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Is transplantation of neurons between species possible?
Can brain tissue from one species be implanted into the brain of another species? Because the brain is tolerant to the introduction of antigens (it is said to be immuno-privileged), I was wondering whether neurons would be subject to graft rejection?
If neurons from another species survive in their new host, would they create functional connections?

To add on AliceD's comment. You should define a specific trait on which you are interested in. For example, you may ask if mice neurons tend to be shorter than human neurons (yes for many motor neurons) or whether there is more myelin on the mice neurons than on human neurons.

Added information to the question, explaining what i mean by "differences"

@AliceD: it now excludes for example differences in size

Ok, I see now, there isnt an "easy" answer to my question. I dont think, continuing this question will lead to any useful information, due to the topics complexity... the question can be closed

@Mystery -  I have focused the question on your last edit. If you wish, feel free to ask any of the other questions in separate questions. It is interesting stuff!

I know of some papers where neural stem cells (of rats/humans) have been transplanted in mice and there is a change (enhancement in vague terms) of function. AFAIK there is some structural difference too (the size of the processes etc). I can answer your question in a while (a week or two) because I need to dig up these papers. Lots of deadlines at this moment.

Short answer
Neural xenografts can survive and form functional connections in the host.
Background
Across-species (xenogeneic grafting) grafting of cerebral cortex from a fetal rat to an adult mouse brain and vice versa, have shown that immunocompetent hosts can reject a graft in less than 30 days. Rejection results in destruction of  the graft tissue presumably by macrophages. Immunosuppression can be used to prevent graft rejection (Mason et al., 1986).
A review article on this topic shows that in the absence of immunosuppression, neural xenografts (donors were fetal to adult-aged) in a rat host brain survive in 37% of the cases in case of a mouse donor, 16% in case of a hamster donor, 9% in case of a rabbit rabbit, 7% from a pig donor, and 0% when human donor tissue was used. Hence, species-separation seems to be a determining factor in xenograft rejection. Induction of MHC-I and MHC-II expression in the xenograft mediates graft rejection in the brain. Hence, despite the fact that the brain is immunopriviliged because of the relative low expression levels of MHC class proteins, it is still sufficient to reject grafts (Pakzaban & Isacson, 1994).
Xenografts have been shown to generate functional afferent and efferent axonal connections with the host brain when grafts of the striatum, substantia nigra, hippocampus and retina were homotopically transplanted.
Functional (behavioral) studies have confirmed these physiological studies. Rats with Parkinson's disease could be successfully treated with substantia nigra grafting from mouse, hamster, rabbit, pig and even humans. Similarly, retinal xenografts have resulted in functional pupil responses, hippocampal xenografts have restored learning deficits, and suprachiasmatic nucleus xenografts have been shown to restore circadian rhythms (Pakzaban & Isacson, 1994).
References
- Mason et al., Neurosci (1986); 19(3): 685-94.
- Pakzaban & Isacson, Neurosci (1994); 62(4): 989-1001.


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Which of these methods is both effective and reliable in elongate muscle and tendon for use in humans: growth factors or stem cell technology
Which method is it the most effective, but also the most reliable for elongating muscle and tendons for clinical trial; using modern growth factor technology or using modern stem cell technology?
Being able to stimulate muscle elongation is a key step towards improving the standard of living for people afflicted with severe Poliomyelitis or people with limb Malformations. There are already techniques to culture living bone implants in the lab from stem cells for human beings. I am looking for an analog for muscle tissue.
Please provide references with your answers.

Modern science might not know the answer to this question, and it might vary by patient. Consider narrowing down the question a little perhaps?

source: Stack Exchange

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If I buy a banana at the market, is there any chance that an insect is hiding inside it?
I watched this horrifying video on Youtube. It shows movement beneath the skin of a banana and then a spider pushes it's way out.
Suffice to say I'm too scared to eat bananas anymore!
I would like to know what is the probability that an insect is hiding inside a banana that I buy at the market? Even if there was just one chance in a million that an insect is hiding inside I would stop eating bananas forever.
I postulate that an insect could lay it's eggs in a banana and then the offsprings would be born inside the banana. Or perhaps an insect tries to eat a small chunk of the banana, it cuts his way out inside the banana, it gets trapped inside, and then someone buys the banana. Both of these ideas are troublesome since I'm not sure if there is air to breathe inside the banana.

The thing that comes out of the banana in the video is not an insect. Where do you plan buying a banana (where do you live?)? In a Wall-Mart at Fairbanks, Alaska or at a local market at Jakarta?

That video could be fake.

If you're scared of insects and insect eggs being in your food you're about to go VERY hungry. https://en.m.wikipedia.org/wiki/The_Food_Defect_Action_Levels

I like the question, but I think the reason you're getting so many down votes (and why I down voted) is because you link to a spider and ask about insects. Remember they are different and this is a pet peeve of entomologists! Did you actually mean to ask about insects, spiders, or anything in between?

That's not why I voted - I voted because I feel it's not on topic and primarily opinion based, and I've spent the last 7 years working with insects :)

Kaleb Lechowski, creator of that video, is a digital creator and animator of critters. I would propose that he did a very good job of rendering a CGI spider to burst from a banana.
Spiders (which are not insects remember) won't eat bananas. In fact, only one species is known to be mostly herbivorous: Bagheera kiplingi.
However, don't eat that banana just yet! The internet is littered with tales of horror about spiders in fruit. Like this Black Widow in a bunch of grapes. There is no bursting out of the fruit like Alien, but what has happened is the spider has unwittingly found itself being picked from its natural environment and transported with the fruit.
Fruit is good. Stay sceptical of internet rumours that are trying to get clicks with fear, and stay measured enough to remember that the benefits of eating (washed, clean) fruit far outweigh the extraordinarily low chance of finding a nasty bug hiding away.

Also I'd suggest many/most insects/spiders are edible, so there's no reason to be scared

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Why is there a compound highlighted in red in a KEGG Module search?
Considering the following module:
http://www.kegg.jp/kegg-bin/show_module?M00115+C00003
why is the compound C00003 marked in red?

It is just a way of highlighting your search term. If you search M00115+C03722, you will see C03722 in red.

where did you search using this syntax?

@Rishika On the browser address bar. You can also do that by going to the KEGG home page and searching.

no data found, did you use this exact syntax " M00115+C03722" ??

@Rishika Just click on the link. If you want to see the actual link just right click and select "copy link location". The syntax is same as the link you posted in the question. I just replaced C00003 with C03722.


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Presence of reaction module in bacteria but not in Eukaryotas (human)
From the statistics page, I found that the Module-M00008 is present only in bacteria and not Eukaryotes. Why so? I noticed that all the compounds necessary or the reaction are present in human body and also all the enzymes required for the reactions are present in human body too. Then why does that reaction not happen in humans?

That module represents Entner-Duodoroff pathway, which is an alternative pathway to the Embden-Mayerhof-Parnas pathway of glycolysis.
Entner-Duordoff pathway exists only in prokaryotes.

so does this mean that the enzymes required for this particular pathway in bacteria are not present in Eukaryotas ?

@Rishika Precisely

so if these enzymes would have been present then which pathway would have had the more probability of occurring?

@Rishika That is a hypothetical question and the only answer would be that it would depend of different regulators of the glycolytic flux (in a manner how the fluxes through glycolysis and pentose phosphate pathway are regulated). Now don't ask me what those regulators could be because this question is as such hypothetical.

But according to the statistics , both the pathways of glycolysis are present in procaryotes, but the Entner-Duodoroff pathway is present only in procaryotes and not eucaryotes ... Any biological reason for this??

@Rishika, to add to this answer, there are three possibilities for discrepancy in coverage. 1) Limited information, i.e. even if the module exists in other species it has not been found (missing enzymes, proteins, etc.). 2) The information has not been added to the database (remember that this resource is manually curated). 3) It actually refers to different evolutionary paths. As WYSIWYG says, this is an alternative pathway. Either only the ancestors of prokaryotes found it or if other species found it, it did not increase fitness and was lost. You will find many more examples.

@Rishika And actually, reading the link to the Entner-Duodoroff pathway in wikipedia, it mentions that some prokaryotes use it as they lack enzymes critical for glycolysis. This suggests that even if "prokaryotes" have both glycolysis and this alternative according to the KEGG Module, maybe not the same prokaryote has both. At least it seems the case here.


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Why lab technicians use indirect (antibody reaction) method for diagnosing?
In microbiology we have two types of microbial diagnosis. The direct method is where we detect the invader's DNA, Antigens or culture to see the exact pathogen while the second, indirect, method is the reacting the antibodies of patient's serum with different reagents.
If we use the indirect method (antibody reaction) and find that they are producing antibodies against a specific disease (let's say streptococcus A) what is the benefit of having found that they are fighting Strep A since the body is already clearly fighting it and putting up the best defence to fight the disease?
Would a doctor really prescribe antibiotics even though here is already an immune reaction against the infection?
If diagnosis and treatment are useless then why do we waste the time to do it?

Short answer: Antibiotic treatment is important because the body can't always keep up with the infection even if it has launched a response.
Background:
First, let's look at what the antibody reaction method is actually doing.

Taking a sample of blood or body fluid
Testing the sample with known pathogens - viruses, bacteria, fungi, etc.
Identifying which infection causes a reaction.

This allows us to determine which infection we are dealing with. This can be especially useful when the infection is hidden in a place we are unable to easily swab - the stomach, heart, a small wound that has already healed. Sometimes this test is just used to monitor how well you are fighting the infection, but it also allows them to evaluate what the best course of treatment is for you. (Reference 1)
Just because the body has an immune reaction doesn't mean that the body's immune system can actually finish the battle against a disease. In the example case of Strep A, you may be able to get over the infection yourself but it will take longer than if you are prescribed antibiotics against it.
See this question on the CDC:

Q: How common is invasive group A streptococcal disease?
A: Approximately 9,000-11,500 cases of invasive GAS (Group A Streptococcus) disease occur each
  year in the United States, resulting in 1,000-1,800 deaths annually.

Note that invasive Strep A usually infects children, elderly, and  immunocompromised people (anyone with a weaker immune system typically).

Unless you have absolutely no immune system at all, there will be an antibody response put out by your body. The NHS goes into detail about different parts of your immune system.
Recall also that Strep A (our example) could divide faster than the body can keep up with. So we would need antibiotic help to fight the disease. Using the "indirect" method we can find a hidden infection.
According to the NHS the antibiotics put a stop to growth and spread which allows the body to come in and finally finish them all off, or they disrupt a process the bacteria needs to survive and kill the infection for the body. Thereby helping the immune system (the body's best line of defence) finish off the infection when it couldn't do it on its own.

It is also worth pointing out that the premise of the question is wrong.  Assaying for an antibody response is rarely used to diagnose an ongoing disease, because the antibody response takes several days to develop; the exceptions are for chronic diseases (hepatitis B or C, HIV) where the pathogens have evolved defenses against the immune system and aren't cleared by it.

@iayork aren't antibodies tested for various diseases? Lepto, dengue, typhoid just to name a few....

They're used to test whether you had the disease, sure. For acute diseases like typhoid and Dengue, they're less useful because they're not detectable for a week or so after the disease starts.

One use of indirect testing is used to test for *exposure** to organisms that we wouldn't just naturally recover from as well. One example off the top of my head is HIV. The first line of testing for this infections is simply to look for antibody responses, but because it is not effectively resolved by the patient's immune response, it is important to know about this infection.
*Also note that because we are looking at antibodies, we only know that the patient has been exposed to the organism, not that they are actively infected. The antibody test is quick and easy though, so it saves money (and probably time) to do this first.
(originally, I included TB in this answer, however it is actually a skin test - not assayed ex vivo via ELISA, so I removed it.)


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How to calculate the percentage of heterozygous cells based on a gene map
I've encountered the following question and am quite stumped by it.
A female with genotype AABBCC has been hybridized with a male that has the genotype aabbcc. The first generation (F1) has been hybridized again (backcross) with offsprings that have the genotype aabbcc. Given the following genetic map, what would be the percentage of F2 offsprings that are heterozygous to all three genes:
A------- 20 MU ------- B -- 10 MU --- C
How should I approach the following question, the brute force approach is too difficult, I keep getting things wrong.

if this is homework please tag it as such and we would appreciate to see some previous attempts at tackling the question. We are not here to do your homework :)

actually, this is a question from an exam I am preparing for. the exam is tomorrow :)

What happens when you draw out all the possible offspring genotypes and calculate the percentage chance?

I get horribly confused and after several attempts can't seem to come to the correct answer, is there no technique to do it without writing down all possible outcomes?

+1 thanks for the edits. I'm not a geneticist, so I hope someone else here may help you further! Good luck tomorrow :)

Units of genetic distance
It took me a little while to understand what MU means. I have never seen MU but rather m.u. for map unit, or cM for centiMorgane.
Solving the problem
This problem got me thinking a little bit. My logic is the following:
Probability of being heterozygous at the first locus
You cross two individuals (we'll call them individual 1 and 2)that are both heterozygote at each locus A, B and C (not to be confused with the alleles A and a, B and b and C and c). We'll start with locus A. The probability of being heterozygous at locus A is the probability that individual 2 gives another allele than individual 1. This occurs with probability 0.5. If the three loci were perfectly independent, then the probability of being heterozygous for a given offspring at all 3 loci would just be $0.5^3 = 0.125$... but that would be too easy so let's keep going with the second locus.
Probability of being heterozygote at the two first loci
So let's assume our offspring of interest, got two different alleles for the locus A. The probability to receive two different alleles at the locus B is the probability that either no individual recombine between A and B or both individuals recombine between A and B. It is therefore: $0.2^2 + 0.8^2$. Put together this probability with the probability that the first locus was heterozygote it gives $0.5 \cdot (0.2^2 + 0.8^2)$.
Probability of being heterozygous for all 3 loci
Finally, we can just keep going with he next locus. Let's assume that the offspring have received two different alleles for both loci A and B. The probability to receive different alleles at locus C is the probability that either both parents recombine (between B and C) or none recombine. This occurs with probability $0.1^2 + 0.9^2$.
Put the whole thing together, the probability of a given offspring to be heterozygote (or the frequency of heterozygotes offsprings if you prefer) is $0.5 \cdot (0.2^2 + 0.8^2) \cdot (0.1^2 + 0.9^2) = 0.2788$
Note that calculating the probability that exactly 2 loci are heterozygous would have been a bit trickier.
Good luck for your exam tomorrow!


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Why does T-cell Cancer Therapy require a large tumor mutanome?
An article I read about Neuroblastoma states that the fact that Neuroblstoma has a small mutanome means that it is not viable to apply the classic T-cell immunotherapy. Why is this so?
The article can be found here: Neuroblastoma: Developmental Biology, Cancer Genomics, and Immunotherapy

The article is also available on PubMedCentral.

Did you get a chance to look at the article @MattDMo?

I changed the link to the article, the authors manuscript is available through PubmedCentral.

Understanding the link between the size of the tumor mutanome and its immunogenicity requires a basic understanding of T-cell development and regulation.
When normal human cells degrade proteins via the proteasome, some fragments of these proteins, called peptides, are bound to specialized cell-surface proteins called MHC. T-cells express a specialized receptor, called the TCR, which recognizes peptides bound by MHC proteins on other cells. The specificity of the TCR, what peptide/MHC combinations a T-cell can recognize, is randomly generated by targeted mutations and VDJ recombination in the TCR genes during a T-cells development. Each clonal population of T-cells (T-cells derived from the same precursor) have a unique TCR that recognizing different peptide/MHC pairs. When a T-cell's TCRs recognize a peptide/MHC combo on another cell, the T-cell is activated.
Because the TCR is generated randomly, many TCRs in T-cell precursors can recognize peptides derived from normal human proteins. To prevent these precursors from becoming T-cells that can attack the body, they are regulated in several ways. Many self-peptide recognizing precursors are destroyed in development, others are converted into regulatory T-cells that instead produce anti-inflammatory cytokines that tune down immune responses. Those those that escape these regulatory processes are later inactivated by other means.
What does this have to do with cancer? Well, most of a tumor's proteins are normal human proteins, and the human body does its best to suppress immune responses against normal human proteins, making it hard to generate an attack against cancer cells with T-cells that recognize normal self-peptide/MHC. Worse, overcoming this protective response could lead to an auto-immune attack on normal, healthy cells. Therefore, we want to make or use T-cells that recognize mutant-peptide/MHC combos. Such cells would not attack or be effectively suppressed in normal tissues, but could attack tumors.
However, to get these ideal, tumor-targeted T-cells, we need the tumor to produce mutant proteins whose peptide fragments ARE DISTINCT from the peptide fragments of normal proteins. Some tumors have far more of these kinds of mutations than others, and not every mutation is immunogenic (not every mutation can be differentially recognized by T-cells). For example, point mutations (single amino acid changes) that activate proto-oncogenes like BRAF don't necessarily lead to the production of structurally different peptide fragments. A larger mutanome offers a greater chance of immunogenic mutations.


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Is 100% accuracy in DNA sequencing possible?
I would like to obtain a complete genome of a canine (with mitochondrial DNA too) at 100% accuracy. Is it even possible with the current technology? The source I have is potential degraded, i.e. dried saliva, dried blood, whisker root, fur roots, etc...

Can you explain what you mean by 100% accuracy. No technique is free of errors. Therefore we experiment a lot of times to improve the reliability.

Current DNA sequencing techniques are based on shotgun sequencing, randomly breaking the chromosomes into small pieces, sequencing the pieces (by various techniques), and then computationally reassembling the pieces by looking for overlapping patterns. This depends on sequencing each piece of DNA multiple times; the more coverage or depth, the more reliable the results. However, especially with long repeating base sequences, 100% coverage is uncommon with small genomes, and almost impossible with large genomes.


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What fraction of sites are expected to be polymorphic?
Question
Consider a very long (eventually infinite) DNA sequence of neutral sites. Consider a panmictic population of constant size $N$ with a per site mutation rate of $\mu$ where all individuals have the exact same fitness.
What is the fraction of sites that we'd expect to be polymorphic in the population (SNPs)?
Motivation behind this question
I am asking this question to verify the results of simulations I run. For example, I run a simulation with $x$ ($x$ will be varying below) neutral sites, with a per-site mutation rate $\mu = 10^{-9}$ and a population size of $N=100$. I run the simulations for 10,000 generations. There is no recombination. When the number of sites:

$x=10^3$ I get 0 SNP
$x=10^4$ I get 1 SNP
$x=10^5$ I get 3 SNPs
$x=10^6$ I get 25 SNPs
$x=10^7$ I get 238 SNPs

Is there a bug in my model or is it what we'd expect given the parameters?
In the human genome, 1 out of 300 sites are polymorphic (SNPs) (ref.). This is a frequency of SNPs that is 100 times greater than what I observe in my simulations. Note however, that the assumption of neutrality and out demographic assumptions would not perfectly hold and this result could pretty far off neutral expectation. My goal is not to reproduce something that look like the human genome but only to reproduce the neutral expectations for the moment.

Have a look at https://en.wikipedia.org/wiki/Tajima's_D. It provides an estimate for the number of segregation sites for a population under a neutral mutation model.

@putnampp Sounds interesting indeed. Does it mean that the expected number of SNP's in a sample of size $n=N$ (I sample the whole population) is $E[S] = 4N\mu\sum_{i=1}^{N-1}\frac{1}{i}$? Therefore, in my case $N=100, \mu = 10^{-9}, E[S] ≈ 1/481939$. Therefore, out of $10^7$ sites I'd expect to have $20.75$ SNPs. Is that right? This is 10 times less than what I observe.

I would agree with your comment. If you were to use the entire population as your sample size you would expect to find roughly the number you suggest. I've written some example simulation software that is capable of performing such evolutionary scenarios (Clotho). You could also check your numbers against MS.

Ok, sounds good. I'll have a look at clotho. If you want an make a short answer out of your comments by repeating the calculation I made. And you'll hopefully get enough reputation to comment in the future thanks to this answer! I'd welcome you link the paper describing clotho as well. Thanks! I've got to understand why I have so much polymorphism now!

Reiterating the above comments. Have a look at Tajima's D. It provides an estimate for the number of segregation sites for a population under a neutral mutation model.
The general form of the estimation for a diploid population is $E[S]=4N\mu\sum_{i=0}^{n-1} \frac{1}{i}$.  Here the mutation rate of is per-genome not per-site, so $\mu=L * 10^{-9}$ where $L$ is the genome size. Estimating the segregation sites of an entire population of $n=N=100$ with genome size of $L=10^{7}$ where each site has a per genome mutation rate of $\mu=10^{-2}$ one would expect that $E[S] \approx 20.75$. So, your numbers seem higher than expected.
I've written some example simulation software that is capable of performing such evolutionary scenarios (Clotho manuscript). Similarly, you can check your numbers against a population generated using MS.

The fraction of polymorphic sites that exist in a population is dependent on the biology of the organism. For instance, you would expect to find different rates of polymorphism in related plants that have different breeding systems, e.g. in Silene [1]. Past bottlenecks are also expected to decrease polymorphisms [2]. So, the answer to your question would depend on the exact species and population that you are looking at.

Thanks for your answer. Yes, I am well aware that pattern of selection (frequency-dependent, purifying selection, spatially or temporally heterogenous environment, LD, etc..) as well as demographic patterns (bottleneck, population structure, range expansion, etc..) affect these polymorphism. I am interested in a theoretical predictions assuming a whole bunch of things. I made those assumptions a bit more obvious in my post.

we included a script to calculate this in supplemental material
http://onlinelibrary.wiley.com/doi/10.1111/mec.13034/full
....single segregating site per locus or up to a maximum of four SNPs, as is expected for short-read genomic data (see attached R script for estimation).

Could you tell a bit more about the method? It's more of a comment now.


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What determines the pathway of a neurological signal?
My question is about the neurological signals. In our body when a signal, for example a hearing signal from hair cells, is built, it goes through a lot of neurons and it passes a lot of synapses. I am wondering how it doesn't lose it's correct path and chooses the right way to auditory cortex? I mean what are the features of a neurological signal that shows it the correct way?
In other words, how can a neurological signal be created and sent through a chain of neurons to the brain, how can it 'know' when entering a synapse contacting multiple neurons which is the correct one for going through it?

please, read this section on how to ask good questions and try asnwering: "Have you thoroughly searched for an answer before asking your question?" This is not only about searching through this site, but also googling

@aaaaaa - I must say this question and related ones are understandable. E.g., folks in computer science tend to compare the nervous system with computer commands and don't understand why an isolated '1' (an action potential) enters up in the correct place without proper guiding info.

i have problem of different kind with given question

Short answer
Neuronal signals neither choose where to go, nor do they carry routing flags of some sort to guide them. Instead, neuronal signals are guided by the hard wiring of the nervous system.
Background
Neuronal signals (action potentials) basically follow a one-way path. When they encounter a cross roads, action potentials are simply propagated to all of those alternatives. External effects of neurons, hormones or drugs may alter these signals, for example by inhibiting action potential formation or propagation.
To take the example of the auditory system (Fig. 1):

Fig. 1. Auditory system. Source: New York University.
One can readily see that the signal from the hair cells are routed into the auditory nerve to the cochlear nucleus, from there to the colliculi in the brain stem and further up to the auditory cortex via the medial geniculate. Basically this is a one-way, straightforward route.
There is complexity in the system, however. For example, the fibers of the auditory nerve bifurcate on entering the cochlear nucleus and make synapses on a number of morphologically different types of neuron. Each of the latter sends its axon out of the cochlear nucleus with a distinctive projection pattern that gives rise to further divergence. Specifically, some cochlear nucleus neurons project directly to the inferior colliculus, whereas others project to various divisions of the superior olivary complex and nuclei of the lateral lemniscus, which in turn project to the inferior colliculus (Irvine, 1992).
But even in this complexity the divergence is basically generated by simple bifurcations. An action potential reaching such a junction by default simply gives rise to two parallel signals; there is no choice involved. Regulation is due to other neurons targeting these pathways.
Reference
- Irvine, The Mammalian Auditory Pathway: Neurophysiology Springer Handbook of Auditory Research (1992).

Ok thank you.  Now my quedtion is what are the features of a specific neurological signal?  I mean for making a fake signal .

@Pedram, I do not understand your follow up question and you should perhaps consider asking a new question. The answer comments should be reserved for clarifications only.

I mean our ear collects sound and make signals and it goes to brain and we hear.Now I want to make a fake signal and the brain hear it I mean here the ear doesn't have any role and we give a stimulation to auditory nerve and it take it to the brain.

@Pedram, I suggest asking a new question on this and carefully explain what you mean with a fake stimulus etc. Comments are not ideal for new questions. Thanks.


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How does the Platypus grow before it eats?
From this fascinating documentary on monotremes it is mentioned that the Platypus is born less than 1 cm in length, but has doubled its size by day three when it begins to nurse. How does the animal grow before feeding?
Surely by conservation of mass there must be some alternate process by which materials are being processed and absorbed by the young animal. Does it absorb nutrients from the air or surrounding environment? Sucking on dirt? Osmosis?

Plausibly, it could grow by intake of water (much like seeds germinating into seedlings). No citation so left as a comment.

The video is quite old and they knew a lot less about the species then.  They probably had to make some guesses.  Any modern reference I find doesn't mention any waiting period before nursing.
It seems to me that were this the case it would be very explicitly studied by now as it would be a real oddity for a mammal.  And we love platypus oddities.
Interestingly, the platypus doesn't actually have teets to be suckled on.  Instead the milk is expressed through their skin and into grooves on the belly that the newborns can drink from.

This doesn't really answer the question.

Why was this downvoted? Is it inaccurate?

Maybe I didn't state it clearly enough but the answer is "it does not".  There is no record of this in any literature I saw, other than the aged documentary provided in the question (with no explanation of the very odd physiology).


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Evolution of the Redundancy of the Genetic Code
In short
Looking at the genetic code, it appears that most redundancy is on the third letter rather than on the first or the second letter of the codon. Why has it evolved this way?

Longer version
In order to compare the relative redundancy accounted by each letter of the codon, let's assume that that every codon occurs at equal frequency. It is probably wrong but useful for the sake of the calculations. Using observed frequencies of codon usage in a given population would change the following probabilities but the question of why some positions in the codon has more redundancy than some others still hold.
A substitution of the first letter of the codon has a probability of $\frac{1}{2048}≈0.00005$ (Stop codon) to be synonymous. A substitution of the second letter of the codon has a probability $\frac{3}{256}≈0.012$ (nucleobases U and G) to be synonymous. A substitution of the third letter has a probability of exactly $\frac{2}{3}$ to be synonymous.
Probability of a substitution to be synonymous given that it occurred on the...

First letter: $\frac{1}{2048}≈0.00005$
Second letter: $\frac{3}{256}≈0.012$
Third letter: $\frac{2}{3}$

Why are there more redundancy on the third position than on the second (which has more redundancy than the first position) in the codon?

ever heard of wobble base pairs? i guess, the reason is that binding of anticodon to codon happens with directionality, 5'-3' (on codon side), that is why when first 2 bases are connected, third one in anticodon has not enough energy to break pairing even if it is very different.

To fully comprehend the concept of wobble base-pairing we need to consider the nucleotide sequences of the anti-codons in the tRNAs that have to "read" the genetic code when the mRNA is being translated on the ribosome.  The nucleotide in the anti-codon's wobble position is, for example, often inosine.  Under the rules for wobble base-pairing an Inosine can potentially base-pair with three other nucleotides.
In real terms that means a cell can use less than 63 unique tRNA genes to decode mRNAs carrying messages made of the 63 different "words" (codons).
In an active cell the Ribosome's A-site, where the charged tRNA binds, is occupied by the incorrect tRNA most of the time (based on the law of mass action where any charged tRNA can randomly diffuse into the binding site).  With tRNAs that can recognize multiple codons (which is what the wobble hypothesis gets us), any given protein can be translated faster (assuming  that correct charged tRNAs are limiting for the polypeptide polymerization reaction).
So those are the practical ramifications of the table that you presented, but the explanation, as for most why based questions about biological evolution, is a retrofit.  Natural selection can only work with the materials at hand, and so we can infer that during the period when this genetic code was finalized that the organisms who used it were more successful than the others.  And the current code is based on whatever the previous one looked like. "Descent by modification" is the original description.
[whoops, sorry about the pedantic voice on the "how selection works" bit, I just looked at your profile and realized you can likely teach me on this subject]


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What is the cause of colours of nail
Why the nails are of white colour from bottom? then why they are pink and again white in the end?

I'm voting to close this question as off-topic because there is not any sign of prior effort on OP 's side.

@AliceD, I don't find the answer by googling with similar phrase. If you know about the answer, can you please share it? Also, why it's off-topic? I think, it fits in biology, isn't it?

@CoolZeroInfinity - That bit of research you just did is what I would like to see in OP's question. As of now the Q is just too easily thrown into this community. We like to maintain a certain question standard.

I think anyone should be able to ask a question here - its not a homework site.

While I agree that anyone should be able to ask a question here, I think we have the right to request that certain standards are met. We have not said this person can not ask a question, but directed them (using the tools available e.g. close votes) to improve the question to meet those standards @shigeta http://meta.biology.stackexchange.com/questions/449/how-much-should-we-enforce-background-research

@CoolZeroInfinity I Googled the word fingernail and got the wiki page, that had enough info to derive an answer

@rg255, I agree. I was searching with different phrase but with anatomy, I can find answer.

The Nightman is giving you a headstart to understand and read about nail colour.
I would like to add a different view to this question from "Colour and Pathology" point of view. Finger nails have been an excellent source of evidence for the initial physical diagnosis process. Nail colour and texture can be an indiator for a wide range of medical conditions.
You may take a look at this link : The hand in Diagnosis Process and discusses about nail pathology.. However this diagnosis gets a little tedious if the patient has colourfully painted their nails with nail polish...
I see many of the answers do include an image - well at the end it's anatomy.

Here's a relative simple and fun to read article to clarify any doubts you have about Keratin in nails being dead or not, for its colour and why it's tough.

The cuticle and matrix are white because the melanocytes there are inactive, so there is no pigment produced. The matrix cells divide and the new cells produce a lot of keratin protein.
The older cells fill with keratin and die, and the new cells push them out of the way – this means toward the end of your finger. This is how your nails grow.
But our fingernail doesn’t look like individual cells. You are
   sloughing millions of skin cells each day, but for a nail the dead
   cells all mass together. Nails only wear away or must be trimmed.
   Individual cells are not lost. The solidity of the nail comes from the
   connecting of the dead cells together by junctions between the cells
   called desmosomes, and by the interlocking of the cells like jigsaw
   puzzle pieces. But there’s more.
Individual keratin protein filaments also become connected so that the entire mass of keratin becomes one solid structure. This is called cornification, like the stratum corneum (the outer, dead layers) of your skin.
One of the two main forms of keratin in your nails is crystalline keratin, which is rigid, stronger, and has an ordered structure - like a tinker toy cube. Transmitted light is less likely to strike an atom and bounce back when the atoms are all lined up, so this is why many crystalline lattices appear translucent.

Great referenced answer, it doesn't address the question though. -1

@AliceD this is my first answer in this site :( well I stated it is a different view :)

The Nail itself consists of dead keratinous cells that shrink upon dying and become translucent. This gives the nail itself its white coloration. The reason it appears pink when it overlaps the finger is because of underlying blood vessels that color the live tissue pink just like your skin, and this shows through the nail itself. The lunula is the most proximal region of the fingernail that is crescent shaped and appears more white than the rest of the nail bed. The reason for the whiter color is that the underlying blood vessels are obscured by a denser stratum basale (one of the lower layers of the skin).
See: Human Anatomy by Martini
If you don't have this book, you could at least start at wikipedia which does describe the anatomy of the fingernail with more or less accuracy: Wikipedia

Interesting answer. +1. A reference or a few links would be great though.

@The Nightman, answer sounds logical, I thought something like same :-) but didn't have any reference. Can you provide any reference please?

Fingernails are not made of dead cells, they are made of Keratin.


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How can bats hear such high frequencies?
I attended a talk that glossed over some biology as it was talking about a certain protein. The speaker mentioned humans can hear up to, often less than 20kHz frequencies, whereas bats can hear up to 100kHz. Presumably this is to do with differences in cochlear anatomy.
What about the inner ear of bats is different form ours, and how does this allow them to hear such high frequencies?

Short answer
Echolocating bats have relatively large sensory epithelia in their inner ear, that may correlate with their high upper frequency limit of up to 200 kHz. The basilar membrane is thinner and stiffer, possibly allowing it to decode higher frequencies.
Background
In terms of the place theory of hearing, the cochlea acts as a frequency transformer, where high frequencies are encoded basally, and low frequencies apically. The cells responsive to sound, the hair cells, are located along the basilar membrane (BM). Going from base (high frequency) to apex (low frequency), the BM becomes wider and less stiff, making it more susceptible to encode low frequencies apically. Note that sound is encoded as a travelling wave, where the point of resonance of a particular frequency corresponds with the characteristic frequency of the hair cells (Fig. 2).

Fig. 1. Rolled out cochlea. Source: New York University.

Fig. 2. Travelling wave and resonance frequencies along the basilar membrane. Source: University of Minnesota.
A study in Microchiroptera species revealed that the basal part of the basilar membrane was relatively narrow and stiff, which increases the resonance frequency of the basal part of the BM and hence may allow it to encode higher frequencies in these bats (Pye, 1966).
Because the high frequencies are encoded basally, it would be tempting to speculate the basal region would be enlarged in echo locating bats. Although this is true in some species, it may have more to do with frequency sensitivity than the upper limit of hearing, simply because a larger surface of the BM allows for more exquisite resolution of the BM. Although there is a tendency for larger BM lengths in echolocating bats, it is not consistent (Davies et al., 2013).
The human BM is 33.5 mm, while the BM of the bat with the highest frequency limit known (200 kHz, Hipposideros bicolor) is only 9.13 mm. However, compared to that of acoustically unspecialized mammals of a similar body size, e.g. Sorex araneus (BM length 4.4 mm) and Mus musculus (BM 7.0 mm) it is relatively long. However, as said, other bats with lower upper-frequency limits have longer BM lengths, e.g., Pteronotus parnellii (13.2 mm) and Rhinolophus ferrumequinum (16.1 mm). Indeed, the BM length has been correlated both with an extension in frequency range as well as enhanced frequency resolution (Dannhof & Bruns, 1991).
References
- Dannhof & Bruns, Hear Res (1991); 53: 253-68
- Davies et al., Front Zool (2013); 10: 2
- Pye, J Morph (1966), 118: 495-510

i really don't see how this is an answer. Any other differences except length of BM? cellular anatomy? Different properties of fluid in the cochlea? I believe there is more to it than page from Encyclopedia Britannica

@aaaaaa, I have added material. Thanks for the suggestion. But what page of Britannica? I haven't used it here? There are three credible references listed.

What's also important is basilar membrane thickness, since that is part of what dictates the resonance at various frequencies (as I understand it, thicker = stiffer = higher frequencies).

@AliceD If being thicker at the basal end promotes lower-frequency hearing, than why are the higher frequencies transduced at the basal end? I know width matters, too, but it seems thickness results in stiffness, which--per given load?--should resonate with higher frequencies. E.g: "Part of the stiffness change is due to the increasing width of the membrane and part to its decreasing thickness." (link: http://147.162.36.50/cochlea/cochleapages/theory/bm/bm.htm)

@AliceD Right--my comment was intended to suggest that perhaps these bats have thicker basilar membranes than humans do. But yes, there are other structural factors (and active tuning) which would also be at play.

@Chelonian I understand, but the Pye article is reluctant to interpret thickness as causative factor, also because it can have the opposite affect, dependent on the load on the basilar membrane etc. Very detailed studies across species could elucidate this, but to the best of my knowledge only gross-anatomical features like the ones discussed in this answer have been addressed.


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What is internal symmetry in membrane proteins?
I have come across the term "internal symmetry" in the context of membrane proteins, but have never found a satisfactory definition.
I'm struggling to figure out exactly what this term means... What plane is this symmetry seen on? Is it dimers that are symmetrical or can a monomer also be internally symmetrical?

Can you please provide the original context? I don't think the concept applies generally...but depending on how weakly one is using the term 'symmetry' it could be in most-any plane and within or across a monomer.

This review paper; Structural Symmetry in Membrane Proteins, made it's way to me soon after I posted the question. It covers the significance of symmetry in membrane proteins. The term is as vague as @Ryan mentioned it could be!

Internal symmetry in this case refers to cases where a part of the protein structure can be superimposed (approximately) on another. It's not a strict mathematical symmetry, more a 'resemblance'
For instance in the 12 transmembrane helix transporters, the first six helices are arranged similarly to the second six, such that if one were to cut the protein in half one would see that the two halves (approximately) superimposed.
Fig 3 of this Nature Micro shows it clearly. http://www.nature.com/articles/nmicrobiol20159 Where the blue helices in 3a could be rotated 180 degrees and then look very similar in arrangment to the yellow helices.


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Which bird of Upper Michigan is it?
While doing morning-walk in Keweenaw Penisula, Michigan; I found this juvenile bird wandering around looking for her mother !
Can someone spot which bird is it?

I suspect that it is a nuthatcher.

A shorebird, perhaps some kind of sandpiper - it's often difficult to ID between species in chicks because they look very similar. (Personally I also don't think you should have touched it, could have taken a photo with out interfering with it).

Hard to identify a juvenile.

Based on the location and picture I believe this a Spotted Sandpiper (Actitis macularis) chick. Once they hatch, they are out of the nest, the one you are holding looks fairly small still, must have hatched recently.
You can find more information about them here.


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Why do humans require vitamin B12 supplementation while herbivores do not?
This question came about from reading the comments of this (very unclear) question, which the author did not properly clarify.
Vegans are often recommended to take vitamin B12 supplements, as the vitamin is not present in sufficient quantities within vegan food. This implies that plants do not produce (or need) vitamin B12 in their metabolic processes.
However, herbivorous animals do not require any vitamin B12 supplementation, yet contain significant amounts of vitamin B12 in their food products.
What, then, is so different about the digestive tracts of humans and other herbivores that prevent humans from obtaining sufficient vitamin B12 from bacterial sources? Can humans be supplemented with gut bacteria from herbivores, allowing them to obtain sufficient vitamin B12 while on a vegan diet without requiring supplementation?

Could be due to 1. non-human herbivoure animals have large cecums in their digestive tracts, located between the small and large intestine where bacterial fermentation takes place. 2. They are mainly depending on bacteria for B12 synthesis. 3. They eat soil which provides cobalt for synthesis :P 4. Humans are hindgut fermenters. It could also be a good reason to observe the dietary habits of these animals in the wild - which are naturally way different from human vegans. Also the metabolism and related biochemical pathways. I am curious to know the answer myself.

The bacteria in the foregut of cud chewing animals (e.g. cows) provide enough B12 and other B vitamins. Uptake of B12 happens mainly in the small intestine. There are lots of bacteria in the human intestine but most fermentation of plant matter happens in the hindgut.
Hindgut fermentation also produces B12 but since this happens past the small intestine it is not sufficient to provide enough B12. Therefore non foregut fermenting herbivores (e.g. rabbits) get their B12 when they consume their own feces, which they do anyway to obtain higher digestion efficiency of plant matter. I would not recommend this process to any vegan human though.
As mentioned by bonCodigo, these animals need to take up enough cobalt, and their requirements for this element are higher than our own.
Source:
Contributions of Microbes in Vertebrate Gastrointestinal Tract to Production and Conservation of Nutrients
C. EDWARD STEVENS , IAN D. HUME
Physiological Reviews Published 1 April 1998 Vol. 78 no. 2, 393-427

+1, I highly recommend that one read this paper, it includes a large amount of information about other species of animals and their nutrient uptake strategies.

Primates are especially interesting as even the most herbivorous of them eat animal sources high in b12 like insects, eggs, or meat. Even gorilla the most herbivorous primate eats insects, and sometimes even have to reprocess their feces to get b12.


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Are there any theories why such an imbalance in chirality of molluscs?
Most gastropods exhibit sinistral  (right hand) winding of their shells. But very few species are anti sinistral. Have there been any theories as to why such a great difference?

"Sinistral" means left-handed. I believe most gastropod species have a dextral coil  (which works out to be your intended meaning).

@BenKovitz If I accept an answer,  it doesn't lock out other answers , does it? I don't believe so. If you have a good answer,  please go for it. Thanks.

It doesn't lock out other answers, but it does discourage them. It says "The OP is satisfied with this answer," suggesting that the conversation—and competition—are basically finished, unless someone persuades you to reconsider. On most SE sites, answerers tend to focus on questions that don't have an accepted answer. Here's a nice message about this on a different SE. I don't have another answer for this question, but I'm very skeptical that "non-independent trials means that no explanation is possible".

@BenKovitz Thanks for the advice. I'm about a year working with SE posts, but still learning the ropes.

Why so many molluscs exhibit sinistral winding?
The estimates of the number of molluscs vary quite greatly between 50,000 and 200,000 species. Of those molluscs species, about 70'000 are Gasteropoda. Gasteropa is most diverse Mollusca phylum.
The winding you describe is present in all Gasteropoda and is often called the torsion. So the answer to why there are so many molluscs that make a torsion is simply, because of phylogenetic independence. The torsion evolved only once in the gastropods. The answer to the more specific question, why is the torsion right handed rather than left handed in all gastropods is 1) phylogenetic independence again. The torsion evolved only once and was therefore either sinistral or anti-sinistral. There is no need for an explanation of why they are all sinistral because the observations are not independent.
Why has the torsion evolved at first place?
One may ask but why did the torsion evolved at first place?. I think the reasons are still to be discovered. The following is a summary of what I read on wikipedia (torsion#evolution)
"Why torsion is bad"
As a result of this torsion, the anus is found next to the mouth which is an obvious hygiene issue and therefore seems rather deleterious. Moreover, there are a whole bunch of issues about organs spinning around and entwining. Also, ventilation seems to be reduced by the torsion which is pretty deleterious.
"Why torsion is good"
However, because there's no "hole" left in the posterior position, the torsion may help preventing sediments. Some have suggested that the torsion may allow to move sensory organs closer to the head. The most likely explanation is that the torsion might have evolved as a defense mechanisms against predation as torsion allow an organism to hide its head behind its shell. Finally, citing from wikipedia:

The evolution of an asymmetrical conispiral shell allowed gastropods to grow larger but resulted in an unbalanced shell. Torsion allows repositioning of the shell, bringing the centre of gravity back to the middle of the gastropod’s body, and thus helps prevent the animal or the shell from falling over.

Note also that

Whatever original advantage resulted in the initial evolutionary success of torsion, subsequent adaptations linked to torsion have provided modern gastropods with further advantages.

Why sinistral rather than anti-sinistral
To repeat myself, we only have one single observation of torsion (as it evolved only once) and this observation is either sinistral or anti-sinistral. It sounds therefore quite likely that stochastic processes have driven the evolution of sinistral (rather than anti-sinistral) torsion. In other words, the first mutation allowing for some degree of torsion was probably causing a sinistral torsion and this is it.
But there might eventually be a more functional reason for why torsion evolved to be sinistral. The reasons would then be related to the already existing asymmetry of organs. For example, anti-sinistral torsion may yield to more entwining between the gut and the respiratory system, or to not squeeze too much the one lung, who'd be smaller than the other one due to the presence of circulatory organs. I don't have enough knowledge in the anatomy of the molluscs ancestors to have a good intuition of whether I'd expect sinistral or anti-sinistral torsion to be more beneficial.

all of what you posted is very interesting and all makes sense, my main interest was in why so many gastropods have right hand coiling, and so few left hand. What evolutionary factor might have selective favor of right hand over left?

I developed the second paragraph and the added a section to try to better address this point.

Good hypotheses. Perhaps worth a rudimentary analysis, study.

Stimulating answer! Here are some reasons for doubt, which could be addressed in an edit or by other answers. 1) How do we know that only one torsion mutation ever happened? 2) Most gastropods actually have dextral coils. 3) A few gastropod species and genera are sinistral. 4) Amphidromus perversus has both. 5) A few sinistral snails appear in populations of mostly dextral snails. (Info mostly from Wikipedia. I am not an expert on molluscs.)


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Why do chickens not try to get up if laid on their backs?
I've seen a few videos about chickens being laid on their backs for a few seconds after which the chickens stay in that position until they are turned over. Comments around the video suggested that lying on their backs is a very unnatural position for most birds and so they don't have any reflexes or instincts that would help them get back up. But this is only speculation. Why is that really happening?
Here's one video demonstrating the effect:
https://youtu.be/R9mzz9jxNsM
I've been told Chicken hypnotism is related to this.

This phenomenon is called tonic immobility. And those speculations you've mentioned are wrong: they do get back on their feet, only remain in that state for a prolonged time, which depends on the distance and eye contact with whoever laid the chicken on its back, as stated here.
From this experiment, it can be concluded, that this behavior in which the animal is immobile is a defense against predation, because most attackers sense motion primary.

+1 would you have a reference for the primary motion-detection of predators?

Sharks do the same thing! I'd link to the Wikipedia article on tonic immobility (https://en.wikipedia.org/wiki/Tonic_immobility).


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Hodgin-Huxley model for a single neuron
I am viewing (through edX ) an introduction course to computational neuroscience. In the second lecture, the Hodgin-Huxley model is considered. I am going over some of the questions and have encountered a problem with one of them (a picture of the exercise is attached below). I have a strong background in mathematics, but my background in biology is yet very poor. I am having a hard time connecting the biology to the math. Can anyone help with this question:

Thank you!!

This is essentially a homework. See out homework policy. You are expected to make an attempt at the answer before asking.

I think that since the question includes the answer and asks for an explanation, this is a legit question

My problem is that I don't know how to even start this question..
The formal answer of the course is that all the answers are correct except number 2.
My original answer was that 1,5,7 are correct.
But, basically, I have a problem understanding what considerations I should use..

The details you provide assume that we are all intimately familiar with the experimental facts and the a priori assumptions that went into the derivation of the Hodgkin-Huxley model, so I don't think you will find much help in this forum unless (a) the correct individual happens to see your post, or (b) you provide more background.  Given that this work was published in 5 seminal papers after World War II, I would not have thought you need to recreate the arguments to learn computational neuroscience. It's really about the molecular physiology underlying transmission of action potentials.

That is actually not the most popular representation of the model. You can have a look at this answer. You can also refer to this book - Mathematical Foundations of Neuroscience by Bard Ermentrout. It is a comprehensive book (includes mathematical models of different neuroscience aspects) and is easy to understand.

Ok. Thank you very much for your answers. I will also have a look in those references. I will attach now, the reference slides for my question. If you will have anything else to add that could enlightening my understanding I will be most greatfull. Thanks!

link

@user135172 edx has course forums where you may find more help

Where are the actual questions?

If you enter the courseware, then it is in the videos of lecture 2. it is the ex which comes after lecture 2.3

Since you didn't get the right answer to #6, let's review the basis for this model.
The basis of the model is precisely the statement in #6: an individual channel has a defined conductance when it is conducting, and if all of them are conducting then the total conductance is the single-channel conductance times the number of channels (conductances in parallel add).
Confusion comes from the fact that, in the terminology used here, an "open" channel is not necessarily conducting. The probability that a single channel is conducting is the product $r^{n_1}s^{n_2}$.
$r^{n_1}$ describes the "activation" process, while $s^{n_2}$ describes the "inactivation" process. These are two separate processes, with the activation process now known to be driven by voltage-dependent changes in the configuration of transmembrane domains of the channel protein, while the inactivation process is a charged part of the protein inside the cell that more slowly moves to block the channel when the cell is depolarized. See this summary by Clay Armstrong, who contributed much to our understanding of these processes.
So in the terminology here, a channel can be "open" (in terms of the $r$ process) but still "inactivated" (through the $s$ process) and thus be non-conducting. It can also be "closed" (in terms of the $r$ process) and "inactivated", in which case it is also non-conducting.
The way this is modeled is that $s=1$ means no inactivation, while $s=0$ means fully inactivated. So that covers question 3. This is in contrast to the activation process, in which $r=1$ is full activation.
Question 4 might be a bit misleading as there may be a hidden assumption that you are starting from being at potential $u_0$ for a long-enough time and then increasing $u$ suddenly (which is how action potentials normally are generated). In that case your understanding of differential equations should make it clear that $\tau_r$ and $\tau_s$ are the time constants for the responses of the $r$ and $s$ processes to a change in $u$. The process with a shorter time constant responds more quickly, so activation precedes inactivation (on the average). The different powers associated with the $r$ and $s$ processes ($n_1,n_2$) might confuse things a bit, but try running this model and you should be convinced.
This might seem convoluted at first, but Hodgkin and Huxley worked out this model based solely on their electophysiological studies (with help from Bernard Katz). It's amazing how this model's postulates of multiple single channels and separate activation and inactivation processes have been so well verified at the molecular level over the past decades.

I see. I think I got most of your detailed explanation. I will also look into the link. Thank you!!


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How significant is the genetic component of homosexual behaviour?
From some basic googling, I found that nobody has ever proven that people are born gay and that environment plays a great part in homosexuality.
I wish to know if there is a genetic component to homosexual behaviour. If so, how significant is that component (in some measure such as percentage contribution to the behaviour). What are other factors that play a role in homosexuality i.e. what constitutes environmental factors?

There is some argument about whether or not homosexuality can be connected to genetics, as I have found two opposing references: http://www.osti.gov/scitech/biblio/5957271
http://www.sciencemag.org/content/284/5414/665.short
(though these are experiments conducted on males)

With reference to the original post, how was your friend in a heterosexual marriage surprising? She could simply be a bisexual.

Possible duplicate of How can homosexuality evolve despite natural selection?

Not a duplicate: One is about whether or not there is a heritable component to homosexuality, the other is about whether selection does/would act against such a heritable component to homosexuality

Related: Is homosexuality an adaptation in humans?

This is not an area I know well, but I'm familiar with a couple of studies that have tried to estimate the heritable (genetic) component of homosexuality in humans. A review paper by Rice  et al (2012) points out that:

Pedigree and twin studies indicate that homosexuality has substantial heritability in both sexes, yet concordance between identical twins is low and molecular studies have failed to find associated DNA makers.

Here is a selection of papers that should be of interest to you:

Pillard & Bailey. 1998. Human sexual orientation has a heritable component. Hum. Biol.
Bailey et al. 2000. Genetic and environmental influences on sexual orientation and its correlates in an Australian twin sample. J Pers Soc Psychol.
Kirk et al. 2000. Measurement models for sexual orientation in a community twin sample. Behav Genet
Rice et al. 2012. Homosexuality as a consequence of epigenetically canalized sexual development. Q Rev Biol.

Kirk et al (2000) find a rather strong heritable component (30-60%), which also differs between males and females (stronger in females).

Abstract
  Multivariate structural equation modeling techniques have been applied to examine the causes of individual differences in responses to several items concerning sexual orientation. To minimize potential ascertainment and response biases, the study sample involved a large (N = 4901) community-based cohort of Australian twins aged 18-52 who answered an anonymous questionnaire on sexual behavior and attitudes. The statistical power of the analysis was increased by the availability of multiple measures of sexual orientation (behaviors, attitudes and feelings), providing stronger evidence for the existence of additive genetic influences on this phenotype than in a previous analysis (Bailey et al., 2000). Estimates of the heritability of homosexuality in this sample ranged between 50 and 60% in females but were significantly lower (heritability of approximately 30%) in males.

Note however that is it often difficult to separate genetic and environmental components in these types of epidemiological data, especially when twins have grown up in the same environment. I'm also not in a position to judge or comment on the quality or methods of these studies.

Be careful about the term 'environment' in these studies. In the breeders equation, which is the model used in most twin studies, "Non-shared environment" is just a miscellaneous bin used to account for all the variance not explained by the other terms. It therefore includes measurement error, developmental noise, etc etc. So even if environment as we usually think of it plays zero role, and it's all chance events during embryonic development, 'non-shared environment' will suck up that variance.

There is a 'genetic component' to homosexual behavior in that genes do predict it to some extent. They don't determine it though. As usual it's an interaction between many factors, most of which we don't understand.

For those you are not familiar with the definition of heritability ($h=\frac{V_A}{V_P}$), you might want to have a look at this post.

I doubt that there is a gene or group thereof directly responsible for homosexuality.
Rather, if there is genetic correlation, it would be something like, a gene which makes it more likely for the mother to not produce enough sex hormones during pregnancy, or for the fetus's brain to react differently or not at all to them. Other causes of an unusual chemical composition of the womb are malnutrition in the mother or environmental causes.
And thus the tendency of the brain of a male to be aroused by female forms, or vice versa, is limited, and this makes it more likely, but not pre-determined, for homosexuality to develop.
(Educated guess)

Please add some references to your answer.


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Do animals commit suicide?
Do we have documented cases of animals purposely and consciously trying to end their own life? What leads to animal suicide, and is it preventable?
I've heard mixed answers from various biologists. Is anyone here capable of providing an answer?

how much googling have you done on your own so far? that might be useful to know

@kmm, arguably the current question is different because of the vertebrate restriction and "purposely, consciously"

@ConnorSmith, they could get killed in the food chain, but I highly doubt they are as mentally messed up as humans though.


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Genetic linkage greater than 50 centimorgans
Classically, the linkage between two loci can be measured in centimorgans (cM), which represents the percent chance that these two loci will recombine an odd number of times (generating a recombinant genotype).
Due to independent assortment, markers on different chromosomes are expected to recombine 50% of the time. As I understand, if one conducts a classic experiment and counts various progeny, then deduces the apparent linkage, values of 50 cM or more are interpreted as "impossible to determine whether on separate chromosomes or just recombines very often". See (source), with grammar corrected:

The final point that we need to make regards the maximum distance that we can measure. Because of the way in which the calculations are performed, we can never have more (than) 50% recombinant gametes. Therefore the (maximum) distance that two genes can be apart and still measure that distance is just less (than) 50 cM. If two genes are greater than 50 cM apart, then we can not determine if they reside on the same chromosome or are on different chromosomes.

Wikipedia gives an analytical solution and also remarks that (d is physical distance):

The probability of recombination is approximately d/100 for small values of d and approaches 50% as d goes to infinity.

However, what happens if the linkage is greater than 50 cM? It seems like classical experiments aside, such a situation is possible in reality.
For instance, yeast chromosome IV is 1530 kb long, and averages 0.31 cM/kbp. Let's take two genes on Chr.IV:

DNF2 is at about +631 kb.
TOM1 is at about +1370 kb.

The physical distance between these is about 734 kb. According to the cM/kbp value, the centimorgan distance is $734\text{ kb} \cdot 0.31\text{ cM}/\text{kb} = 228 \text{ cM}$ . How to interpret this 228?
If I mate a haploid yeast which is DNF2 TOM1 with another which is dnf2 tom1 (lowercase indicating minor allele rather than deletion), then sporulate them, what is the chance of getting spores with DNF2 tom1 or dnf2 TOM1 genotypes?
I realize that the cM/kbp value is only a simplification and that in practice linkage is a more complex phenomenon. Nevertheless, it seems plausible that several crossover events can happen on Chr.IV since it is so big. This includes the possibility of 1, 3, 5 and more crossovers which would create a hybrid (assuming they all happen between these two loci), as well as the possibility of 2, 4, etc crossovers which would create a non-hybrid spore (at least as far as our chosen markers are concerned).

Understanding the statistics we use when talking about recombination rate is an important question that is unfortunately too often dismissed in an intro course to evolutionary biology or population genetics and that is misunderstood by many. I have a partial understanding of it but hopefully, I'll manage to write a decent answer.
#Short answer
A recombination rate and a genetic distance (in centiMorgan) are two different things. While the recombination rate is bounded between 0 and 0.5, the genetic distance is bounded between 0 and infinity. There is a one-to-one function from the genetic distance to the recombination rate. For small recombination rate, the recombination rate and the genetic distance take very similar values but for greater values, the recombination rate is much lower than the genetic distance.
#Long answer
There is a tiny bit of math below. These equations are mainly for curiosity as one can understand the answer without understanding the maths behind it.
Definitions of $r$ and $M$
You are getting confused between two different statistics

The rate of recombination $r$ between two loci
$r$ is the probability for two loci to remain in the same gamete after recombination occurred. This probability cannot be greater than 0.5 ($0 \le r \le 0.5$).
The distance in Morgans $M$ (or more commonly in centiMorgans) between two loci. $M$ is the expected number of cross-over that occurs between the two loci.

Morgans and centiMorgans
You will note that I talk in Morgans rather than centiMorgans, which is not typical in the literature, but it helps at conveying the intuition of what it means. If $150$ centiMorgans $=$ $1.5$ Morgans. For two loci distant by 1.5 Morgans, the expected number of cross-over between the two loci is 1.5 (by definition). Below are some more explanations on these two definitions with some drawing :)
Case study with loci A and B
While $M$ and $r$ are closely related, they are not exactly the same thing. Consider the following sequence with the loci A and B
---[A]------------------[B]---

Let's assumed the two loci are very far apart and $M=2$. The probability of having exactly $k$ crossovers is therefore given by a Poisson distribution with rate $M=2$
$$P(k) = \frac{e^{-M}M^k}{k!}$$
Let's say for a given case that $k=1$ (a single cross-over occurred). This cross over is represented by a "/" below
---[A]-------------/----[B]---

Here clearly the two sequences at loci A and B will be separated. Let's say now that $k=2$ (two cross-over occurred).
---[A]---/-----/--------[B]---

Here, even if crossovers have occurred, the two sequences at loci A and B will remain together. Only the sequence in between the two cross-overs will come from the homologous chromosome.
Relationship between $r$ and $M$ - in words
You might see it coming from the previous section. The probability $r$ of these two loci A and B to be separated via recombination is the probability of an odd number of recombination events to occur between them (knowing that $M$ is the expected number of cross-overs).
Relationship between $r$ and $M$ - in equation
Let's calculate first the probability $p_{even}$ that an even number of cross-overs occur. This probability is just
$$p_{even} = \sum_{k = 0}^{\infty}{e^{-M}M^{2k} \over (2k)!}$$
, where I just added the constant $2$ before $k$ at both the numerator and denominator. With some algebra and trig, one can show that
$$p_{even} = \sum_{k = 0}^{\infty}{e^{-M}M^{2k} \over (2k)!} =
e^{-M}\sum_{k = 0}^{\infty}{M^{2k} \over (2k)!} = $$
$$e^{-M} \: cosh(M) = e^{-M}\left ( \frac{e^{M} + e^{-M}}{2}\right ) =
{1 + e^{-2M}\over 2} $$

As, $r = p_{odd} = 1 - p_{even}$,
$$r = 1 - {1 + e^{-2M}\over 2} = {1 - e^{-2M}\over 2}$$
Here we go! We have our relationship between $r$ and $M$! Let's graph it
#Relationship between $r$ and $M$ - on a graph
I just graphed the above equation in Mathematica (Plot[y = (1 - Exp[-2 M ])/2, {M, 0, 5}])

Here is the same graph but zoomed on lower values of $r$ and $M$ (Plot[y = (1 - Exp[-2 M ])/2, {M, 0, 0.1}])

We clearly see from the graph that for low values of $M$, as $M$ increases $r$ increase quasi linearly ($M≈r$). For greater values of $M$, $r$ still increases but slower and slower until reaching an asymptote / plateau at $\frac{1}{2}$. $r$ is indeed bounded between 0 (when $M=0$) and $\frac{1}{2}$ (when $M=\infty$).
Note, the fact that the sum of probabilities of every even $k$ in a Poisson distribution is always lower or equal to 0.5 is an interesting math fact in itself!

From a deleted comment by @emre : You should start with
$p_{even}=\sum_{k=0}^{\infty}\frac{2}{2}\frac{d^{k}e^{-d}}{(k)!}$. Because, simply, $\sum_{k=0}^{\infty}\frac{d^{2k}e^{-d}}{(2k)!}\not=\sum_{k=0}^{\infty}\frac{d^{2k}e^{-d}}{2(k)!}$

@Remi.b As AliceD pointed out, some of your math was wrong. I modified it to be valid, and to still demonstrate the equality in question by using common trig identities of $cosh(x)$.

Just to be clear, markers on different linkage groups (chromosomes) do not recombine 50% of the time. It is just that unlinked mutations co-segregate 50% of the time.
This is a direct quote from Strickberger's textbook "Genetics" 3rd ed. 1985 p 397:

>
  After many tests involving numerous sex-linked genes, the entire X chromosome of D. melanogaster was mapped and found to have a length of 68 map units. This, however, does not mean that there is a recombination frequency of 68 percent in a linkage experiment between yellow and bobbed which are at the extreme ends of the X chromosome.  As explained previously, no more than 50 percent recombination is expected between any two loci, since only two of four chromatids in a meiotic tetrad are involved in any particular crossover point.  In fact, the actual recombination value observed between yellow and bobbed may be even less than 50 percent in a linkage experiment for the simple reason that not every X chromosome bivalent may have a crossover in that particular interval.
  <<

1 percent recombination = 1 map unit

Now that we know what this 68 does NOT mean. Can you explain what it means and how to interpret it?

If you are trying to use meiotic recombination between visible markers to construct a genetic map of a chromosome then you will need multiple linked genetic markers. Once you order the markers with respect to each other then you do additional mapping crosses to get accurate recombination rates (cM) between the pairs of adjacent linked markers. Then you sum those distances up to get the total length of the linkage group in map units.

So if you have know that two genes are tightly linked to the two telomeres: TEL-A----Z-TEL, and you have a couple more well-placed genes between them: TEL-A-----D----------H---------Z-TEL.  If A is 18 cM from D, and D is 20 cM from H, and H is 30 cM from Z then the total distance from A to Z is 18 + 20 + 30 = 68 map units. If however you  mapped the distance between A and Z using just those two markers you would calculate that they co-segregate 50 percent of the time, and may be unlinked. So if you know they are linked but you get 50 cM then you know you need more markers for your map.

Yes, that's exactly what I would be suggesting to include in the answer :)

You're killing me! (by which I mean LOL). Sorry, I wasn't trying to be deliberately dense or obtuse. I was confused because I know you have a rep of like 10X mine, and that you are an expert on evolution (among many other things), but for some reason my frame of mind when I wrote those comments was "he genuinely doesn't know, so I will try to explain it explicitly" and I didn't clue in at all to the StackExchange mantra subtext of improving my existing answer. I am almost totally off of Bio, I just found it too frustrating. So once my initial enthusiasm wore off, I drifted away.

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


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Help identify this worm-like thing
Many instances of this worm-like creature were found in a water system for a mountain cabin in the Sierra Nevada mountains of the US, in late June / early July.  The water system collects water from an enclosed spring.  Can you help identify this creature?
Clues:

The worms have two "points" on their heads.
They can stretch out and be long and thin, or when poked (or are resting) they contract into a small blob.
Here is a picture of a single worm with markings shown.

Here is a picture of a few worms, somewhat contracted.

Here is a movie of them moving, in natural light.
Here is a movie of them moving, with backlight.
Here are pictures of their undersides and their internal structures.

Whenever I pull some out of the water and put them into a tupperware with the same water, they only survive for around 24 hours, after which they seem to disintegrate.  Here is a picture of about 20 of the worms after about 24 hours, the bulk of them have halfway-decomposed and form a heap in the upper right.  After another day it'll just look like debris in the water, you wouldn't even recognize that there were worms in it.  There is a piece of bacon in there because some suggested putting it there to test if they were leeches, but this disintegration happens repeatably and regardless of the bacon; please ignore the bacon.

Someone suggested that they are trematodes, but there are no snails, frogs, or other creatures in the storage and collection sections of the water system;  we have looked very closely.  There may be something within a 30-foot section of pipe, but we doubt it.

Can you help us identify this creature?  Even just possible families of creatures or general categories would be helpful for us.

My first thought, based on the two "points", is that they're slugs, but I think most water slugs live in salt water. This page seems to suggest that freshwater slugs are all tropical, but might have a useful lead.

Are leeches supposed to like bacon ? I thought they needed fresh blood.

@bli - leeches are attracted to odors as well. In swampy areas, it's not uncommon to find a leech or two on a carcass that's been in the water.

@JeffAmelang Thanks for good photography and description effort.

I am not too sure but this looks like Polycelis sierrensis.
Though it is apparent that the worm in your pictures is a tricladid planarian, I was not too sure about the species and the geographical distribution.
However, from the Smithsonian list of freshwater planarians in North America, I deduced that this should be Polycelis sierrensis which is found in California and Nevada (Kenk ,1973).
The EOL page on this species also concurs with the geographical distribution. Moreover, the shape and dimensions of the worm, as described in EOL, matches with that of the ones you have got.
I could not find a picture of P. sierrensis but this is how a general Polycelis looks like:

Wow, a google image search for Polycelis sierrensis shows this image as the first result, at least for me.

@user151841 Same here. But the caption just says Polycelis sp. but this one does look like the worms in the question.

Thanks so much for taking the time to answer, WYSIWYG.  We really appreciate it.

The overall shape appears to match that of a flatworm or planarian, but those don't have eyestalks. Also, in the images you posted, none of the worms appear to have the characteristic eyespots of a flatworm, although they DO look planarian-like in some photos:

If they didn't look so thin, I'd say they were common garden slugs. We get them all the time down in Southeast Texas, and they're attracted to humid areas, especially wetness. They usually have thicker bodies, though:

I've never put salt on a planarian before, but the behavior you describe is exactly what happens when a common slug hits salt. They curl up into what looks like a wad of gum, then shrivel up into a blackened husk. On the other hand, slugs are definitely NOT mountainous creatures. And they're definitely NOT leeches, which we also get down in Southeast Texas.
Based on your location and the images, you're probably looking at some sort of freshwater planarian. They're most likely in the source spring itself.

Their capacity to elongate / contract and their two head lobes make me think they are Planarians.
The two points  on their heads must be their eyes: https://en.wikipedia.org/wiki/Simple_eye_in_invertebrates#Ocelli_or_eye_spots


text:
Critical discussion: Gene expression and systems biology allows us to understand the control of complex traits
I'm having a bit of trouble tackling this question. Any help on what I should write about or the points I should mention would be much appreciated. I keep seeing articles about eQTL and QTL are these relevant as well?

What should be the question's title, is it theoretically or what?

In your question's current form, it may not receive many answers.
Please take a look at our homework policy faq.
Here you will find information on how to improve your homework question so your
fellow users will be more inclined to help. Thank you.

@ FloriOn it is Critically discuss

@cagliari2005 thank you im havin a look at the policy now

what's eQTL? Expression quantitative trait loci?

yes its Expression quantitative trait loci?

Turns to be too long for a comment.
If you are looking for explanation of the title/question, than it is following (roughly).
If we get information about gene expression from all different cell types, and extract also interactions between those genes (if a gets higher then b gets lower), this will allow studying multigene traits. E.g., life quality, height, mental disabilities, cardiovascular risks etc. Thing is that for most health problems that stem from single gene variation we already know named gene, or can easily find it out.
More complex issues are often hidden in statistics, links are not so clear. So, for example, autism is described by genetic variations (so far) only in less than 30% of cases or so. In other cases there is no genetic predisposition or strong evidence. Mainly that is so because many genes interact to produce final trait or illness. Looking with microscope one gene at a time will not provide information about it.
You should look into multi-gene traits, maybe pick your favourite illness (e.g. autism) and see how it is hereditary (tip: not fully). Whole-genome sequencing is important tool in tracing such issues because it gives wide overview and a lot of genetic information about patient.

"Looking with microscope one gene at a time will not provide information about it." Never saw a gene under a microscope. You should rephrase that to something like: "Studying one gene at the time will ..."

@cagliari2005 metaphor


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Is pulse rate measurable in the capillary bed and venous vasculature?
Pulse rate is easily felt when gently pressing the arteries in the wrist or neck region (Fig. 1).

Fig. 1. Feeling the pulse at the radial artery. Source: Wikipedia
Arteries supply the thin vasculature in the capillary bed where the blood flow encounters a large increase in resistance due to the narrow vasculature and blood flow is reduced, albeit the pressure may still be relatively high. The capillary bed, in turn, feeds the venous system (Fig. 2), characterized by a low blood pressure and relatively slow and continuous blood flow. This steady, slow blood flow is apparent during blood sampling procedures from the veins in the arm, where I have never noticed any pulsatile flow by visual observation (anecdotal evidence, but quite representative I'm sure).

Fig. 2. Blood vessels. Source: Aruba trial.
Is there an observable/measurable pulse in the capillaries and veins, or is blood flow continuous in these vessels?
PS. This question was re-formulated based on a deleted question posted by @laggingreflex and credits go to OP.

I asked the original question but mine was probably a lot dumber :) as I was basically just asking whether blood flow was continuous in the arteries of the wrist itself (something I mistakenly imagined were the case), to which the answer would've been "duh no" because if it were you wouldn't be able to measure the pulse. Yours is a great question though, clearly much more than just an interpretation. +1

@laggingreflex - your question was not dumb and in fact pretty interesting! My knowledge on behavior of pressurized fluids is next to nil, so I'm curious to the answers.

If it adds to the context, I was trying to learn how exactly does a sphygnomanometer help in measuring the blood pressure and I encountered this line on Korotkoff sounds page: "As the heart beats, these pulses are transmitted smoothly via laminar (non-turbulent) blood flow throughout the arteries, and no sound is produced." which kinda sounds like the pulsating flow of the blood from the heart becomes smooth and continuous in the arteries (unless I'm misunderstanding). Anyways I'm curious and looking forward to the answers as well.

@AliceD can you include the original question in yours? And why wasn't the original question edited include this aspect?

@bonCodigo - question was removed - edited my Q to explain

This is interesting @laggingreflex http://biology.stackexchange.com/q/35817/8709

In the capillary bed? Absolutely! In the venous return? Depends!
I had to build one of these for class. In short: you can tell how oxygenated the blood is by its color, but you have to correct for how much blood there is: The dilation of the arterioles and capillaries with the heartbeat increases the size of the area being measured, and changes all sorts of properties including conductance. There's a neat heartbeat monitoring method method that involves putting two electrodes on your arm, one at the wrist and one at the elbow, and measuring the increase in conductivity every time your heart beats and your arm swells.
Depending on heart rate and all sorts of other things, there's not usually a detectable heartbeat in the veins right outside the heart (see the CVP, which is pretty much flat). However, the jugular venous pressure is the pressure of the internal jugular vein that drains the head, and that has heartbeat oscillations (not one-to-one, there are "echoes" and other weirdnesses because it's almost connected to the heart. See here for more).
In sum: The capillary bed absolutely swells and contracts with each heartbeat, but in the veins blood usually just oozes along. There are a couple exceptions but mostly they're silent.
(The Korotkoff sounds you're talking about are a fluid dynamics thing. When the veins are regular-sized they're wide enough to permit laminar flow(where all the blood moves in a straight line), which is smooth but still pulsatile. Like these guys the blood flow starts and stops but is in sync with itself. When you compress them you increase the Reynolds number and you get turbulent flow, which you can hear because it's making noise.)

"I had to build one of these for class" : Can you share how you build it or/and an accessible manual for it?

A complete description would be too long for comments. As far as a manual you could try this but I don't advise you try this at home. It's not life-threatening per se but you'll probably need to solder things onto other things.


text:
Are there histones present in the cytoplasm?
In this paper the authors depleted core histone heterodimers H3-H4 at 90 % from the cytoplasm of Xenopus oocytes. They state that their concentration is in the order of 6 uM.
My question is, are histones found in cytoplasm besides the nucleus location? (ignoring the newly sythesized ones), and if so, is there any known function?

I can't access that paper, how did they deplete the histones? Did they use siRNA?

@user137 The experiment was done with cell extracts. Histones were depleted with anti-histone antibodies and Protein A coated beads.

This is quoted from the paper: The cytoplasm of Xenopus eggs contains a large stockpile of core histones in complex with specific chaperone proteins. Histones H3 and H4 are stored as soluble heterodimers… This paper may also interest you: http://www.nrcresearchpress.com/doi/abs/10.1139/o06-082#/doi/abs/10.1139/o06-082

In early embryogenesis, cell division called cleavage occurs every 30 min and there is no transcriptional activity. Oocytes have accumulated important gene transcripts and synthesize the proteins at right times. However, histone is one of the most abundant proteins and it would be difficult to supply enough histone proteins during early embryogenesis while oocytes translate other gene transcripts regulating differentiation.
This is my speculation, but the article calls cytosolic histones "stockpile". Just in case, I don't mean that I deny some other roles of histones in cytosol if there are any.


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How does pressure measured by sphygmomanometer translate directly to blood pressure?
As per my understanding a sphygmomanometer when wrapped around the arm and inflated only measures the pressure of the air inside the cuff, doesn't it? How does that translate directly to the pressure value of blood flowing across the artery?

Korotkoff sounds!
The blood pressure measurement process is fairly cool, and goes like this.

Inflate the cuff to well over plausible blood pressures (250mmHg or so).
Slowly deflate the cuff while listening to the artery.
When you start to hear sounds, that's when the systolic blood pressure is higher than the cuff pressure and the heart can squeeze a little blood through the cuff, which makes a little squirty noise.
As cuff pressure continues to drop it stays between the systolic and diastolic blood pressures and therefore bloodflow stops and starts and creates audible turbulence.
When the artery stops making noise, the cuff pressure is below the diastolic blood pressure and the cuff has no effect on the artery, so it goes back to laminar flow that doesn't make noise.

Measuring the pressure of the cuff is just part of controlling the pressure of the cuff. You could conceivably measure blood pressure by submerging their arm in water(mercury would not require a conversion, but vats of mercury are unpopular in doctor's offices) and listening for Korotkoff sounds and measuring the depths where they start and stop.
Edit: The actual question here is how does cuff pressure physically change the arterial surroundings, not how do we link the two clinically.
The body is mostly water, and water is incompressible. For small strains(amount of deformation) flesh isn't that springy and mostly "flows" like water. When you pressurize the cuff around the arm, the flesh of the arm equilibrates to the cuff pressure the way balloons equilibrate to the air pressure, only less dramatically because water is mostly incompressible. For small pressures and large cuffs, therefore, the cuff pressure is the pressure on the artery wall, and by listening for Korotkoff sounds while varying the cuff pressure the blood pressure can be roughly established.
The reason why you don't lose all blood flow to your extremities while diving underwater is because the systemic pressure on all of your body raises your internal blood pressure, making the net external pressure on any part of your body zero. (The cuff works by exerting a relative pressure difference on part of your body.) At high altitude the sphygmanometer is still accurate-ish because the cuff pressure relative to the atmosphere is still the same as the blood pressure, relative to the atmosphere. If you had air for blood(or any compressible fluid) your veins would collapse underwater. This is why your ears hurt while diving deeply if you don't equalize them: your ear is full of compressible air, and at depth the air attempts to shrink more than the flesh around it, pulling things out of place painfully.

Thanks for the answer, but please bear with me as I might be missing something very obvious here because even though I did understand how Korotkoff sounds help in the measurement, yet I'm still having trouble understanding how exactly do these readings on the sphygmomanometer (like 120mmHg for systolic pressure) actually relate to the pressure that's exerted by the blood on the walls of the artery? Doesn't the sphygmomanometer only measure the pressure exerted by the (compressed) air on the walls of the cuff? How does this pressure directly equate to the blood pressure?

When it comes to pressure differentials, the body is essentially incompressible(it's mostly water and water is mostly incompressible). The cuff is long enough and the arm fluid enough so that as long as nothing moves very far, the pressure on a long enough part of the arm is the pressure inside the arm. Your arm is too viscous to "flow" out of the cuff but otherwise it's not unreasonable to treat flesh as a surprisingly stationary liquid.

okay I understand that, the arm can be treated as stationary liquid, but I'm afraid I still don't see how that answers my question? Actually I'm slightly more confused as to how the arm comes into discussion at all? weren't we just talking about the artery and the cuff? I'm definitely missing something very obvious and I very much appreciate your responses.

The artery is embedded in the arm, isn't it? When the arm is under pressure, the artery is under pressure. The cuff doesn't pressurize the artery directly (it'd have to be surgically implanted) it just pressurizes your arm and relies on the arm to transmit pressure to the artery. Come to the chat, this is getting too lengthy for comments.

I see. Even earlier I imaged the cuff is directly choking on the artery but what I still don't get is how the pressure on the walls of the cuff measure pressure on the walls of the artery (or the hand, if the pressure is transmitted). I guess it's more of a physics question then, I'll have to spend some more time thinking about it. Thanks for your replies, really appreciate it.

One last thing, I was wondering about something you brought up >"You could conceivably measure blood pressure by submerging their arm in water" That's very intriguing point. 200mmHg = 0.26atm and 1atm is 10m deep in water so 200mmHg = 2.6m deep in water? Now if a sphygmomanometer applying 200mmHg on the arm basically stops the blood flow, does that mean that in 2.6m deep inside the water the blood flow would also be stopped? This is clearly not the case. Have I mistaken somewhere in my logic?

(Oh we should totally go to chat these are fascinating questions but they're drifting off-topic.) If you managed to get your arm 2.6m away from your body, that's exactly what would happen(maybe you have very long arms). If you brought your body with you, the body-wide pressure increase would increase your blood pressure systemically and cancel out the increased outside pressure. The closing is a relative pressure effect where the pressure on the arm under the cuff is higher than the pressure on the rest of the body. That's why it still works at altitude.

Ah, makes perfect sense. That was pretty much the only question(s) I had right now. Thanks very much once again!