text on which you've encountered those terms.

It's in the first chapter of "Ecological Speciation" from Patrik Nosil pp 5. He gives examples on measures of divergence in the first table. The examples are from Jiggins and Mallet 2000; and Barton and Hewit, 1985.

Clustering and Clines are two fundamentally different approaches to target the population structure problems. Because many results in classical population genetics are derived from a panmictic population, it is natural to extend them to multiple panmictic populations with some degree of gene flow in between, such as Wright's Island model and Kimura's Stepping stone model. In these discrete models, we view each subpopulation as a breeding group and hence the clustering algorithm can be used to a large number of individuals to classify them based on which subpopulation they belong to. It is 100% valid if the real population is actually discrete (such as in Galapagos), but not so if the real population is distributed continuously in space. In the latter scenario, cline may be more appropriate to describe the spatial variations of the population.
You can check Montgomery Slatkin and Nick Barton's papers on cline theory back in 1970s and 1980s to get the details, but the general property of a cline is that if divergent selection is the primary cause of the cline, then the cline steepness is proportional to the selection differences, but there is a characteristic spatial scale of variation $\sigma/\sqrt{s}$, below which any spatial structure will likely to be swamped by dispersal ($\sigma$ is the mean dispersal distance of an individual, and $s$ is the selection intensity).So Even if the cline is a step function, which is not realistic at all, the cline will still be of finite steepness. As long as $\sigma$ is not zero, you will not get a clear-cut boundary between the two sides of the population, thus invalidating the assumption of clustering algorithm. However, although clustering is not very rigorous in a continuous population, we can still use it to make qualitative explorations of our genetic data and population structure, in fact many people prefer to use that because they are conceptually clear and easy to manipulate in a computer.


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Why can Anaphylaxis lead to death?
Why can the immune system kill its host?
It is always better to just take up the insect poison, or peanut protein etc. instead to kill the host by preventing the breathing.
Is it just a modern symptom or did humans always have to fear death from anaphylaxis after an insect sting?


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Appearance of Karyotypes in educational material
Most actual karyotypes online appear as single chromosomes (unreplicated). I was under the impression that a micrograph of the replicated chromosomes was taken during metaphase of mitosis and thus should show up as duplicated sister chromatids instead of single chromatids post anaphase.  Are the arms of the chromatids just so close to each other that they are hard to distinguish?

Many karyotype images, especially those used for introductory educational purposes, have been edited to show a regular human 2n. For example this image has been edited to depict a regular 2n (46) compliment of human chromosomes.

While this image is unedited and shows the replicated homologous pairs in metaphase:

So the first image you supplied does not show replicated chromosomes consisting of two chromatids for each of the chromsomes in the first pair?

Correct, the first image shows the normal 2n of 46 chromosomes arranged in 23 homologous pairs. The second image shows the replicated chromosomes at metaphase with the sister chromatid pairs arranged in tetrad with their homologues. If you look closely at the second image you can even see the centromere holding the sisters together.

This is incorrect; both images have been edited (to form pairs), and both are from cells in metaphase, which therefore have sister chromatids present.  (One is human and one is bird.) Both have chromosome images which clearly show the pinched waist caused by the centromere.  Some show the division between the chromatids, but the contrast in the second makes this easier to see.

I don't see the difference either

Can you add your sources to the figures?

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Dealing with Repetitive Bases in DNA?
I have been given a project involving a plasmid that contains long stretches of Adenine (60 or 120 bases each). These PolyA stretches are interrupted by the occasional G or C.
I understand that performing PCR, cloning, DNA synthesis, mutagenesis, and sequencing on repetitive sequences is difficult. What techniques and practices should I follow to improve the accuracy when dealing with these PolyA sequences?

What exactly are you trying to do with this plasmid (more spef. this PolyA tail). Do you need to amplify it, digest it etc... depending, different strategies can be implemented to minimize error with the polyA tail

@AdamRadekMartinez Let's say I wanted to replace those interrupting G's with an A. How does site directed mutagenesis work when you have more than 1 potential site? How do you sequence the DNA to verify that the mutation worked?

You can use much longer primers (up to 70bp or so), such that they span the repetitive region you want to change and some more specific sequence to anchor the primer (assuming your vector allows). If the multiple sites you want to change are within range of one another, you can order primers with 2 or more mutagenised sites - though expect your efficiency to drop. Your other option would be to do multiple rounds of mutagenesis, altering one position at a time.
I would then simply try these primers on a gradient PCR using a good enzyme like NEB's Q5. Trying to find a temperature for the correct size band will likely be key.
The real problem you're going to have though probably isn't the cloning, it'll be proving it. Homopolymer stretches are a real problem for sequencing, and the longer they get the worse it is. Automated sequencers find it difficult to tell between, for instance, 29 Adenines, and 30 adenines in a row. When your sequencing results are returned, if your sequencing is off by a base or two, it will be pretty much impossible to tell if your sequencing was wrong, or your construct was.

Okay, one of the main problems with polA tails is with PCR, which is a method commonly used in molecular cloning, specified mutagenesis etc...
One problem with PolyA tails and PCR is with the primers. Since A's only have 2 hydrogen bonds, instead of 3, this can make it hard to design good primers in this area. If you want to amplify this region using PCR, you may have troubles designing primers since it is recommended that you have a lot of G and C's (espically near the ends for stability). Thus, creating blunt ends, mutagenesis etc will be more difficult.


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Recombination frequency
From Campbell Biology 2017, unit 15, test your understanding question 5:
Using the information from problem 4, scientists do a further testcross using a heterozygote for height and nose morphology. The offspring are tall upturned snout, 40; dwarf upturned snout, 9; dwarf downturned snout, 42; tall downturned snout, 9. Calculate the recombination frequency from these data.
Why is the correct answer 18% and not 22%? My reasoning is that you should do a 9 + 9 = 18 and 40 + 42 = 82, and then do an 18/42 = 22%.

If you post this sort of question, like any other question, it must be self-contained. This question refers to a problem in a text book, so is only comprehensible to someone with that text. Hence it is off-topic here and I have voted to close. Please take the tour and read the help on asking questions before posting again.

For recombination frequency you have to consider the whole population of the offspring (not just the offspring that got not recombinated), means 40 + 42 + 9 + 9 = 100. Then you have 18 recombinants, and your recombination frequency goes with 18/100 = 18%.


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Identify the bird
Please identify the birds and tell about its details

I found this bird in Hyderabad, India

Why those downvotes?

That is an Australian shell parakeet, or budgerigar. It is a type of seed eating parrot native to Australia. They live a nomadic lifestyle, and inhabit scrublands, open woodlands, and grasslands. They are good mimics -- considered to be one of the top five talking species. Very commonly sold in pet shops. There is an entire Wikipedia page dedicated to it:
https://en.wikipedia.org/wiki/Budgerigar

I found this bird in India not Australia

The species is distributed across the world as a pet. Sometimes they escape or are purposely set free. If the local climate is suitable, they can survive and even establish local colonies. For example, books on Florida (USA) birds include the budgerigar (e.g. Florida's Birds: A Field Guide and Reference). It would not be surprising to find them in India.

The bird was stranded at my house and I have rescued it and put it in the cage and the bird keeper said them to be the love birds so I purchased an another male bird of the same kind and kept them together.... And unfortunately the next day morning they both died ...... I didn't know the exact reason of this incident.....can anyone help me out with this...!


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Which eradicated viruses still have remaining stockpiles?
Other than smallpox, I'm curious to know if there are any other stockpiles of eradicated or nearly eradicated viruses, and if so where are they located?
Thank you.

I'm voting to close this question as off-topic because it is not about biology but about social policy.

If you ask this question on the history or politics stack exchange sites, I'll answer it for you ;)

again, I don't think this information would be publicly available in many cases because rogue nations involved in developing biological weapons would likely keep their research a closely guarded secret.

There are only two eradicated viruses, and one "nearly eradicated", and all have known stocks. For the purpose of this question, it's completely irrelevant to talk about "rogue nations"

Only two viruses have been eliminated in the wild to date: Smallpox (humans) and Rinderpeste (cattle). As the question notes, smallpox stocks still exist. So do Rinderpeste stocks; see Identifying and Reducing Remaining Stocks of Rinderpest Virus, which is from 2015, but has no indication that the stocks were to be destroyed in the near future.
The only virus that is "nearly eradicated" is poliovirus (human) and there are still many stocks of polio, although organizations are working on reducing their number ("Toward Eliminating Poliovirus—In the Lab).

Thank you so much for this information--it's exactly what I was looking for for my med school presentation.  Do you also know if there are any established stockpiles for other, non-viral infectious agents that are becoming progressively eradicated (e.g. Plasmodium falciparum, Dracunculus medinensis, Treponema pallidum pertenue)?


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Modern Classification of Introspective Psychopharmacological Drug Profiles?
In the effort to better relate neuronal mechanisms to states of mind, it makes sense to have - in addition to pharmacological classifications of drugs and imaging/physiology classifications of their effects - classifications of the states of mind they evoke, according to introspective reports.
I have been unable to find such a data-driven classification in the literature (I would imagine a cluster analysis of reported terms, or a factor analysis of ratings on statements could be appropriate). Instead, "subjective effects" classification seems to be restricted to single-substance profiling, and elsewise is remarkably top-down - based on ad hoc models by the same authoritative people or entities which commonly make psychoactive substances available to consumers (introducing confirmation bais). I'm wondering if there's anything else out there?

A couple things...1) This might be better suited for psychology.SE, and 2) I think you might be having too high a view of the state of neuroscience. Very few psychoactive drugs are truly understood from an imaging/physiological/pharmacological nature; they are pretty much all classified by their effects. Consider anesthetics, for example. Drugs like propofol, isoflurane, etomidate, etc have diverse chemical and pharmacological profiles - we group them because they cause anesthesia.

What you suggest could be done but I ponder on its usefulness. Say we relate mood swings with 60% serotonin and 40% GABA. Does that mean that if we have mood swings we adjust our serotonin and GABA levels accordingly? I think modern neuroscience is aiming at a more in-depth understanding. I suggest instead that we'd need to know which circuits it up- or down-regulates.


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Is the human lifespan still expanding?
Description
200 years ago, the human lifespan was roughly 35 to 40 years long. And it has doubled in length since then.
Question
Will the human lifespan continue to expand in length?

Is this question about maximum human lifespan, or about population lifespan as health and general living conditions improve?

@GrahamChiu it's a question about whether it's still expanding or if it's at it's maximum length.

And what does it refer to?

@GrahamChiu the human lifespan...

So, you're asking about the maximum life span any human might attain? Like a 4 minute mile.

@GrahamChiu yes.

If you mean to ask whether or not humans will be able to continue increasing their life expectancy without an upper bound, the answer is no.  If you're asking if people live longer now than in the past and whether we can expect to see further increases, I'd guess that the answer is yes for most of the developed world, with the exception of the United States.  The same is probably true for most of the developing world; it would definitely be true in the developing world if western corporations started paying them fairly for their labor or resources, but that's getting into an answer for a different stack exchange website.
I suppose I should qualify the "no" to unbounded life expectancy, because it could come down to definitions of alive.  I don't think that it is outside the realm of possibility for science to provide techniques to artificially extend life; if we can start growing organs in labs, we might be able to just go change out our heart or kidneys much like we take our cars to have the tires changed. If you could figure out a way to take care of the circulatory / nervous system, too, who knows?  As it stands, though, our cells have an upper limit on the number of times that they can reproduce because we don't have enough telomerase in somatic cells to prevent the eventual shortening of telomeres (special sequence of base pairs located at the ends of DNA molecules) to the point where they no longer protect the DNA during replication and the cell eventually dies as a consequence. Hell, if we could just figure out how to take care of that we could probably chalk on some extra time - then we can see which system would be next to fail and take us out.

And drugs to lengthen telomeres?

You will find here on the UN World Population Prospects plenty of data and visualization about change in life expectancy over time (among other things). The data also include predictions until year 2100.
For example, here is the life expectancy data and predictions over time for men in Morocco.

and here it is for women in Norway (note that x-axis range differs between the two graphs)

I picked two random countries but the general trend is very consistent among countries.

Is the human lifespan still expanding?

Yes, life expectancy is still increasing in pretty much all countries and is expected to keep increasing.

What about maximum life span?

@GrahamChiu What do you mean? Are you asking about the change in the maximum lifespan through time or maybe about whether a theoretical asymptote should exist?

@Remi.b Not sure what is motivating the comments/question here but there was a recent paper (could be 5 years old now maybe? or older, time goes fast) that made a statistical argument that maximum lifespan reached a peak some years ago and has not risen since. That is, all gains in life expectancy since then have come by delaying earlier deaths, with no effect on prolonging the longest lives, and that new supercentenarian records are only because of increasing world population and nothing more. Sorry I don't have the reference.

There were also papers in response rebutting the original argument.

It might have been this one: Dong, X., Milholland, B., & Vijg, J. (2016). Evidence for a limit to human lifespan. Nature, 538(7624), 257. I'd also add that in the US life expectancy has dropped over the last couple of years. That doesn't necessarily mean the trend is not positive, of course.

Lifespan has obviously increased so I thought the question was asking about limits to maximum life span through time.  has that remained static since the appearance of the modern human?

@BryanKrause there's also this one, which I remember citing before the Dong paper came out: ( https://link.springer.com/article/10.1007/s10522-008-9156-4 ).
When I ask questions like this to my mentors (I'm an undergraduate and have been working with aging for the last ~3 years), I usually get some variation on a long sigh. We can make other animals live a LOT longer than normal. And humans have been living longer on average, but our maximum hasn't changed much. Lifespan, especially human lifespan limits, is a really hard-to-pin-down thing.

Whilst the graphs show rising life expectancies the rate of growth appears to be slowing, ie would (were this purely a matter of statistics/mathematics) reach a peak and analysis might reveal when and how high. Of course it is not purely statistical; the underlying reasons for the rise are an accumulation of better food, living practices and medicine. Food and living practices are likely to reach a peak for extending lifespans - in places may have peaked already. Medicine remains a wild card that could deliver more, but not necessarily across the whole population.


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Using cell concentration
I am doing an experiment in which I plate for example 3x10^5 cells, and every day I have to count the cells growing. I find the number and a convert it in x10^5. In my graphs I have to use the cell concentration. I am not sure which units are used for cell concentration. Is it ml, μl or anything else?

This site is for questions about biology. Your question is a basic question about units which you could find by an internet search. The units you cite are units of volume. You have my sympathy if you don't know what concentration means but you'll have to find out elsewhere.

Use cells/mL, I find it easier to discuss that way. Also look at it like this: Cells grow exponentially, so you can express your concentration axis on a log scale.

@David Thank you but you could answer more politely:)

What is a concentration
A concentration of cells is the number of cells per unit of volume.
You are free to choose the units you like
It is very much up to you to chose the units you want as long as they express a concentration. There is no right or wrong.
You can express your graph in cells per liter or in 100,000 cells per $\mu$l or in billions of cells per ml, all would be correct. Of course, some are more intuitive than others. I would advice you to avoid expressing in cell per square meter or in billions of cells be nanoliter because the numbers will be very small and very large respectively and will not convey much intuition.
A good intuitive unit
I don't know what kind of concentration you have in you data but a priori, I would recommend expressing your concentration in cells/ml is quite intuitive.

Really! If you respond to this sort of question the site's quality standards may not be met any longer

Yes, I agree with @David. Not every question deserves an answer.

Every question deserves an answer please think out of the box!:)

@Claudia In fact, not every question deserves a question. Some questions that are too broad, unclear, not about biology, do not show any effort and others are typically considered as off-topic and should be closed here. I personally considered your question very introductory and by its nature only remotely related to biology but I'd have a hard time to imagine where you'd ask your question otherwise, so I decided to answer it. But it was a little bit of a limit case in my opinion. Anyway, if you think I've answered your question, you can click on the check mark.

@Claudia btw, it is usual to get its question closed when you arrive on stackExchange. It takes a bit of time to learn the rules here. Welcome to Biology.SE.


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Genes & Map Units
Two genes of a flower, one controlling blue (B) versus white (b) petals and the other controlling round (R) versus oval (r) stamens, are linked and are 10 map units apart. You cross a homozygous blue oval plant with a homozygous white round plant. The resulting F1 progeny are crossed with homozygous white oval plants, and 1,000 offspring plants are obtained. How many plants of each of the four phenotypes do you expect?
The answer is: 450 each of blue oval and white round (parentals) and
50 each of blue round and white oval (recombinants).
Here's how I solve it: BBrr (homozygous blue oval) X bbRR (homozygous white round) gives four times BbRr (heterozygous blue round). Then BbRr (the resulting F1 progeny) X bbrr (homozygous white oval) gives BbRr, bbRr, Bbrr, and bbrr. I don't get how the numbers 450 and 50 are related to the 10 map units apartness, but BbRr (blue round) and bbrr (white oval) are parentals.
Source: Campbell Biology 2017, page 313.

According to my book, a map unit is a unit of measurement of the distance between genes. One map unit is equivalent to a 1% recombination frequency.

What is the definition of map unit according to your book?

@LinuxBlanket, I'm Viktor but I have to have at least 50 reputation to add a comment.

Related: Genetic linkage greater than 50 centimorgans

I don't get how the numbers 450 and 50 are related to the 10 map
  units apartness,

Understanding how to use the map unit information is the point of the question.
If the B and R genes were unlinked, a gamete with the B allele would have a 50% change of having the R allele, and a 50% chance of having the r allele.  It would just be luck which chromosome went in to the gamete with the B-containing chromosome.
But in this question, the B and R genes are on the same chromosome.  Given the breeding scheme, the F1s have one Br chromosome, and one bR chromosome.  Unless crossing over happens, the gamete that gets B has to get r as well.  Crossing over happens 10% of the time.  So instead of the gametes BR, Br, bR, br all being equally likely coming from the F1, their odds are actually 5%, 45%, 45%, 5%.

The two chromosome copies that bear the alleles in the F1 are
B-{10 map units}-r  -  Blue oval
b-{10 map units}-R  -  White round

As you said, one map unit is equivalent to a 1% recombination frequency. Ten map units = 10% recombination frequency. It means that the progeny will have a blue round/white oval phenotipe only 10% of the times, while 90% of the time it'll show the parental phenotype.
Hence the 450/50 (90%/10%) proportions of the F2.

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


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Why is suicide inhibition considered a catalytic reaction when the catalyst is irreversibly modified because of the reaction?
I understand that this might be meaningless semantics, but I'm confused and would appreciate clarification.
I've always been taught that, a catalyst is, by definition, a substance that is increases the rate of a reaction but is not consumed by the reaction. Enzymes are a subset of catalysts, so all enzymes must share catalyst properties. From my understanding, suicide inhibition irreversibly modifies the enzyme and consumes it during its normal catalysis reaction.
How can an enzyme that is consumed during its normal catalysis reaction still be an enzyme? Wouldn't it make much more sense to call it a reactant?

People are people. If you give them strychnine they die, but they are still people. Enzymes are enzymes, if you poison them with inhibitors they ‘die’, but they are still enzymes. Yes this question is meaningless, and it hardly justifies the description of semantics. And next time you post, please read how to ask a good question first and quote your sources, not your understanding.

It's not clear what the confusion stems from, but perhaps it was from the first sentence of the Wikipedia article, which says:

Suicide inhibition ... is an irreversible form of enzyme inhibition that occurs when an enzyme binds a substrate analogue and forms an irreversible complex with it through a covalent bond during the normal catalysis reaction.

This might mislead someone by using the phrase "during the normal catalysis reaction", which I suppose could be interpreted as saying the enzyme only catalyzes reactions involving the inhibitor.  That is very much not the case.
The normal action of the enzyme is with some other molecule, the normal substrate of the enzyme, and the catalytic reaction produces and release the product, leaving the enzyme in its original form.
In contrast to this, the inhibitor is an analogue of the normal substrate molecule, that is to say, a molecule which is very similar (in the target region at least) to the normal substrate molecule.  Because of the similarity, the enzyme will cause the inhibitor to undergo the same chemical reaction as the normal substrate. However, the inhibitor will thereby become active in a way which causes it to irreversibly bind to the enzyme and thus, unlike the normal substrate, will never be released.


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Is one single antibody binding its antigen enough to elicit an immune response?
IVIG (intravenous immunoglobulin) is derived from plasma of more than 1000 donors. I wonder if in this preparation is one antibody present that recognize its antigen after infusion - if this is enough to elicit an immune response? Thanks

This is a wonderful question, because it addresses a common misunderstanding.
Short Answer: We have no clear data about the effectiveness of a one single antibody molecule in the immune response of an entire organism, but since many different antibodies can recognize the same pathogen, and . Just as antibodies in a healthy individual are able to find, bind to antigens, and produce an immune response, antibodies from transfusions of IVIG can do the same. They can block, opsonize, activate complement, and regulate B-cells and T-cells.
Long Answer: Surprisingly, brilliantly, our innate immune system is able to generate transmembrane and secreted proteins that bind every possible antigen (or almost every possible antigen, depending on who you ask). See my answer to this earlier question, and the associated general references. We get very excited when we teach this. With our focus on teaching the diversity of antigens and binding regions, it is easy to get the idea that there is a single unique antibody for every possible microbial invader. For students that really take in the problem of antigen diversity and the solution of antibody diversity, this question, or some variation, often follows: how can a single antibody ever do any good? Usually, with some wonder about how to quantitatively match up this diversity with any specific pathogen. This is an example of that question. Here is the answer:
Many different antibodies can recognize a pathogen
A single pathogen has many many antigens, or molecules that, e.g., an antibody could bind to. A single antigen has many epitopes, or specific binding sites for an antibody paratope (the part of the Fab region of an antibody that is specific to the binding site). A single paratope can bind more than one epitope. This is called cross-reactivity. Additionally, a single epitope can be bound by more than one paratope. A good discussion of this principle can be found in Chapter 4 of Frank's Immunology and Evolution of Infectious Disease.
Antibodies are produced in massive quantities
Lauren Somparyic, in How the Immune System Works, estimates that, in the pre-immune state, of the roughly 3 billion B-cells, a single clone is comprised of about 30 cells. Each clone contains many copies of the transmembrane version of its single antibody, and many different clones (as discussed in the paragraph above) will recognize a single pathogen. Once exposed to a pathogen, B-cells that recognize it divide many times over, undergoing a series of changes beyond the scope of this question. At the end of this process, plasma cells, the B-cell progeny that produce secreted antibody, then each secrete hundreds to thousands of antibodies a second. Without ongoing antigen stimulation, many of the plasma cells die, but long lived plasma cells migrate to the bone marrow and continue to secrete enough antibody to allow for the rapid response seen in a subsequent exposure to the same pathogen. The majority of antibodies in the blood of a healthy adult come from these long lived plasma cells in the bone marrow. You can read about this process in chapter 3 and 10 of How the Immune System Works and chapter 7 of Abbas Basic Immunology. Essentially, the circulating antibodies in the $\gamma$-globulin fraction of plasma contain large numbers of each antibody produced in response to exposure to a pathogen. Because of this, we don't have to wonder how one lone antibody in the vast expanse of an organism can be effective in response to many pathogens. We have many, many antibodies that can do this.
IVIG
IVIG is from, as the OP states, pooled samples of antibodies from many thousands of blood and plasma donors. 75% of these are IgG antibodies, meaning they've already undergone class switching and are a result of exposure to antigen. I'm not aware of a good study that clearly catalogues the populations of different clones in IVIG samples, but we can say the set of antibodies in IVIG represent the collective immune memory of the population from which it was pooled, but behave in a similar way to the circulating antibodies in a healthy adult.  You can read more about this here and here. Because of this, the same principles discussed in the above paragraph apply here. We don't have to worry about the lone antibody lost in the massive sea of the human body. Even pooled from thousands of donors, each dose of IVIG contains many, many antibodies that can recognize each important human pathogen.
Transfused antibodies retain their effectiveness
There are a variety of clinical uses for IVIG, but there is clear evidence that the antibodies in these samples retain their effectiveness in their roles as effectors of the immune system. Not only are the antibodies in IVIG effective at blocking and neutralizing pathogen receptors and toxins, but they activate and clear complement, opsonize pathogens and damaged cells for clearance by neutrophils and other phagocytes, control and regulate the B cell population, and interact with the T-cell population, much as they do in the healthy individuals who haven't been given IVIG. The NEJM article I linked above discusses much of this (though it focuses on modulation), this review, which you can access without a paywall, also discusses this.

Generally we think of this as "passive immunity" in which the antibody does not necessarily initiate any immune response.  It may simply inactivate its target. However, sometimes inactivating the target might require the antibody to activate complement and/or trigger phagocytosis. In any case, I thing the answer to the question is "No," assuming that the target is more than one cell, virus, or toxin molecule.

This is the start of an answer but needs more details and sources.

Antibodies in IVIG have both their Fab and Fc regions. They can do more than just bind. The can certainly generate an immune response.


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How do cells relocate transmembrane proteins from one side of the cell to the other? Is it possible?
Is there a process by which cells can relocate proteins residing on the cell membrane in areas of low demand to that of a high demand location somewhere else in on the cell? What's that process called?
Through protein catabolism, cells can break down the proteins into their individual amino acids and then reuse these resources to build new proteins in needed locations. This process seems inefficient if the cell simply needs to move a transmembrane protein (for example integrin or cadherin) from one side of the cell to the other.
I hope the question is clear. I haven't taken a biology course since early high school (8 years ago) so if there's something i need to clarify let me know!

Transmembrane proteins can move laterally through the plasma membrane (see fluid mosaic model) and this movement can be actively directed along the cytoskeleton. The following paper is the most salient example that I found of transmembrane proteins moving from one side of the cell to the other:
Moss WC, Irvine DJ, Davis MM, Krummel MF. 2002. Quantifying signaling-induced reorientation of T cell receptors during immunological synapse formation. PNAS 99(23):15024-15029.

Productive T cell recognition of antigen-presenting cells (APCs) is normally accompanied by the formation of a cell–cell contact called the “immunological synapse.” ... T cell receptors are recruited in bulk within the first minute after the onset of activation...

The following figure, adapted from the paper, shows the time-lapsed movement of GFP (ie fluorescently) labelled CD3, which is part of the transmembrane T-cell receptor complex, during synapse formation with an APC:

Time is in minutes, and zeroed at first contact between the two cells. I've put a red dot on the T-cell and a blue one on the APC in the DIC images (left panes); hopefully that proves more informative than annoying. The right panes show GFP fluorescence and thus CD3 localization. As time progresses, CD3 is re-localized from one part of the membrane to another (the synapse). There is supposedly a video of this is in the supplementary information of the article, though I was unable to open it.
The rate and directionality of the movement implies that an active process is occurring, rather than simple diffusion. However, they did not find the actual mechanism for movement and I haven't found any follow-up papers in a brief search (though many subsequent papers implicate the cytoskeleton in this movement). Just to show that movement of transmembrane proteins can, in fact, be actively directed by the cytoskeleton, I refer you to this paper:
Grabham PW, Foley M, Umeojiako A, Goldberg DJ. 2000. Nerve growth factor stimulates coupling of beta1 integrin to distinct transport mechanisms in the filopodia of growth cones. J Cell Sci 113:3003-3012.
They show that membrane-spanning integrins are moved along actin filaments of the cytoskeleton by myosin motor proteins. Expectedly, the abstract does a good job of summarizing the paper:

The cycling of membrane receptors for substrate-bound proteins via their interaction with the actin cytoskeleton at the leading edge of growth cones and other motile cells is important for neurite outgrowth and cell migration. Receptor delivered to the leading edge binds to its ligand, which induces coupling of the receptor to a rearward flowing network of actin filaments. This coupling is thought to facilitate advance... [T]ransport was dependent on an intact actin cytoskeleton and myosin ATPase...

Here's a few more papers I found, but did not use, in case anyone is interested: one, two, three.

@BryanKrause Thanks! And likewise, obviously; I thought they’d work hand in hand.

As this is my first question I've asked on this site, I am VERY impressed with the quality of the answers, thanks! My lab has seen hints of this happening when using epithelial cells with fluorescent labeled E-cadherin protein. When stimulated on one side with external E-cadherin protein, it seems the E-cadherin inside the cell decreases in areas far away from the stimuli and correspondingly increases in the area of the stimuli.

@SethH You're welcome, and that sounds like an interesting experiment.

The breakdown and reassembly of proteins is a ubiquitous process within cells, and yes this is expensive but transport is expensive, too, and recycling has the added benefit of dealing with proteins that become misfolded or otherwise damaged as well as allowing for transcription and translation to regulate overall protein levels. The Toyoma & Hetzer 2013 review (see references below) cites estimates of the median protein half-life in a non-dividing mammalian cell to be about 43 hours, though they discuss some exceptions that do last much longer.
However, it is possible to relocate transmembrane proteins via vesicles.
Essentially the same way proteins are put in the plasma membrane in the first place, but in reverse. Endocytosis is often taught as a way that cells (often macrophages are used as an example) take in materials from the outside world, but it is just as applicable to internalizing chunks of membrane. Nature has an entire 'web focus' on entocytosis reviews.
One situation where this happens is in synaptic plasticity; receptors can be internalized or trafficked to the membrane to decrease or increase the potency of that synapse, respectively (see Carroll et al., 2001), but similar processes occur all over (and some proteins constantly cycle back and forth; see Trowbridge et al. 1993 for a more general review, though a bit dated).
However, to your specific question, I don't know specifically of examples where transmembrane proteins are literally cycled from one side of the cytosol to the other. There may be examples I am not aware of, but my understanding is that it is more typical to think of a "store" of certain proteins in endosomes, from which they can be trafficked to the membrane and reinserted via exocytosis. Probabilistically, some will be transported from one place to another, but not so much in a stepwise fashion.

Toyama, B. H., & Hetzer, M. W. (2013). Protein homeostasis: live long, won't prosper. Nature Reviews Molecular Cell Biology, 14(1), 55.
Carroll, R. C., Beattie, E. C., von Zastrow, M., & Malenka, R. C. (2001). Role of AMPA receptor endocytosis in synaptic plasticity. Nature Reviews Neuroscience, 2(5), 315.
Trowbridge, I. S., Collawn, J. F., & Hopkins, C. R. (1993). Signal-dependent membrane protein trafficking in the endocytic pathway. Annual review of cell biology, 9(1), 129-161.


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How does one calculate Rx/a in population genetics?
The ratio of sex-linked to autosome mutation frequencies (R) is Rx/a =(2/3)(2+ α)/(1+ α) for X-linked genes and Ry/a = 2 α /(1+ α) for Y-linked genes. How does one calculate Rx/a, in order to find α?


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DNA replication during Mitosis
I am a bit confused.
During Meiosis, DNA is replicated to form a cell with half the DNA and likely to have variations.
But since the replication process of meiosis and mitosis are the same, why do DNA in different cells of an individual organism not have variations? Or do they have variations that are just not expressed?

Welcome to Bio.SE! In order to ask a good question, you are expected to show some research effort. Did you try googling "differences between mitosis and meiosis"? It could lead you to the answer!

Individual cells do have variations, those are just not inherited as during mitosis you don't produce gametes.

So can DNA in hand skin cell and leg skin cell be same

Think of Meiosis as a means of producing half the genetic material you (and your partner) need which, once combined, produces offspring that inherits genetic material from the both of you. Think of Mitosis as a means of producing a full, exact (as exact as possible anyway) copy of chromosomes during cell division =)
Meiosis - results in a cell with half the genetic material (haploid), which is later fused with a similar haploid cell from the opposite sex (gametes) to produce a single cell with a full set of chromosomes (diploid cell). I.e. a sperm and an egg (each haploid) which fuse to produce a zygote (diploid). Important to note that during Meiosis, there is cross over between chromosomes, so that you end up with genetically diverse gametes (i.e. each haploid cell is different to one another - part of the reason your kids don't all look exactly the same).
Mitosis - results in a cell with a full genetic copy of the cell it was replicated from. That zygote will replicate using mitosis again and again until the organism dies. During Mitosis the cell tries to preserve as much of it's integrity as possible, so there isn't cross over. But the process isn't perfect in humans - each division results in shorter telomeres, and a cells also accumulate mistakes that result in "bad code" being passed on - UV damage for example.
With regards to expression, there is the concept of epigenetics - you may inherit certain genes, which (through various mechanisms) will be "locked" and not expressed in yourself, but may be expressed in your children. You might notice that kids have characteristics of their grandparents which aren't present in their parents.

In meiosis crossing over takes place which leads to variations
 in chromosomes while in mitosis no crossing over takes place


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Breathing with Clogged Nose during Sleep
This just happened to me recently, I was trying to sleep with clogged nose, so I tried breathing through my mouth. As you can imagine it was hard, but I managed to sleep deeply.
So I became curious, how does our body know whether to breathe through the nose or the mouth especially when we have a clogged nose during the time when we are in deep sleep?
NOTE: I tried researching this, but most result just shows how to clear clogged nose before sleeping

Comments are not for extended discussion; this conversation has been moved to chat.

Most people with colds/allergies/stuffy noses don't die in the middle of the night. Why?
Prevention of oxygen deprivation is powerfully regulated. If insufficient air intake is possible through the nose, the mouth opens automatically (regulated by the autonomic nervous system. If you exercise, at some point, nasal breathing isn't enough, and you start mouth breathing. It's not conscious.

The autonomic nervous system (ANS)... is a division of the peripheral nervous system that supplies smooth muscle and glands, and thus influences the function of internal organs. The autonomic nervous system is a control system that acts largely unconsciously and regulates bodily functions such as the heart rate, digestion, respiratory rate, pupillary response, urination, and sexual arousal. This system is the primary mechanism in control of the fight-or-flight response.
Within the brain, the autonomic nervous system is regulated by the hypothalamus. Autonomic functions include control of respiration, cardiac regulation (the cardiac control center), vasomotor activity (the vasomotor center), and certain reflex actions such as coughing, sneezing, swallowing and vomiting. Those are then subdivided into other areas and are also linked to ANS subsystems and nervous systems external to the brain. The hypothalamus, just above the brain stem, acts as an integrator for autonomic functions, receiving ANS regulatory input from the limbic system to do so. (emphasis mine)

The answer is a complex interaction between blood pH and oxygen/CO2 receptors and the autonomic nevous system.

As a point of emphasis that I think is lost to novices of biology, the brain (and the rest of the nervous system) does a lot that you are not aware of - it seems that people often have some intuition about their "subconscious" and they think of all this high-order pseudo-Freudian stuff, but the nervous system is so good at just handling the day-to-day 'boring' nitty-gritty operation of the body that people take it for granted and it just seems magical... Respiration, circulation, digestion, all hardly noticed unless something is quite wrong.


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What is cephalostatic theory?
I just came across this theory while solving problems. I looked for it all over Google but couldn't find the actual theory. I guess I can learn it here.

Name the book in which you found that term pls.

The exact term "cephalostatic theory" apparently does not occur in any results indexed by Google (at least, until they index this question):
https://www.google.co.uk/search?q="cephalostatic+theory". This makes it even more important to know where you came across it, but also are you sure you've gt the right term?

A cephalostat is head holding device used in orthodontic analysis; cephalometric analysis being the clinical application of cephalometry - the analysis of dental and skeletal relationships of the human skull.
Cephalostatic theory then, I would assume, is the body of work regarding that relationship.


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If senescent cells are removed by the immune system, how can they contribute to ageing?
It is said that senescent cells, also called zombie cells, can cause biological ageing.  These senescent cells are also killed by immune cells. It does not make sense as to how they cause ageing if they are removed?

Who says that senescent cells are killed by the immune system? Do you have a source for that?

Here is a review article talking about immune killing of senescent cells....Cellular senescence: Immunosurveillance and future immunotherapy  https://www.sciencedirect.com/science/article/pii/S1568163718300114

here is a link from a blog....https://www.fightaging.org/archives/2016/03/how-the-immune-system-recognizes-senescent-cells/

In an healthy individual, senescent cells are likely removed by the immune system.  However, as we age, our immune system becomes impaired and may no longer be able to kill senescent cells.  Senescent cells can then accumulate and promote age-related diseases.


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What is "integrated spindle activity" in plain English?
From a research article:

To determine if a combination of spindle parameters allowed for a better group discrimination, integrated spindle activity (ISA) was calculated by integrating over time the amplitude of each detected spindle (and by dividing by non-REM sleep duration). We found that integrated spindle activity was markedly reduced in amplitude and number of detections during the first sleep episode in the schizophrenia group in relation to the comparison and depression groups (Figure 3A).

Is this ISA parameter calculated using integrals? I vaguely recall integrating functions in the university, but by now I've forgotten all - that was too long ago. And I don't know how one would "integrate" not functions (like we did in the university) but spindles. And what is the meaning of "over time"?
In short, I'm curious what this ISA parameter stands for. Is there a way to describe it in plain English?

Wouldn't this be subject to variance due to electrode impedance and inter-subject variability? It doesn't appear they normalize these measurements- unless I'm missing something>?

@LindseyCrown For the comparisons they are making it's probably fine to not normalize; in Fig 2A it looks like the spectra overall are comparable across groups. Inter-subject variability doesn't matter because that's the whole point of their comparisons: testing whether the differences between groups are large enough relative to inter-subject variability to not likely be from random chance.

Integrated spindle activity is just this paper's measure of the intensity of spindles. It isn't really a term of art, there is no defined thing "integrated spindle activity," it is just a description for their method of quantifying spindles, or in other words operationalizing their definition of spindle activity.
Spindles are brief bouts of (relatively) high-frequency oscillatory activity that occur occasionally during sleep - often they are called "sleep spindles."
Figure 1 of the paper you link shows their method for detecting and measuring these spindles.

Ferrarelli, F., Huber, R., Peterson, M. J., Massimini, M., Murphy, M., Riedner, B. A., ... & Tononi, G. (2007). Reduced sleep spindle activity in schizophrenia patients. American Journal of Psychiatry, 164(3), 483-492.
In summary, the top trace is a raw EEG trace. Spindles are present in this trace, but the authors want to quantify spindle activity in some way. By filtering between 12-15Hz, the spindles become more obvious (middle): they are the high-amplitude things bracketed by vertical lines.
On the bottom, they have rectified and smoothed the signal to approximate the amplitude of the spindles (that is, they aren't interested in the area under the curve in the middle plot, which has negative and positive going components, they just want a measure of the whole event).
They are defining the integrated spindle activity as the integral (i.e., the area under the curve, just like in calculus) of bouts of activity that exceed some threshold, indicated by the area shaded blue.
In summary, to answer your question, there isn't really a better or simpler English way to say "integrated spindle activity" without losing information for the reader - they are indeed referring to mathematical integration. You could say something like "total spindle activity" but then it is much less clear how exactly you are quantifying spindle activity. Probably the best plain English description of integration is the 'area under the curve' of a function or measurement, though this isn't a perfect mathematical description.
As someone who is familiar with general methods for analyzing electrophysiological data, it was pretty clear to me what they meant by "integrated spindle activity" before opening the paper - this is a fairly common way to report the amplitude of oscillatory activity, because it captures both average amplitude and duration in a sensible way.

A pretty good approximation is to say that they are summing the activity  of (rectified) spindle events, since we are talking about discrete signals.

And what is the meaning of "over time"?

This procedure presupposes that they have identified the beginning and end of a spindle event, hence the integration is done within that interval.
There are plenty of ways to calculate a discrete integral, for example by using Riemann sums or just taking the regular sum, but none of the details matter much for all practical purposes in signals such as those dealt with in the cited paper.


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Why does the pulmonary artery have higher glucose concentration than the pulmonary vein?
If the pulmonary artery have higher glucose concentration than the pulmonary vein, does it mean glucose will be consumed during gas exchange?
That confused me because gas exchange is something like diffusion and shouldn't consume any glucose

So what about the red cells flowing in the pulmonary artery? And its endothelial cells?

@GrahamChiu So during the gas exchange, red cells will proceed cellular respiration as soon as it absorb oxygen?

I didn't say that

I said that because glucose will be decomposed in order to proceed cellular respiration.
Edit: I didn't know that red cells don't have mitochondria

https://biology.stackexchange.com/a/34753/22415

I still don't get it. If glycolysis does not require oxygen, then why glucose will be metabolized during breath exchange? Breath exchange seems have nothing to do with glycolysis.

Lung tissue is living and requires glucose. The answer is correct.

@nongoodnurse the answer should mention the role of the bronchial arteries. As it stands it is misleading.

Gas exchange doesn't but the cells of the tissue it occurs in do consume glucose, even the cells in the walls of the artery will consume some.  The cells in the lungs still need to be fed and only one of those two vessels has flow going into the tissue so it is the one that has to carry that glucose into the tissue.


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Is it possible to produce bread using only microorganisms?
I am wondering if it is theoretically possible to produce bread using only microorganisms. If one lists all the chemical components, proteins fermentation time, etc., is it then doable to combine the needed (engineered) microorganisms in one bio-reactor, let them do their thing and produce the wanted product (bread in this case)? Maybe there is a review paper on this topic but I haven't found it yet.
My background: Molecular biology, I know too little about microbiology and bio-reactors, etc.

What do you mean by "only using microorganisms"? Do you mean with no flour at all?

blue green algae and brown algae might be a candidate, it is already used as a minor source for gluten free bread, you would need to specially breed them however to get the right protein to starch levels

@LinuxBlanket Yes, flour provides the structure of the bread. So I can imagine that if an bacteria species is engineered in such a way that it produces every component of flour then it could be possible to produce bread without flour, right?

I would take this question to WorldBuilding. They love the hypothetical 'What if - how can we" type of questions. And shouldn't any Molecular Bio person have a solid understanding of MicroBio and reactors??? At least in my time, ages ago, I received quite some training in that arena during my bachelor's Biochem

It looks like that yeast has been engineered to produce starch.
First of all, the authors had to knock out the genes responsible for the glycogen metabolism pathway (both glycolysis and gluconeogenesis). Then they introduced eight genes known to belong to the amylopectin biosynthetic pathway. The authors succeeded in having starch granules in yeast.
You could start with this yeast strain to produce your bread. You'll probably need to at least dry them in order to reduce them to some sort of flour (probably a hard one, since the yeast would be rich in proteins); otherwise, some means to purify starch grains from yeast should be devised. Then you'd mix them with water and regular baker yeast and maybe you could obtain a bread-like food!


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What species is this "talking" bird?
This YouTube video shows a bird which appears to repeat some sounds (not speech though) after a human. Here're some cropped screenshots from the video:

What species is this bird? Can it actually mimic human speech, or are these sounds in the video its natural sounds?

A location would help narrow it down.

Unfortunately the only information I have is this video. I wasn't the one who filmed it, so I can't add much information aside from what is contained there.

It is a black-collared starling (Gracupica nigricollis).
According to the title of this other video, which is the same footage uploaded by another user and could be the original one, it has been recorded in Thailand, where the black-collared starling is common.
Also, from the same Wikipedia page:

In Thailand the collared starling is sometimes kept in captivity and taught to speak.


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Is there a way to remove hemoglobin from pig kidney homogenate without deactivating enzymes?
I would like to measure different enzyme activities in centrifuged pig kidney homogenate. I get out of range errors at 450 nm. The samples are still reddish after centrifugation. Is there a way to remove hemoglobin without deactivating / removing enzymes? Thanks!


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Is there any way to tell if a gene is functional for an individual with only a reference sequence and the individual's sequence of the gene?
I have gene sequence of a ton of individuals within a subspecies from cdna and the ncbi IDed sequence as well. Is there any way to tell using just the sequence that the gene for an individual is non-function or only partially functional?

In general, no.  There might be specific cases where you can, like if there is a stop codon, or a frameshift mutation early on, or someone else has seen your exact variant and experimentally proved that it has no function.
But in general, you cannot predict function from in silico data alone.

It is possible to get a prediction of the change caused by a mutation using programs like Sift or polyphen(only for human proteins), but these are only rough estimates

I don't know your level of knowledge, so this may seem very obvious to you, but...

Translating it into the six frames gives you some hints. If the sequence has degenerated and is full of stop codon, then it's nonfunctional.
Align the sequences with Mega or AliView or whatever, then translate them. If there is a frameshift mutation in your sequence, it becomes very visible within the alignment and chances are that the sequence isn't functional anymore.
Find information about the protein's domain in Pfam and look closely to the alignments in the functional domain. If otherwise conserved residues are mutated, this should ring a bell. (Since all your sequences will be very similar to each other, you may want to add some sequences of the protein of other species, so that you can find more easily the active residues within a domain)


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What percentage of a complete Denisovan genomes lives on in the union of the sets of overlapping pieces in extant humans
In studies like this one mapping out distributions around the world or the analysis described in this article (suggesting a contribution from a non-Denisovan but Denisovan-like unidentified hominin to Melanesian populations, various single digit percentages are given of an average as high as 6%.
One complication in talking about this is what we mean by percent. Just through shared DNA we'd have over 99%, if we knew which DNA was shared. There are surely other complications, like how do you count repetitions toward the percentage, etc. But I mean to ask what percentage of  DNA that is DNA descended from introgressions adds up to, if you put together the different and overlapping pieces various people have.
I realize it may also be hard to pin down exactly what one would mean by a Denisovan genome -- as I said one of the linked articles suggests there may at least one Denisovan-like hominin species represented in the introgressions.
Note: Someone already asked this about Neanderthals.


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Vine To Tree Root Grafting
I am experimenting with grafting multiple heartleaf philodendrons(philodendron cordatum) to the root of an oak tree(quercus). If the grafting is successful, the next step is to cut the root from the trunk, cap it, and place it in a long rectangular potter. The experiment to follow this will be to sustain the tree root with the philodendrons, and symbiotically use the philodendrons to sustain the tree root. Does anyone have experience in this type of experimental research and advice to provide?

I don't think this will work. Grafting will usually work between the same species and sometimes between the same genus. You're talking about grafting Philodendron cordatum to Quercus robur. The former is a tree from Europe, the latter a flowering plant from Brazil. They aren't compatible in the slightest. The graft will never take.
One possible route you might want to consider that may be more successful, but a lot more difficult, is using agrobacterium tumefaciens to infect a mix of cells from the two species. If you have a homogeneous mix of individual cells in culture, infect it with A. tumefaciens, the resulting gall will contain cells from both (incompatible) species. How they grow from there is unknown.


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For how long can animal body cells survive outside the body?
I'm researching on the topic that if bacteria have souls then animal cells and plant cells also do for an article.
1) Is there a way to make any of the body cells survive outside the body for a reasonably long time?
2) What is the longest time that human cells have survived outside the body?
3) Can we consider each human body cell as a living thing, the same or more complex than a bacteria? Why? Why not?
4) If a cell is unable to survive outside the body, is it considered to be not a living thing in biology?
5) What are the properties of a living thing definition that animal body cells do not meet?
6) What is the stance of biologists on animal cells being living things?

Whoa whoa whoa. Too many questions. Choose one or two of them, not more. You can ask the other ones in another question.

Partly duplicate of: https://biology.stackexchange.com/questions/7053/can-you-consider-a-human-as-alive-or-is-it-the-cells-on-the-body-that-are-alive?rq=1. Disregarding all talk about "souls", the question revolves around the definition of life.

depends which ones, and the temperature, and protection, and robust attributes.

HeLa cells would be a classical example of a human cell that can live indefinitely outside of the body.

I am voting to close as too broad because the post contains way too many questions!

The concept of soul is undefined in science. Please use terms that are clearly defined or define them in your post.

The soul part might be better suited to the philosophy site, or to the one for your religion of choice. For survival (in culture) outside a body, AFAIK the record is HeLa cells, which have been cultured since 1951: https://en.wikipedia.org/wiki/HeLa

I think it is very likely that this will be closed as "too broad" in the near future, but if you plan to narrow it down to (2), then you need to clarify whether you mean a cell line or an individual cell. Either way, it should be fairly easy to answer (incidentally if you mean option 2 then it's not far off https://biology.stackexchange.com/questions/45790/which-are-the-last-cells-of-the-human-body-to-die, but that doesn't have an answer yet).

As @LinuxBlanket stated, that's too many questions. But I thought this interesting so wanted to answer anyway.

I'm researching on the topic that if bacteria have souls then animal cells and plant cells also do for an article.

Since there's no evidence of "souls" anywhere, the topic is moot. I encourage you to read this.
Concerning your main question

Can animlal body cells survive outside the body? For how long

That has nothing to do with a soul - if souls did exist, then they'd only really matter when the organism dies. So how long something lives has nothing to do with your topic.
You should also think about what "alive" means, as there isn't a solid definition in Biology. usually the definition is around replication and/or metabolism, but then would you say a virus is alive? If yes, what about prions? If you cut a tree to the stump, when exactly does it "die"? Where do you draw the line?
OK, to answer your questions.

Yes. Think of a cell as an enclosed unit that metabolises and respirates. As long as the cell gets what it needs to continue those two processes, whether within the tissue or in a synthetic setting, it'll "survive". See this.
So as I explained, you can keep a cell ticking along as long as you can keep those basic processes going. At some point, a cell will want to replicate. So now you have to think - is my 1 surviving cell becomes 2, then 4, etc., then cell number 1 dies, am I still classing it as survival? If you want to keep cell number 1 alive indefinitely, you can adjust its environmental conditions to slow the pace of its life - cool the cell down, chemical reactions for metabolism and respiration slow down and the individual cell will "live longer". You can even freeze a cell for years then thaw it, and it will continue to live. See this.
That's for you to figure out. I encourage you to look up the definitions of cells, tissues, organs and organisms.
If a cell dies, it's considered dead. Even in biology.
Again, the definitions of "living" aren't set in stone. Personally, I reduce a living thing into these two requirements:

Something that replicates
Something that metabolises

But, I would say that animal cells meet the requirements of the general consensus more than viruses and prions (they replicate), but less than plant cells. This might be a good start to exploring why. But in short, animal cells tend to work together as tissues. Plant cells are a little more viable on their own. You can take a plant cell and grow an entire plant from it. You can only do the same with an animal if you use stem cells.

You should be able to answer that question yourself now =)

"this is called 'death,' namely a release and separation of the soul from the body." --Iamblichus | @Ronald Greeff -- soul is immaterial: no physical instrument can detect and measure soul. If you deny the existence of soul, you are against Pythagoras, Aristotle, Plato, Plotinus, Porhyry, Iamblichus . . .

@MartinKlvana "that which can be asserted without evidence, can be dismissed without evidence". If no physical instrument can detect and measure soul, how did lamblichus could conclude that the soul existed in the first place? Just because I disagree with the Greeks, doesn't make me "against them". Pythagoras' theorum's grounded in maths, so it's difficult for it to be contrived. But they didn't have the scientific instruments of today, nor the discoveries of Newton, Einstein, etc., to test their assumptions and correct their errors.

@RonaldGreeff The 4 point is about if the cell doesn't have the ability to survive independently can it be considered alive according to biology. Not if it is dead, is it dead.

1) Is there a way to make any of the body cells survive out side the body for a reasonably long time?

HeLa cells have been living outside of their owner's body since 1951. Admittedly, cancer cells are trying hard not to die in the first place...

Cell lines are cancer cells or virally or chemically transformed cells that can continue to replicate indefinitely, as long as they get fresh media. Primary cells are native cells that are grown in culture, but they eventually die off. Some primary cells are short lived, both in vitro and in vivo, like neutrophils. Other primary cells can grow, differentiate, and replicate for weeks, particularly if growth factors are supplied.

I think it is unlikely that cells have souls, especially not culturable cells.


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Are there wounds which never completely heal?
I have a cut on a knuckle which occasionally opens (usually during winter), to disappear after some time (it is usually fine during the summer). This is going on for years now and yes, I will show this to my doctor (it is more a nuisance than anything else but there is the risk of infection).
Then during a recent discussion about the Vietnam War, the story of Phan Thi Kim Phuc was mentioned and I recall that I read years ago that she said (quoting from memory) that "[her] wounds still open, usually in summer".
I was wondering what is the mechanism of such wounds which heal, but not completely (to reopen after some time or on some conditions).
Her story is horrific and the extent of her wounds (and also the nature of the wound - inflicted by Napalm) make me think that there may have been some changes in the skin so deep that the consistency of the skin is not there anymore (wildly speculating).
In my absolutely minor case, however, there are no particular reasons for the wound to open - it is just closed and then, sometimes, decides to reopen to re-heal some time afterwards. Since this is otherwise healthy skin (it looks perfect when the cut is closed) I wonder if there are mechanical or chemical reasons for these behaviours?

Yes, there is a mechanistic (and an environmental) reason for the same lesion to occur and heal every year. You can alter this with some effort, though. Use a high quality moisturizer for your hands year-round, and wear gloves outside in the winter. If you adhere to this, your skin will not break open.  After a few of years of this, it will have really finished healing itself. This is much cheaper than moving to the tropics, where it would not occur (but other things will.)


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Do different people have the same number of mitochondria in comparable cell types?
e.g. will a lymphocyte in one person have roughly the same number of mitochondria as a lymphocyte in another person.

I can't provide a reference but I believe mitochondria are sparce in lymphocytes, perhaps 6-10 per cell but their numbers vary depending on the cells activity so I don't understand why you want to compare numbers between different people.

Careful in asking for the number of mitochondria. In a non-dividing cell, mitochondria are normally organized in a net-like structure (more here: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4672710/). Maybe it'd make more sense to ask about the number of mtDNA nucleoids.

".... The number and shape of mitochondria vary dramatically in different cell
types and can change in the same cell type under different physiological conditions, ranging from multiple spherical or cylindrically shaped organelles to a single organelle with a branched structure (a reticulum). The arrangement is controlled by the relative rates of mitochondrial division and fusion, which are regulated by dedicated GTPases that reside on mitochondrial membranes' In addition, the total organelle mass per cell can be regulated according to need.
For example, a large increase in mitochondria (as much as 5-10-fold) occurs
when a resting skeletal muscle is repeatedly stimulated to contract for a prolonged period."
Alberts, Bruce; Alexander Johnson; Julian Lewis; Martin Raff; Keith Roberts; Peter Walter, Molecular Biology of the Cell, 5th Edition.
As the Paragraph above explains, it can be assumed that due to different metabolism in different people, a specific number of mitochondria in the same cell types for different people may not be assumed.

No, because there are 3 different types of muscle fiber, each containing different numbers of mitochondria, each correlating with a different requirement for oxygen and glycogen.
You also have different muscle types throughout your body - cardiac muscle, smooth muscle, skeletal muscle.
Different people of the same group (e.g. region) will have minor genetic differences which will result in different proportions of muscles and muscle type distribution in their bodies.
Different people across groups (e.g. different countries) will also have different environments to deal with, and different strains on their muscles, which result in muscles developing differently over time. People in Kenya run for miles to get water, and require high-endurance, while people in California spend a lot of time in the gym doing weights, which require less endurance and more power.
This goes into a lot of detail.
I would expect that this is true for other cell types as well, as different environments and differences in genetics will result in different requirements for cellular metabolism, all of which will dictate the number of mitochondria needed.


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Is it genetically possible for these to be the parents?
In a human, assuming no mutations, is it possible to have a child with this phenotype, given the phenotype of the parents?
The mother, Alice, has black hair and brown eyes. The father, Bob, has red hair and green eyes. The child, Clare, has green eyes and black hair.
From what I know of genetics, and experimentation using a simplified model, called the 'Genetic Heredity Calculator', this should not be possible.
Being green eyed is apparently a 10%. chance, however resulting in a black-haired child isn't supposed to be possible.
Of course, my understanding of genetics is far from complete. Is it possible, and if so, what is the likelihood that this is the result, knowing nothing else of the parents' genetics, aside from them being caucasian British?
My question revolves around Alice, who has hair well within the commonly perceived range of 'black', which I here define as <7 lightness in HSL, having a child with Bob, a redheaded man, which I shall define as a man whose hair colour in hex is greater than 3:2 r:g, and >30 Lightness in HSL.
Such precision is not required, but exists to put the question in context.

I don't think our understanding of the genetic basis of hair and eye colour are good enough to give you probabilities for offspring to have certain combinations or shades of colours. The possible phenotypic range for these traits always contains at the very least the two parental phenotypes. One parent has black hair - why would it be impossible for a child to have black hair?

I think I found the tool you refer to and it's certainly not to be taken seriously. It output 100% brown hair colour for children of one black-haired and one blonde-haired parent. My parents are that exact combination, and they have one blonde, two brown-haired and one black-haired child.

many genes code for hair color and eyes, not just one. and the chromosomes can be split into 2-3 pieces and jumbled.

unlikely but possible
Eyes. As you already indicated green eyes are possible just through recombination, in fact lighter color eyes are always possible due to mutation. All the major eye colors use the same pigment anyway, it is just amount and depth that varies, so it is not discrete genetic trait meaning ballparking is the best you can do.
Hair. All the necessary genes are present in the parent pool so it is possible. Brown and black hair are just different levels of the same pigments not due to the absence of a pigment like red hair. There is also more than one combination to get both black and brown hair.  If both parents lacked the same pigment (both redheads) it would prevent black or brown hair but this is not the case so black hair is indeed possible, unlikely but possible. Worse hair color genes can be hidden by dominate ones so you can't even guess the parents genes so any estimate will be just guesswork.

Do you have any kind of rough estimate as to how likely it would be?

not aa good one the genetics of hair color is not well understood the physiology of it allows for it however. black and brown are caused by the same pigments so for a really rough back of the envelop you could say half the chance of brown hair, so around 25%,

The genetics of eye colour and hair colour is not easy enough so that we can answer. There are two main issues. 1) The traits in question are quantitative (takes continuous values) and not discrete which makes the expression "brown eyes" a little inaccurate and undefined. 2) Those traits are polygenic traits. In other words, there are a lot of loci that affect eye colour and hair colour and pretty much everything end up being possible.
So, yes it is possible, although it would be more likely that Claire has brown eyes.

Updated for precision

Is it possible for Claire to have 'black' hair?

@Armatus Yes, definitely. Sorry that was a mistake. Thanks for pointing that out

Roughly how likely is having the correct hair colour?

Your follow-up question is partly undefined. We would need an exact measurement of what you call "black" and "red" 2) I would not know anyway and I don't know if there is any study on that.

I did exactly that! Read the question.


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Check on 23andme what type of CYP2D6 substrate metabolizer I am
CYP2D6 is responsible for the metabolism and elimination of approximately 25% of clinically used drugs. Which SNPs do I need to check on 23andme in order to determine if I'm a poor or ultrarapid metabolizer of CYP2D6 substrates, and how reliable would the results be?
I've found one article on this topic, but I'm not sure how accurate it is, and it doesn't cite sources.
PS: why isn't this information more readily accessible to 23andme users, given the relatively large risks incurred by not knowing one's reaction to a large number of drugs?

Unless your polymorphisms have been tested against a particular drug, you can't extrapolate a starting dosage for it based only on your genotype.  It's better to actually take the drug, and change dosage based on observations.
See this paper
https://www.ncbi.nlm.nih.gov/pubmed/24935087

CONCLUSIONS AND RELEVANCE: In this meta-analysis of randomized
  clinical trials, a genotype-guided dosing strategy did not result in a
  greater percentage of time that the INR was within the therapeutic
  range, fewer patients with an INR greater than 4, or a reduction in
  major bleeding or thromboembolic events compared with clinical dosing
  algorithms.

.

why isn't this information more readily accessible to 23andme users,
  given the relatively large risks incurred by not knowing one's
  reaction to a large number of drugs?

Because no-way no-how does 23andMe want to be in the business of giving medical advice.  Nor should they be, because for most things, we have no idea how to convert genotype knowledge anything medically actionable.

This is the case for all genotype guided dosing strategies I'm aware of, even if the polymorphisms have been tested against a particular drug.  So far, clinical effect is always better.

That was my understanding too, but I phrased it like I did lest there be exceptions unknown to me.


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Resources to learn about marine life
I recently saw the documentary series Blue Planet 2 and was mesmerised by it. Can someone recommend me some resources to learn about marine life? I am particularly looking for those that detail the habits and lifestyles of marine organisms.
P.S. - Hope this is the right stack exchange for this question

There are a lot of marine documentaries out there. These are some that I know of:
Shark (2 episode series in 2015);
Deep Ocean;
Life in the Blue;
Ocean of Giants (Nat Geo);
Ocean Giants (BBC);
Humpback Whales;
Ocean Voyagers (whales);
The Polar Sea;
Swimming with Killer Whales;
Ocean Wonders (no narration, just under sea footage of animal behaviour);
Martin Clunes: Man to Manta;
Nature's Great Events: Diaries (a couple episodes of marine ecology);
Dolphins: Spy in the Pod (a view on dolphin activity using dolphin-shaped cameras);
I watched these off YouTube:
Alien Reefs;
The Giants of Rurutu (whales);
Mucky Secrets: The Marine Creatures of the Lembeh Straight;
Reef Life of the Andaman;
Secrets of the Australian Ocean;
Oceans of Contrast (spends a lot of time on life on land revolving around the ocean, but there's reef life as well);
The Incredible Glowing Creatures of the Deep Sea: Documentary on Bioluminescent Sea Life;
Documentary on Coral: African Wonderful Coral Reef
Conservation type documentaries:
Sharkwater;
Mission Blue;
Chasing Coral;
Blackfish;
Sonic Sea;
A Plastic Ocean;
Shark Men (If you like reality style television series. They capture, tag and learn about sharks to protect them)
If you want a more in-depth resource for learning, you can also YouTube search "marine biology lectures"


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Apical dominance in plants
Could someone help me understand a few concepts related to apical dominance
1) why auxin is a dominant over other hormones?
2) how exactly the mechanism of apical dominance works?

Which link did your research produce, and what concept from that link is it that you don't understand?