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Is cyanocobalamin toxic?
I see that cyanocobalamin is not naturally occurring, and is synthesized in vivo to methylcobalamin. As part of the synthetic pathway, cyanide is broken off. All opinions I can find are that this isn't a problem as cyanide is naturally occurring in many foods anyway, and is safely detoxified via the the Rhodenase pathway.
However, given its synthetic creation and vast prevalence as the primary B12 source in nearly all supplements, I was curious if any actual studies did exist to rule out potential (albeit minor) long term cyanide toxicity for this synthetic form of B12. I'm unable to find a single study where cyanide toxicity  was directly tested for, only studies stating that RDA in excess of 1000 times the daily dosage isn't lethal.
I understand no evidence currently exists for cyanocobalamin toxicity, but this wouldn't be surprising if there aren't any studies done in the first place.
Would anyone be able to reference an actual study that directly measured levels of potential cyanide toxicity for cyanocobalamin in any animal or humans?

What is the reference to carcinogenicity? Cyanide is not carcinogenic. You can check here for doses of cyanide that are considered safe.

Mistake in the title sorry, corrected now.

The NIH RDA for vitamin B12 is 2-3µg/day. Cyanocobalamin has an $M_r$ of 1355, of which 26, or less than 2% ($CN^-$) is cyanide.
Since the Minimal Risk Level for cyanide is 50µg/kg/day, your studies are correct in that 1000x the RDA of vitamin B12 in the form of cyanocobalamin is not lethal, and furthermore is expected to not cause any negative effects even in the most sensitive of individuals.
This holds true even if 100% of the cyanide ligands dissociate from cyanocobalamin, which is unlikely to be the case in practice due to cyanide being a very strong binding ligand.
Cyanocobalamin contains too little cyanide, and is consumed in too low an amount, to cause cyanide toxicity. The dose makes the poison.

A common mutation in the Methylenetetrahydrofolate Reductase gene (hetero & homozygous), implicated in a vast array of diseases, is prevalent in some populations as much as 38% Source* - and requires excess supplementation of B12 & folinic acid in order to complete the pathway for homocysteine -> methionine. A vast quantity of anecdotal reports show dosages up to 5mg B12 per day alleviate symptoms. Surely at this level the cyanide would start to matter if cyanocobalamin was supplemented, even if just 1% did break down?

@user4779 It seems that there is no issue, even in your case of extreme overdosage of cyanocobalamin (100µg cyanide daily). Assuming 60kg body weight, one has to take 3mg cyanide daily to reach the MRL.

I guess there's no arguing with the current numbers and evidence, given the studies of the MRL in rats. Thanks to you and WYSIWYF for providing the link to the cyanide toxicity.

Potassium cyanide is added to the cobalamins produced by bacteria to give rise to cyanocobalamin. CN is strongly bonded to Co and will not easily dissociate, thereby making this form of B12 inactive. Therefore, it has been argued that cyanocobalamin is not a good vitamin supplement and other variants such as hydroxycobalamin or methylcobalamin should be used. Displacement of CN from the complex would be energy expensive and even if the reaction is efficient the amount of cyanide released would not be in the toxic concentration. The CN-Co bond is so strong that hydroxycobalamin is used as an antidote for cyanide poisoning; it forms cyanocobalamin by displacing OH with CN.

 Source: Wikipedia and the cross references.

Interesting, but for the molecules of B12 that are bioactive, I believe the cyano group dissociates as free cyanide. Just curious if any such effects have been studied, as free cyanide also breaks off in Amygdalin and that has been linked to cyanide toxicity in comparable dosages I believe.

@user4779 Generally the bond between the Transition metal and cyanide is very strong.  It would not easily dissociate. Even if it does, the minuscule concentration would not be toxic. For all practical purposes you can assume that CN- does not dissociate from the metal. Even potassium ferrocyanide K₄Fe(CN)₆ is non-toxic.

I believe CN- does in fact dissociate from cyanocobalamin, as otherwise it would not be bioavailable as vitamin B12.

@MarchHo It should to a little extent but CN is much stronger ligand than others. And B12 bioavailability of cyanocobalamin is very low.

@user4779 In case of amygdalin the CN is not complexed with a metal. It is covalently bonded with carbon and is close to a hydrolyzable group.

Wouldn't an enzyme be able to easily perform this synthesis regardless of how tightly bound it is?

@user4779 enzymes are not magic molecules. If enzymes could do that easily then why should cyanide poisoning happen at all? Cyanide can be and is removed from cyanocobalamin when it is converted to active form but I assume that it would be very energy expensive and therefore won't happen in a large scale.


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Why do fingers swell during cold winters?
When exercising, tissue in the hands may swell. This may be caused by the muscles generating heat, which leads to blood being pushed to the vessels closest to the surface of your body to dissipate the heat. This response triggers perspiration and may contribute to hand swelling (Mayo Clinic).
This all makes sense. But why do fingers swell during the winter in freezing temperatures? It is referred to as chillbains and may affect the toes as well. See the following picture of chillbains affecting the fingers:

I'm voting to close because you asked the same question once and that has been put on hold, Please edit your original question so clarify, so that can be reopened. The original, practically identical question: http://biology.stackexchange.com/questions/31679/why-do-fingers-swell-during-winters

I have edited what else

Well, I've re-read your original post, and as @WYSIWYG said in the comments you already tagged blood circualtion and you also mention this in your post. It is most likely because of that. So you have most likely answered your own question in your post. Also I don't remember experiencin such phenomenon, although I've never watched closely. So this claim stands on personal / anecdotal evidence. If you could provide some reference, that this is indeed a common thing that would help. Also details on how exactly does the swelling happens would be a plus.

The reason for the swelling is the question @poka.nandor so providing that as detail would answer the question...

continue: if you could provide a more clear focus on what you're interested in more than "or what?".  Basically if we simply things enough most things in our body happen because of blood circulation....  your cells respireI'd suggest something like: "I suspect it is because of increased blood ciriculation. Can anyone confrim? If it is the case why is there increased blood flow and how does it cause swelling."

@AliceD well yes, I misphrased that part. i meant the conditions when the swelling occurs, like after how much time, touching anything cold, doing any exercises, or just in general standing in the cold, does it happen when gloves are put on or only when the OP is barehanded etc.

Question edited. @Bhavesh - if this question edit is not to your liking please feel free to roll back.

@NandorPoka it may be personal / anecdotal, but it definitely happens.  Come to Canada during January, and I'll show you.  ;)  I've observed that the degree to which it happens is directly related to the speed at which you heat up the fingers.  For instance, if you stay out in the cold  for a while and get them a bit wet, then come in and run warm water over them to heat them up, they'll almost definitely swell - frequently to the point of being painful.

From the website of Dermatology New Zealand I learned the following:
Chilblains are due to the constriction of blood vessels in cold conditions. Cold causes constriction of the small arteries and veins in the skin to reduce heat dissipation. This is normal and temporary in nature. However, rewarming after cold exposure may result in leakage of blood into the tissues and swelling of the skin. This can occur several hours after exposure to the cold in temperate humid climates. It can be aggravated by sun exposure.
Chilblains are less common in countries where the cold is more extreme because the air is drier and people have specially designed living conditions and clothing.
Chilblains are more likely to develop in people with poor peripheral circulation. Other contributing factors include genetic predisposition, diabetes, smoking and connective tissue disease such as lupus erythematosus.

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How can green algae be both multicellular and unicellular?
How can green algae be both multicellular and unicellular? What are the cases in which it can be both uni and multi cellular?

"Green algae "is a broad group. You should add details to your question. And why the "organic-chemistry" tag?

Because Algae are represented across four kingdoms, namely Bacteria (unicellular prokaryotes), Plantae (multicellular eukaryotes), Chromista (multicellular eukaryotes), and Protozoa (single-celled eukaryotes).
For example, I. Chlorophyta is unicellular:

I. Chlorophyta. Source: University of Wisconsin
While kelp can become huge and can form underwater forests:

Kelp. Source: Nature
Reference
Guiry, J Phycol 2012; 48, 1057–63

-1. The taxonomic classification (the four kingdoms mentioned) utilized here and the corresponding habituses are at best inaccurate or incomplete. Moreover the question was about green algae (Chlorophyta), I don't see how this answer addresses it.

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Parameters for Fitzhugh-Nagumo model of Action Potential
I'm a high school student who's currently in AP Biology, so my background in biology is quite limited. I'm interested in mathematically modelling action potentials.
Doing a quick google search, I discovered the Fitzhugh-Nagumo model, a simplified case modelling the voltage of the cell during an action potential as a second order differential equation $ C \frac{d^2V}{dt^2} + \epsilon(V^2-1) + \frac{V}{L} = 0$. I want to solve this equation numerically, but I can't find the numerical values of $\epsilon$, $L$, or $C$ online. What are some reasonable parameters for this model for a human neuron?

A high school student would wants to solve a differential equation numerically. Woah. I definitely did not have your level in math and programming when I was in high school. +1.

I didn't know about the Fitzhugh-Nagumo model. I quickly scrolled down this paper and this scholarpedia article. Maybe you can indicate where your differential equation come from and link to some info about the meaning of the parameters $\epsilon$, $L$ and $C$.

This is actually not the Fitzhugh-Nagumo model of the a neuron, however it is highly related to it. I believe the the Equation you have there, is capable of oscilations for any positive values of $\epsilon$, $C$, $L$. I generated this graph with the parameter values all set to 1.  Note how it is very similar to a sine wave.

I believe you where trying to write Van der Pol's equation here:
$$C\frac{d^2V}{dt^2} +\epsilon (V^2-1) \frac{dV}{dt}+ \frac{V}{L}$$
Note the subtle difference of multiplying by the first derivative.
Here is again a image with all parameters set to 1

The Fitzhugh-Nagumo equation can be found on wikipedia here and on peer reviewed  scholarpedia here. For reference it is a two state model described by the equation:
$$ \frac{dV}{dt}=V-V^3/3-W+I$$
$$ \tau \frac{dW}{dt}= V + a -bW$$
A common value for the parameters are $a=.7$,$b=.8$,$\tau=12.5$ $I$ can be anything really, I used $I=.5$ to generate the graph below. Also note that the model wont spike if I below a certain value. The Fitzhugh Equation is is slightly more general, but does simplify to the Van der pol under the assumption $a=b=0$. Here is the graph of it with the constants I described.


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How far in can non-extremophiles live, in Earth?
I am a high school student. I'm doing a project where I need to find a planet in our galaxy that might be habitable. Then I need to create an organism that could live on that planet and justify everything about it Ex: Sight, whether or not it can see and why or why not / Touch / Smell / Respiration / Central Nervous System / Cell Count... My final outcome must have these and a lot more.
I just need to justify and explain where it lives on the planet I have chosen. I found a planet (Kepler-422b) which was described as being one of the most Earth-like planets, in terms of size and temperature, yet found. Since it is very Earth-like, it made my job a bit easier. But the planet orbits a red dwarf star that is cooler than our star, and this planet is -40 degrees Fahrenheit (80 degrees cooler than earth) so my organism will have to live in the ground of the planet and rely on the core for warmth. But I do not know how deep organisms can go into the Earth. Can someone please help me? I have done a lot of research and spent a lot of time trying to find this but extremophiles are the only organisms listed.
Thank you so much for helping me.
An extremophile is defined as a microorganism, especially an archaean, that lives in conditions of extreme temperature, acidity, alkalinity, or chemical concentration. Like the Tardigrade. Im sorry I did not make this clear initialy

Can you define what is an extremophile? It seems difficult to answer question when this is not properly defined.

https://en.wikipedia.org/wiki/Gliese_422_b - It's like 10 times more massive than Earth - it's really not earthlike. Have you thought it out well? Also it's unconfirmed, so may don't even exist...

Welcome to Biology.SE and what a great project, it sounds fascinating!
A few years back there was an expedition that drilled down to the deepest layer of the ocean's crust. Down there they found hundreds of different species of bacteria (mostly Proteobacteria) surviving largely on hydrocarbons and other minerals found in the rock. The deepest (that was sequenced) was found 1391.01 mbsf (meters below sea floor) and survived at a temperature of about 102°C (215°F). Like I said, there were several species sequenced, so you could really use any of them that match your needs as at least a start to your organism.
This is the deepest point I know of that we have found life, and, considering your project, I don't think you have need to go much deeper. I assume Kepler-422b has liquid water (obviously not at the surface, but perhaps a few miles down)? If so, there is a chance that the water goes relatively close to that depth already.
I hope this helps and good luck!
CDB
Source: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2974637/
Edit: If you are looking for a multicellular organism that survives deep enough underground to rely on core warmth, I suggest Halicephalobus mephisto, a nematode living about 1.3 km underground at about 32°C (90°F). This is still considered an extremophile, however it is multicellular with a digestive tract, nervous system, etc. I apologize for the confusion in my initial answer and thanks to jamesqf for noticing my mistake. If you are not content with any extremophiles (even multicellular) please let me know and I will do my best to find something else. Again, I am very sorry for my error.

I think that living that far down makes them extremophiles, pretty much by definition.  And for the OP, the planet could have an ice-covered internal ocean, like Jupiter's moon Europa.

As far as I know these species of bacteria are not officially considered extremophiles, I could be wrong though. I will pin-point a specific species and research it's classification tomorrow to confirm this though.

@jamesqf it would appear that you are correct. The mere fact that these bacteria can survive in this environment makes them extremophiles. For instance, Ralstonia pickettii was one of the species found and it can survive high concentrations of heavy metals and low nutrition, making it both Metallotolerant and Oligotrophic, however this species is not officially classified as an extremophile. This situation seems to be a double edged sword; an organism living deep enough underground to keep warm would need to be Metallotolerant, however an organism living on the surface must be Psychrophilic.

Just out of curiousity, when you say "not officially classified", who/what is the official doing the classifying?

You know, I'm actually not sure. I assume that it would be the team who discovered it. Usually anywhere you get reliable information on classification will specifically note that it is considered an extremophile and cite what type, but I'm not sure who officially decides.

Thank you so much, this really helped a lot and saved me a lot of time! Your answer was great, I guess it was a little silly of me to think that an organism could live that far in the Earth and NOT be an extremophile. The Halicephalobus mephisto looks great, I will be able to use this very well. Again, thank you, all of you

No problem, I'm very glad I could help! Again, what an awesome project, from what you've said you seem to be doing a great job with it! Good luck and have fun!


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Primer Design With Primer-BLAST
I am trying to design primers for sanger sequencing snp detection. In the past I have used Primer-BLAST, but I'm trying to pick up KRAS codon 12 mutations. The problem is that in Primer-BLAST you specify refseq gene ID and so it doesn't seem to design primers outside of the gene locus. This means that my primers will sit on the SNP. Is there a way to tell Primer-BLAST the exact locus I am trying to sequence? Or is there a better way of doing this? Thanks.

You can manually restrict the design ranges in Primer-BLAST screen.

First of all you should enter the targeted sequence. In this case, it will be NC_000012.12 which corresponds to chromosome 12 that has KRAS gene.
You should determine the position of variant that you interested in that chromosome. The KRAS G12D -or rs121913529- variant is in 25245350. position. You can find the position of specific variant on dbSNP.
For Sanger sequencing, the recommended size is 600-1000 bp. So, we should select ranges +/- 300-500 bp apart from the variant position.
For the left primer we choose From:25244850 To:25245050; for the right primer we choose From:25245650 To:25245850. And then submit.
Here are the primer-sets that you are looking for. :)

So actually for the way I phrased the question, this is the correct answer and I appreciate it this works for me trying to get G12D. But the problem I am trying to get at as well is what if the variant I am trying to pick up is in one of the first 100 bases listed in the RefSeq accession number. So the for primer 'From' number should be something like -350. Can this be done?

I understand your question. Unfortunately, it is not possible. I suggest that instead of using RefSeq ID, you can enter larger sequence -such as chromosome-.

yeah that makes sense, that's sort of what I figured. Thanks.

For sequencing primers, I've always used this tool to great effect. You can set up how many bases you want to include before your target, and define how to divide large exons and set up no. of overlapping bases. I think this is what you ask for in your comment to the previous answer.
http://ihg.gsf.de/ihg/ExonPrimer.html

glad to be of service :)


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What is the probability of fixation for a mutant under fluctuating selection?
Here is an answer which explains how one can model the frequency of an allele that is under fluctuating selection (the selection that varies through time).
Not, thinking about fluctuating selection, there exist several derivations of the probability of fixation of an allele present at frequency $p$ with selection coefficient $s$ in a finite population of size $N$. For example, Kimura (using diffusion equations) approximated the probability of fixation $P_{fix}$ to be
$$P_{fix}≈\frac{1-e^{-4Ns} }{1-e^{-4Nsp}}$$
How to model the probability of fixation (in a finite population) of an allele that undergoes fluctuating selection?
I welcome one to answer by using whatever type of fluctuating selection. It might be an alternate of $s_1$ (uneven generation) and $s_2$ (even generation) or $s(t)$ might be a sinusoidal function of the time $t$ (in generations). Or $s$ might be drawn randomly from some distribution.

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Difference between pulse and blood pressure
I'm a very naive and biologically illiterate person, and from what I've read on the internet I'm not really sure I understand the difference between pulse and blood pressure. I'm guessing for most of you this is trivial so I'm hoping for something clear for someone of my "level".
On a side note, I speak french, and we have two words: pression / tension (artérielle). One of them must be wrong since they mean totally different things and makes things even more confusing.
But from what I could gather, are the next statements correct/accurate or am I completely off?

The blood pressure is the fluid's movement "strength" in the veins (or "arteries", please edit my post with the correct english word)
The "tension" is the force applied on the veins itself, kind of like when you're pulling a rubber band
The pulse is just the wave of blood moving, which creates different tensions over the vein and whose movement is created by the pressure.

The blood pressure is the fluid's movement "strength" in the
  arteries (or "artères", please edit my post with the correct english word)

Blood pressure is a measurement of the strength of flow through the arteries. (I.e., the force per unit area exerted by the blood on arterial walls.) So replace vein with artery and your definition is correct.

The "tension" is the force applied on the veins itself, kind of like
  when you're pulling a rubber band

In cardiovascular terminology, hypertension and hypotension are used interchangeably with high and low blood pressure (even though technically tension uses force units and pressure uses force/unit area units). Your definition sounds more like arterial tensile strength, which is the ability of the artery to withstand pulling forces without breaking (which decreases with age).

The pulse is just the wave of blood moving, which creates different
  tensions over the vein and whose movement is created by the pressure.

Pulse is an indirect measurement of heart rate. So, yes, it's the rate of the "wave of blood moving." It creates different "pressures" measured by systolic (the "wave" in your terms) and diastolic (the "trough") whose movement is created by the force (of the heart walls contracting).

There are many articles on pulse and blood pressure, but here's an analogy:
Think of the blood as a heavy iron block you are trying to move by hitting it with a sledgehammer.  Blood pressure is how hard you hit with the hammer.  Pulse (heart rate) is how often you hit with the hammer.
This analogy can be taken further if you like:  There is also stroke volume which is how far the block moves each time you hit it with the hammer, and cardiac output, which is how fast the block moves on average as you hit it with a hammer (depending on the pulse and stroke volume).  Vascular resistance is the friction on the block that makes it hard to move (demanding more blood pressure...)

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How can I create R8 (homopolymer repeat) filter without using illumina pipeline?
illumina instruments have built-in -or online- analysis software for variant analysis (CASAVA). This software can filter out the false positive variants near the homopolymer repeats (AAAAAAAA) and filter them with "R8" tag.
Is it possible to make homopolymer repeat filter without using illumina's own pipeline? (with another software?)
P.S I noticed that, GATK have HomopolymerRun script that makes similar job. But it is no longer supported and recommended.

Yes you can do it with perl or awk or other such languages.

Does it mean that there is no software for such filtration? Should I write my own script? There should be an easier way.

People have made such scripts. Try this one called prinseq. It runs on perl


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Our muscles give us the ability to move our arms but....?
I have a strange question, but let me tell you something first.
If you think of this carefully, then you realize something, please try this right now:
Contract your muscles only so that your arms move without you doing it. You can't.
The way it happens is that you move your arm (or you do something or whatever you call it), then your muscles contract.
If our muscles weren't there, then we wouldn't be able to move our arms.
We don't contract our muscles, we move our arms, then our muscles contract automatically. So the muscles contract themselves, but what gives us the ability to make our arms move after deciding when we want to move our arm?
We can't contract our muscles so that our arm moves, we make that movement, then our muscles contract, but you can't even feel it because it's so light.
This is hard to explain.
So what gives us the ability to make our arms move, but not the muscles? I'm telling you, some people won't even understand, but this is real.
Thank you.

I have tried to edit your question for language and grammar. I tried to keep the revised text as close to your original intent as possible, but if I have made a mistake, feel free to revert the edit or edit it yourself.

Your brain is responsible for interpreting your spatial "I want to reach that way" and converting it into the proper muscle contractions. You're pretty good at it because you've had a lot of practice, you started working on that skill when you were a baby.

This question sounds more like philosophy than biology.

You are trying to connect two neural circuits which are not linked. The muscles act due to discharge from the motor cortex (which gets input from the frontal and prefrontal cortex) which is not directly involved with thought process.

I am a bit confused as to what you are asking. You don't move your arm, like your suggesting, ever. No one does, and no one can. You contract your muscles which happen to move your arm. The movement of the arm is the result of your muscles contracting, not the cause.
How it happens is that your brain sends a signal to your muscles (which you cant feel). The muscles get excited and they contract. The instant your muscle contracts your hand begins to move. In the end your bones are like sticks, and your muscles are the ones that pull the stick in different directions, in order to achieve flexion and extension.
Might i suggest you read up on the musculoskeletal system (http://kidshealth.org/teen/your_body/body_basics/bones_muscles_joints.html) ?

I understand what my question is now, what causes the signals to be sent, how are the signals sent, before the muscles are even contracted.

If I have satisfactorily answered your question, please click the green tick mark to accept my answer, and if you found it helpful, please do consider upvoting the answer also.

your answer is not answered im afraid lets see if you can answer the above.

Can you please be specific as to what exactly you are asking please?

my question is now,  what causes the brain to send signals. what do we do to cause the brain to send signals, so if I want o lift my arm, then what is it that gives the brain to send signals. what comes after the intention to lift arm, and before the brain sending signals.

This is quite different to your first question which you asked. Please start a new question for this.


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Ribosomal DNA references sequences
I'm having a bit of trouble with searching for this piece of information. I'm doing a study related to phylogenetic susceptibility of hosts to pathogens (based on a recent Nature publication), specifically to flu. This requires knowing the reference 18S ribosomal DNA sequence for chickens, wild ducks, horses, pigs and humans (amongst others). Is there a resource that enables us to easily download these?

I presume you have tried the usual sources (NCBI, ensembl etc ?)

Yes, I have tried the usual sources, my biggest question was whether they had a "reference" genomic 18S rDNA sequence, or if the NCBI sequences themselves were reference sequences.

Considering the chicken is sequenced, I'd say that its the same thing. tbh I am not too sure of what exactly you ant, but for ll intent and purposes, you'll be using the sequences from below for your analyses

For birds you can start by searching 18s in http://birdgenenames.org/cgnc/
But generally NCBI Nucleotide database, should provide you with all information and accession numbers. See this broad search: http://www.ncbi.nlm.nih.gov/nuccore/?term=18S+ribosomal+RNA+gene
Adding species specification and other parameters, you might find what you are looking for. For example, see chicken 18S ribosomal RNA gene

I may be jumping the gun here, but assuming that you haven't searched NCBI or ensembl, I'd do that first.
Essentially all genomic information is maintained by a collaboration between US NIH, EU EBI and Japan. All databases are synced to each other, and hence the data should (theoretically) be the same (in practice it never is). I'd suggest you pick one server and stick to it.
In my lab we prefer to use NCBI, but that differs from lab to lab.
You can search NCBI by following the tutorial here (http://www.ncbi.nlm.nih.gov/guide/howto/find-published-info-gene-sequence/) or ensembl bu following the tutorial here (http://www.ebi.ac.uk/training/online/course/ensembl-browsing-chordate-genomes/how-search-ensembl)
A sample search for chicken gives you this (http://www.ncbi.nlm.nih.gov/gene/100861561) with three entries for genomic dna and one for mRNA. I'd choose a complete sequence over a partial sequence.
You might also want to look up in their help the meaning of cds (coding sequence; you'll encounter it)


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How many mitotic divisions do haploid cells undergo before fertilization?
Background
This question is about human physiology and gametogenesis. A spermatozoid is not necessarily the direct "offspring" of a diploid cell. Stated differently, a spermatozoid cell can be the offspring cell of another haploid cell. I am saying "can be" and "is not necessarily", but the correct formulation might be "always is". A given spermatozoid might eventually be the descendent of 1000 generations of haploid cells before (going back in time) finding the diploid ancestor (the one who underwent meiosis II). I'd expect the same to be true for ovules although I'd expect that a given ovule have fewer haploid descendent before (going back in time) finding the diploid cell.
Question

How many haploid generations preceded a typical spermatozoid/ovule that could eventually fertilize an egg?
How does this answer vary with age and sex?

In its most beautiful form, the question is:

What is the distribution of the number of mitotic divisions that happened in the father/mother of a given individual?

Any answer that would offer a step toward answering these questions are welcome!

You may have a look at this post. Haploid gametes do not naturally undergo mitosis but haploid stem cell can be produced, that can give rise to an offspring.

Do you have evidence that haploid gametes naturally undergo mitosis? I was under the impression that they do not undergo mitosis naturally at all.

@March Ho I think OP meant Meiosis II ?

I don't fully understand the comments. When I say meiosis I mean meiosis II indeed (I edited the post). I supposed that after meiosis II mitosis occured to increase the number of gametes but I might be totally wrong (I think I remember that from a Bachelor course).


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Woodpecker pecking, an effective evolution?
I was sitting out on my balcony earlier and saw a woodpecker land on a tree nearby. It began pecking at the tree, and did so about five times, in intervals of about four pecks each time, before finally giving up and flying away. My question is quite simple, were woodpeckers gifted(did probability glean favorably upon) with a positive form of evolution? Does the reward justify the amount of energy they have to exert for food? Were they given an improper and doomed form of evolution?

Welcome to Biology.SE! What do you mean by "were woodpeckers gifted with a positive form of evolution?" and "Were they given a improper and doomed form of evolution?". Do you mean "Is the pecking behaviour of woodpeckers adaptive or should they better do something else of their lives?" Out of curiosity, do you know which species you were looking at? (it might not matter much)

@Remi.b "should they do something else better with their time". And no, I could not see it for it was partially a silhouette, it just looked like a traditional woodpecker to me. I live in Kansas city near the border of Missouri if that matters at all.

I mean, if pecking trees didn't help woodpeckers survive, they wouldn't do it. They're specialized to exploit the food niche of bugs in trees. The reward does (biologically) have to justify the energy they exert for food, or else the woodpecker would die.

The question does not deserve downvotes. I upvote in reaction to the downvotes.

@Luigi: I would look at it the other way around.  If they didn't get enough food energy from pecking trees (and eating the bugs they find there), they would have starved to death long ago, and there would be no woodpeckers around.  The fact of their existence demonstrates that they can survive.

As a +1 to @Remi.b , would downvoters care to explain why this question is bad? I cannot see why this question is in any way lacking in research effort, at most it is slightly unclear.

@MarchHo Unjustified downvotes is kind of a regular thing when it comes to Stackexchange and its off-branches. In my opinion, downvotes should require a comment, but that's just me.

@MarchHo I haven't downvoted but can imagine that downvoters feel that the Q lacks research effort (many misconceptions of the evolutionary process) and is unclear, i.e. 2 out of 3 of "This question does not show any research effort; it is unclear and not useful". These problems have also been mentioned in earlier comments, so further comments pointing this out are redundant.

@jamesqf I think you and I are making the exact same point. The first sentence of my comment maybe should read: "I mean, if pecking trees didn't help woodpeckers survive, they wouldn't do it, because they would already be dead."

@Luigi: Yes, we're saying the same thing, just looking at it from different directions.  As with so many other evolutionary questions, there's an inherent circularity: the reason X evolved to do Y is because it did, and if it's around & reproducing it's successful.

My question is quite simple, were woodpeckers gifted with a positive form of evolution?

Though this has been addressed in comments, it's an opportunity to address a popular mind frame about evolution, that is anthropormorphizing it.
Evolution does not think or bestow in the sense that a philanthropist might. Evolution does not doom or treat unfairly as a dictator might. Evolution is merely the process of predominantly random changes in genetic material that result in a change in the expression of that genetic material. If it is a change that radically affects expression of a critical gene (say, that encodes the structure of hemoglobin), the organism experiences a lethal point mutation and ceases to exist. Evolution for that organism stops there; if death occurs before reproduction, the mutation is lost.
Evolution seems beneficial because the environment exerts selective pressures on life: if two animals (say, birds) in the same habitat (say, woodlands) eat the same food (say, larval insects), competition for resources exists, decreasing the numbers of both animals. However, if a mutation (say, a marginally different beak shape) allows even a slight chance that the animal will have a competitive advantage, it is kept in the population. A staggering number of mutations similarly either harmless or advantageous may eventually allow two animals to inhabit the same habitat without competition - a net gain for both animals.
But there's no gift involved. Just a mind-numbing number of non-lethal mutations over a mind-numbing number of years, under the influence of the selective pressures of the environment. You don't see all the mutations that were deleterious, resulting in countless deaths and dead ends because you are standing in one point in time, seeing what exists around you now. The woodpecker seems almost fantastical.

Were [woodpeckers] given an improper and doomed form of evolution?

Evolution follows the same principles for all species: predominantly random mutations without rhyme or reason or form. If you want to speak of doomed animals, look to mankind's effects on the environment in the last 2000 years, or the last 20. When ecological niches are wiped out, that, not evolution, dooms an animal. The Monarch Butterfly is a poignant example of dooming a species by destroying it's habitat.
A great way the understand selective pressures of habitat is to read about marsupial evolution in Australia. The effect of ecological niches on evolution is very clear.

When I say "gifted" I mean "did probability glean favorably upon". And I know how evolution works; my question was more or less about sustainability of the species given their current scope and path of evolution.

@Krythic - it is as sustainable as any species given its current scope and path of evolution. That's evolution. :-)


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What is the reason behind high resting membrane potential of pacemaker cells?
Pacemaker cells have high resting membrane potentials of -50 to -40 mV, whereas normal cells have their resting membrane potential around -70 mV. Which ions, and what kind of channels are responsible for the high resting potential of pacemaker cells?

According to my knowledge their is a slow influx of sodium ions which causes action potential and during depolarization their is influx of calcium ions and while repolarizing their is efflux of potassium ions. But I want to know specifically what is the reason behind slow influx of sodium at the start of action potential and if their are any other ions involved in this.

The pacemaker potential is interesting (to a biologist) as it involves your typical Na/K channels, Ca channel, as well as a funny current (If) or alternatively called hyperpolarization-activated current.

The funny current is a mixed sodium-potassium current that activates
  upon hyperpolarization at voltages in the diastolic range (normally
  from -60/-70 mV to -40 mV). When at the end of a SA potential the
  membrane repolarizes below the If threshold (about -40/-50 mV), the
  funny current is activated and supplies inward current, which is
  responsible for starting the diastolic depolarization phase (DD); by
  this mechanism, the funny current controls the rate of spontaneous
  activity of sinoatrial myocytes, hence the cardiac rate.

Pacemaker activity (or spontaneous electrical activity) of the
  sino-atrial node is based on the presence of a special phase called
  the diastolic depolarization during the action potential, in which
  cells depolarize spontaneously towards the AP threshold. Animal
  studies (mostly conducted on rabbit heart) have identified that this
  net inward current during the diastolic depolarization phase is the
  result of a complex interaction of multiple inwardly and outwardly
  directed ion currents....

Verkerk, Arie O., Antoni CG van Ginneken, and Ronald Wilders. "Pacemaker activity of the human sinoatrial node: role of the hyperpolarization-activated current, I f." International journal of cardiology 132.3 (2009): 318-336.
Also this

The SAN is a complex tissue with regional differences in morphological
  and electrical properties.Animal studies have revealed that
  pacemaking in SAN cells follows from diastolic depolarization driven
  by a net inward current, which results from an interaction of multiple
  ion currents. Inward currents are activated during diastole:
  hyperpolarization-activated pacemaker current (If), background Na+
  current (Ib,Na), sustained inward current (Ist), T- and L-type Ca2+
  currents (ICa,T and ICa,L, respectively), and Ca2+-release activated
  Na+–Ca2+ exchange current (INCX). Conversely, outward currents are
  deactivated: rapid delayed rectifier K+ current (IKr) and slow delayed
  rectifier K+ current (IKs). The relative contributions of these
  currents to diastolic depolarization are a matter of debate.

Verkerk, Arie O., et al. "Pacemaker current (If) in the human sinoatrial node." European heart journal 28.20 (2007): 2472-2478.
Might I suggest you read up on the papers mentioned above?
You might also be interested in this:
Noma, Akinori. "Ionic mechanisms of the cardiac pacemaker potential." Japanese heart journal 37.5 (1996): 673-682.

The Last reference provided by you was very useful and it had answers to most of my doubts and questions.


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Oscillatory electrical system using a chain of neurons
Many daily activities that we perform are result of inbuilt oscillatory circuits in our body. For example walking, breathing, heart beat, blinking, etc. The coding and decoding of stored memory also happen via controlled oscillations. The link http://en.wikipedia.org/wiki/Neural_oscillation contains information about neural oscillations. It says in here that a single neuron, an ensemble of neurons and activity of brain may exhibit synchronised oscillations. It is also said that these oscillatory circuits can control all the parameters of oscillations i.e. frequency, phase and amplitude.While above are true for neurons as a part of bigger systems, my question is related to study of isolated neurons.
There are many instances of studies of artificial neural circuitary created on a customized substrate(Micro Electrode Array) by masking techniques. Also there are loads of ongoing research to study the simple neural circuits in temporal and spatial domain by electrical interfacing of semiconductor and nerve cells using Field Effect Transistor(FET).
I want to know if these kind of oscillations are unique to some special kinds of neuron? Is the control of oscillation parameter possible in every neurons and isolated neurons? Can a neuron or any other cell exhibit change in action potential independently? Do other cells except neuron and pacemaker cells exhibit oscillation? Can a single neuron exhibit memory?
Can a simple circuit like below generate oscillations?
Suppose I culture the neurons on a substrate in a controlled way such that one neuron is connected to only one other neuron in a linear fashion and the last neuron is connected to first. Assuming we supply the ions if there is loss, can a clock pulse of varying frequencies be generated, where the frequency is the function of the no. of intermediate neurons and their length.
It would be a great help if somebody can provide information about softwares to simulate simple neural circuits (If available).

What is your analysis on this? Theoretically you can build a continuously oscillating system but there will always be some loss. If the neuron never runs out of energy then it would keep firing. The period of the oscillation and the nature of the steady states depend on system parameters. Your question is broad and you have not made any effort to find an answer to the question. Therefore I am voting to close this.

Agreed with @WYSIWYG - No neuron ever evolved to live like a bacterium. This is too theoretical and probably more suitable for another more theoretical SE site.

I'm voting to close this question as off-topic because it is too theoretical for Biology.SE

ps - I ran a few searches on Scholar and there is really nothing to be found (search terms autostimulation&neuron, self-wired neuron and the likes).

@AliceD FHN model is continuously oscillating system.

@WYSIWYG - yes, but it is a model not applicable to a biological system. That is my issue with this question.

@AliceD yeah.. This case has to be specifically modelled.

I wanted to know about generating clock pulse using neurons by giving its own signal as feedback

Suppose for example I culture the neurons on a substrate in a controlled way such that one neuron is connected to only one other neuron in a linear fashion and the last neuron is connected to first. Assuming we supply the ions if there is loss, can a clock pulse of varying frequencies can be generated, where the frequency depends on the no. of intermediate neurons

Interesting add @DivyaPrakash, I retracted my close vote.

single neurons can act as oscillators without the need for feedback, simply by the interplay between various channels.

@AliceD please, can you explain more? If possible give the answer to my question too.

I vote to re-open this (edited) question. At least there are some theoretical studies on such systems, and also relation to how such constructions can't explain the scalar property.

Original poster (question author) did not provide any evidence of even basic research, using google, or pubmed, or google scholar. Hence, it should be closed

I'm voting to close this question as off-topic because OP did not provide any work on answering question. This might be asked in chat room, rather than Bio@SE. Although, I might be wrong

Short answer
A single pacemaker neuron can generate oscillatory behavior.
Background
Given our exchange in the comments, I will focus on single neurons with intrinsic oscillatory behavior. For example, thalamocortical relay neurons and inferior olive neurons have intrinsic oscillatory properties, mainly through the interaction of a hyperpolarization-activated cation current (Ih) and a low-threshold activated Ca2+ current (IT) (McCormick & Huguenard, 1992, and Fig. 1).

Fig. 1 Model for an oscillatory inferior olive neuron. Source: Bal & McCormick (1997)
Rhythmic burst firing is created through generation of a low-threshold Ca2+ current (IT), which activates fast action potentials mediated by Na+, K+, and Ca2+ currents (INa, IK, and ICa, respectively). Entry of Ca2+ in the cell during fast action-potential firing and low-threshold Ca2+ spiking result in after-hyperpolarization through activation of a Ca2+-activated K+ current. This afterhyperpolarization activates Ih. Combined activation of Ih and decrease of a Ca2+ activated K+ current (IK,Ca) results in depolarization of neuron, which activates another low-threshold Ca2+ spike. In this manner, Ih modulates frequency of oscillation. In addition, tonic activation of Ih also contributes to average membrane potential, and therefore to presence, strength, and frequency of oscillation
in these neurons.
Regarding the series of sub-questions - these are quite varied. Perhaps it is better to generate another one or two focused, well-formulated questions on this. For now, I will answer them curtly below. Further, the papers I linked contain a wealth of information, and the McCormick & Huguenard (1992) paper is a detailed modeling study. Both papers are awesome and the authors are three of my all-time favorites so far.
I want to know if these kind of oscillations are unique to some special kinds of neuron?
Answer: Yes quite unique, because Ih channels are quite unique (they have been called "funny currents") and they are not present in every cell.
Is the control of oscillation parameter possible in every neurons and isolated neurons?
Answer: No, as the molecular machinery such as Ih channels may be lacking in most other cells.
Can a neuron or any other cell exhibit change in action potential independently?
Answer: That depends whether the cells are coupled through synapses or other means.
Do other cells except neuron and pacemaker cells exhibit oscillation?
Answer: Yes, some cells start to oscillate, for example in the degenerated retina (modeling work only) and there are non-neural cells that when cultured spontaneously start to oscillate.
Can a single neuron exhibit memory?
Answer: Yes, through long-term potentiation or depression.
References
- Bal & McCormick, J Neurophysiol (1997); 77:3145-56
- McCormick & Huguenard, J Neurophysiol (1992), 68(4): 1384-1400


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How do minute changes in an organism, as a result of evolution, get carried over to next generation
The theory of evolution states that random variations in organisms occur to better suit their surroundings. We take for example a bacteria's flagella. There's a bacteria who has a tube kind of structure that it uses to inject toxins in other cells. Structure of flagella and this tubular structure is very similar. So biologists state that this is clear evidence for evolutionary process wherein this tubular structure underwent gradual changes that resulted into a flagella.
Now my question is, minute changes did occur to this tubular structure, but how do those changes get carried over to the next generation? Almost all components of a cell are created as per the instructions coded into DNA. So does it mean that every minute changes that occur to an organism get recorded into DNA so that they can be carried over? In above example, assume, that a few proteins got accidentally attached to the tubular structure that will help the structure to rotate. Now when this temporarily changed bacteria gets divided into a new one it will have lost that change. So to actually carry over this "beneficial" change would the bacteria have changed its genome? How does this happen? What is the basal mechanism that supports evolutionary changes?

Changes to the organism don't get recorded in the DNA, changes on the DNA generate differences in the organism

As populations expand, generation by generation, they will inevitably
  run into limits on resources. Not all individuals in a population are
  exactly alike as some will have traits that give them an advantage in
  survival. A change in any aspect of the environment can suddenly turn
  what had been just another variation or variant into either an
  advantage or a disadvantage  If a selective pressure (i.e. change in
  the environment), acts against or upon the differences between the
  individuals in a population, you get natural selection, which, through
  time, can cause a population to evolve

http://rmitchellbioanthro.weebly.com/uploads/2/3/7/6/23767919/natselinanutshell.pdf
Evolution consists of two essential things:
Random mutagenesis (in this case a slight change that occurs in the DNA, that causes a slight change in the protein to show up)
The second stage of evolution is natural selection. After the mutagenesis event, nature rigorously selects for the mutation. If the mutation has a fitness cost to the organism, it gets removed (the organism doesn't survive). By removing all things that are more costly than beneficial, nature selects for the fittest.

Take the examples of beetels here (http://evolution.berkeley.edu/evolibrary/article/evo_25)
Very rarely does the external environment directly change the DNA code (you can argue about epigenetics, but that's a different can of worms). Changes in the environment usually dictate the survival of organisms with different traits. In fact what usually happens is a change in the DNA code occurs naturally due to mutagenesis and that change undergoes the rigours of natural selection.
So in you case what might have happened is (I am postulating here, I would recommend a literature search to verify this), your bacteria had a tubular structure that it used to inject toxins in other cells. Some bacteria (due to genetic variation in sexual reproduction) had mutations that allowed it to move this tubular structure. This allowed it to survive more efficiently, and hence reproduce more. Eventually this population of bacteria, slowly replaced the bacteria who had no locomotor control on their "tube", and hence one stage of natural selection has occurred. Now this happens again and again, till the efficiency of the locomotion is optimal.
Might I suggest you read this book ?
Bonner, John Tyler. The evolution of complexity by means of natural selection. Princeton University Press, 1988.

So a fully functional protein can form out of random mutation? Or does that too evolve? Can you give me any links of evidence?

Usually it's due to SNPs and INDELs that you get new versions of proteins.  But again, that's rare where a new protein rises out of nothing.  It's a very iterative process,  and usually the proteins that make the  cut are well conserved from then on.  Usually,  due to genome duplication events,  one gene may code for the protein and the copy will not be under the same selection pressure,  allowing it to accumulate mutations and experiment. Was I able to answer what you were asking?

I'm not a biologist, just have a lot of curiosity in how molecular machinery in cells work. So I have no idea what SNP and INDEL is. Could u tell me the full-form? And I read somewhere that malfunctioning or wrongly folded protein does a lot of harm to cells so will randomly and then successively forming proteins cause problems?

@Shades88 Basically they are small changes in the DNA code. Single Nucleotide Polymorphisms and Insertions Deletions. Anything that causes harm to a cell will cause cell death, and thats the end of that story.

The two other forces of evolution are drift and meiotic drive. Michael Lynch fairly convincingly argues that complexity rarely if at all originates from natural selection.


text:
Why can we control our breath rate but not our heart rate?
Even though we cannot survive for more than few minutes if we stop breathing or if our heart stops, why is it so that our heart beat is controlled involuntarily while breathing can be voluntarily controlled to a certain extent. I just noticed that blinking of eyes also falls in this category; though we involuntarily blink and our eyelids close involuntarily in bright light, there is still voluntary modulation. What kind of evolutionary changes and natural selection could have led to these kind of voluntary modulations i.e. cortical control over these processes?

Perhaps to make tasks like eating and speaking possible. Note that you cannot voluntarily stop breathing indefinitely.

You already know why these processes cannot be voluntary. There is some level of voluntary control on breathing but it is overall involuntary. So if that is your question then you should note what @canadianer said.

evolution does not have consciousness or will. It does not make choices. Living beings are formed through mutations, natural selection,genetic drift etc.

@WYSIWYG involuntary and unconsiously doing something is different.

@DivyaPrakash they more or less mean the same. Moreover I never mentioned the word "unconscious".

Many unconsious activity like walking, writing, understanding and interpreting language are possible even though none of them are quite certainly involuntary action

@canadianer while eating and speaking breathing could also have been stopped involuntarily. There is no reason for making it voluntary to eat and speak.

@DivyaPrakash There is no debate here about subconscious control of voluntary activities. You still have to clarify your question. Plus your above comment to canadianer just sounds philisophical and not scientific.

I specifically want the answer in terms of certain evolutionary advantages if possible.

@DivyaPrakash Evolutionary advantage of what?? Little voluntary control on breathing or heart beat being involuntary. I am sure you know why that latter is advantageous.

@WYSIWYG Little voluntary control on breathing, I guess. As for the advantageousness of latter I am going to research more about what could happen if heart beat was made voluntary.

Let us continue this discussion in chat.


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Why is translocation of food in the phloem still a debate?
I currently take tertiary-high school biology and I am taught that translocation of food in the phloem occurs by the pressure flow hypothesis.
I would like to ask why it is still a hypothesis, and what are arguments against it. If possible are there any scientific literature or journals for me to chew on? Thanks in advance.

The wikipedia page provides some of the opposing arguments, but doesn't necessarily source them.
http://en.wikipedia.org/wiki/Pressure_Flow_Hypothesis


text:
Does the DNA of a tadpole change after it becomes a frog?
Does the DNA of a tadpole change after it becomes a frog? In other words what changes take place as a tadpole becomes a frog, and does this metamorphosis affect the DNA in any way?
I would appreciate your help. I am doing research for a book I'm in the process of writing. If you can refer me to research material, I would appreciate that also.

Welcome at Biology SE! Your question in the title is valid, but your second question is, I beg your pardon, so unscientific that I think this question will be closed. I suggest to read basic biology textbooks to get basic understanding why organism transform from one to another in an instance. in short it does not work like that.

Is your question a better fit for worldbuilding.SE? If so, we can migrate it there.

Thanks for your reference to the world-building site. I have posted my 2nd question there. Enjoy your day--CC

I'm voting to close this question as off-topic because it has no biological basis.

the question has been edited to probably fit the rules... should we conider reopening this?

Your germline DNA remains the same no matter what you do in the growth process (The DNA of a child is the same as the DNA of the adult). What does change is the expression of the DNA (transcriptomic profile), other regulatory factors (Epigenetic modifications), alternative forms of the same DNA expressed differently (splice site variations and alternative promoters) things like that.
Your somatic DNA does undergo small changes, caused by (retro) transposons, and in a few cells, like the mature B and T cells, they contain only a small subset of a few essential genes (that give them their specificity to an antigen), and other small changes like that (credit: mdperry, see comments).

Thank you for answering my 1st question in layman's terms. I appreciate your time. As for the 2nd part, which is basically a "what if", I will try your world building site.--Best regards, CC

DNA gets methylated in certain places.. That is the only "change" that happens with DNA.

We need to make a distinction between somatic DNA and germline DNA. In vertebrates with an immune system, the B-cells that produce antibodies all contain rearranged DNA in their antibody light chain and heavy chain genes (for example). Similarly the T-cells contain rearranged T-cell receptor genes. These are all somatic cells. In contrast, the germline DNA remains intact and identical until meiosis and the recombination that accompanies crossing over. This fundamental observation (somatic rearrangement) was shown in 1975 by Susumu Tonegawa and Noburo Hozumi.

Also, transposable elements are active in somatic cells of many species and introduce DNA rearrangements.


text:
Question regarding an Escherichia coli reaction
With respect to this link
http://www.biocyc.org/ECOLI/NEW-IMAGE?type=REACTION&object=RXN-14479
Here the enzyme is mentioned and the two reacting compounds. Now , my question is
1. When these two compounds react, do they initially get attached to the enzyme before reaction?
2.If they Do both these compounds get attached to the enzyme, what is such an interaction called? Protein compound interaction??

As far as I can tell, enterochelin esterase (Fes) utilizes an Alpha/Beta hydrolase fold to catalyze it's reactions, which means there's a triad of catalytic amino acid side chains. Where Fes differs from other proteins in the pathway is an amino terminal lid domain which confers specificity to the substrates of Fes ((1) dictates this forms a deep pocket in the protein). I'm having trouble finding the exact catalytic amino acids, but homology modeling between IroE and Fes from the same source shows this may be a triad of Glu, His and Ser. If we kind of visualize what a catalytic triad's mechanism looks like, and the following image is a generic lipase/esterase catalytic site,

A sort of transition state is formed between the target molecule and the serine, where the water reacts with help from the asp/glu and histidine to catalyze the hydrolysis. You'd just call it protein-ligand interactions.

Okay now I found this article in wikipaedia : http://en.wikipedia.org/wiki/Ligand , this has got a list of ligands... but the reaction I provided, doesnt contain the list of ligands as mentioned in wikipaedia, then how is it called a protein ligand interaction? Is it because the compound may contain a ligand group which binds to the protein which is why you called it protein ligand binding?

In biochemistry, we'd refer to the ligand as anything that forms a complex with the protein. That includes inhibitors, substrates, etc. The ligand that binds to the active site of the protein is it's substrate, and the following wikipedia page explicates ligands from a biochemical perspective.


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Is there any biological support for the concept of "chakras"?
Is there any support in modern biology for the ancient concept of "Chakras"?
I've seen the concept of 7 chakras linked to the major endocrine glands in the human body (pineal,thyroid, adrenal, testes, etc). This makes some sense, however, I've seen other numbering start to talk about 14, 21, etc number of chakras, which makes me skeptical.  Are chakras real?

I think the question should be migrated to skeptics.SE. In the same time, it will be very important to very accurately defined what is meant by "support for the concept of chakra". Does it mean "Is it true that there is more energy flowing at key points on our body" or does it mean "does medicine such as  effective?". Does it means something else?

If you agree, I think you can flag your own question to ask for migration. Again, I think (might be wrong) that the question will need some remodelling to make sense of "support for the concept of chakra".

I think no matter what definition of chakra you use, it's not suitable for a science based site.

I'm voting to close this question as off-topic because this question would be better suited on Skeptics.SE. Also I would suggest to clearly define what you would call a "support for the concept of chakras".

@canadianer I'm afraid I must disagree with you there. The chakra is, like many things, a guess, a "theory" if you will, developed through someone's observations to explain a concept that they do not understand. This is human nature, to wonder about something and attempt to explain it. Is this not science? Wonder is at the very heart of science and an attempt to explain an observation comes soon after.

Whether this theory is right or not is obviously arguable (not only for this theory, but for many, many others as well), however I do not think it should be closed. I think it would most likely fit in a little better over in Skeptics SE. though.

@CDB If you think it belongs at skeptics SE, then it sounds like you actually agree with me ;)

@cdb a guess is not a theory.

@canadianer It definitely belongs on a science based website, otherwise you would get some pretty scientifically unsound answers. I just don't think this should be it. Than again, this is a website specifically created to answer questions regarding biology, so perhaps it should be answered here?

@dustin Good point, I should have said hypothesis. My apologies.

As is the question is fit for neither sites. You need to define better, not just by referencing to an other page, what is the concept of chakras you reference to. Then if you can formulate a "common claim" Skeptics is a good place to ask if this claim is right (see the closest to a guideline for skeptics at http://meta.skeptics.stackexchange.com/a/2512 ) otherwise you can move it to the beta Health site  http://area51.stackexchange.com/proposals/66048/health but I think here is not a bad place to ask.


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Does crude oil or kerogen contain ancient DNA?
According to wikipedia by the formation of oil there are a lot of organic materials present including DNA. Is it possible that this DNA is conserved somehow for millions of years?

I don't see DNA mentioned at all in either the petroleum or kerogen articles...

I'm sure if you look hard enough you could probably find some nucleotides or other components of DNA/RNA. Finding intact nucleic acids would be very hard, even under ideal conditions, DNA doesn't last forever, and this oil has been under high heat and pressure for a long time.

@MattDMo Organic material = DNA along with other biomolecules.

@user137 What about the kerogen? It was not under high heat...

According to some of the DNA decay kinetic studies, it is not possible to extract older DNA than 6 million years. But ofc. that is just a model, we have to wait another 6 million years to prove it. :D Interesting topic btw.

@inf3rno Your odds may be better there, but I don't know how long DNA lasts in an anaerobic sludge. Depends on pH, temperature, residual nuclease activity, etc. And the DNA decay would probably begin by nicking and cutting the long DNA into shorter and shorter strands. Eventually, even if you could pull DNA out of the sludge, it would be too short to do much with. That being said, some work has been done to sequence well preserved DNA from Neanderthals and other ancient organisms, though these samples were much more recent than oil and kept under better conditions.

@user137 Yepp, I reached the same conclusion.

@user137 Feel free to add an answer with references.

@inf3rno That's the problem, I don't have references.

@user137 http://scholar.google.com/scholar?as_ylo=2011&q=million+years+old+dna

@inf3rno the wording of your question implies that Wikipedia states that there is a lot of DNA present along with other organic materials. It would be better to [edit] your question to clarify this.

@MattDMo edited.

According to Live Science, the temperatures are in the 120 to 300 degree-Fahrenheit range (48-148 degree-Celcius) when crude oil is forming. DNA in "dry" conditions completely degrades at temperatures above 190 degree-Celcius. Which means that there could be DNA in the oil itself if there are some surviving cells, however, outside the cells there are DNases which will chew up DNA.
So the DNA they are talking about is like the DNA studied by Gong et. al, where they're looking at the live bacteria in the crude oil, which would be descendants of the bacteria that was around when the oil first began its degradation from organic material.
On both NCBI and PLOS ONE there appear to be a number of papers studying the bacterial growth in crude oil. Which would be why you may have seen articles about DNA in the oil.

This does not answer the question with a yes or a no.

The thing is there is no REAL answer to what DNA is actually being looked at. It is possible that there is DNA in the oil itself is being looked at but most likely they are looking at the DNA of bacteria that's growing in the oil @MarchHo.


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Specificity of the immune system
We know that the adaptive immune system recognizes foreign particles when their proteins are expessed of the the surface of T-cells, complexed with MHCs. But MHCs present only short peptides of length 8-11 amino acids long. How is it that every antigen has one characteristic 8-11 residues long stretch in some protein of its which none of the host's protein has. Conversely, how is it that this 8-11 amino acid long peptide, which the body is recognizing as foreign is not found in any protein of any cell of our body?

For starters, your conception of antigen presentation seems a bit off, but that's not the crux of your question. There's around 10^15 different sequence permutations for a peptide 11-mer. Despite that, it's actually likely that highly conserved regions of some proteins will be present in both the pathogen and the host. T cells will not recognize them, however, as they are negatively selected in the thymus.

This is not completely true. One part of the adaptive immune system actively recognizes and tolerates own oligopeptides.

@inf3rno Which component is that?

http://en.wikipedia.org/wiki/Regulatory_T_cell "Regulatory T cells are involved in shutting down immune responses after they have successfully eliminated invading organisms, and also in preventing autoimmunity cells." - Ofc. most of the self-reactive T-cells are destroyed by negative selection, or probably (I guess) transformed into regulatory T-cells. I have to read more in the topic, but it's too complex, I have to write a program, which can maintain a knowledge graph.

Another part of the puzzle: http://en.wikipedia.org/wiki/Regulatory_B_cells

@inf3rno I don't think Tregs can be said to be actively recognizing self antigens. It seems that Treg recognition of self is an exception rather than the rule.

I would rather say that your model is coarse-grained, while this one is fine-grained, but you are right, most of the T cells do not behave that way. +1

@canadianer yea, it should be APCs, wrote T-cell by mistake. One more thing, how did you arrive upon 10^15?

@Bio_geek24 Very rough rounding of 20^11

The immune system is the most beautiful, complex biological process that operates on a scale that it can be termed as engineering.
MHC polymorphism:
MHC's have two particular properties that give it flexibility in the face of the antigen: Its polygenicitcy (it contains several different MHC class I and MHC class II genes with different ranges of peptide-binding specificities) and secondly, MHCs are polymorphic (having multiple variants of each gene within the population).
Note: MHCs are also called HLA (Human Leukocyte Antigen)

So as you can see, there is a lot of possible variation possible. I'd recommend reading through this:
http://www.ncbi.nlm.nih.gov/books/NBK27156/
From the source above:

The outstanding feature of the MHC molecules is their extensive
  polymorphism. This polymorphism is of critical importance in antigen
  recognition by T cells. A T cell recognizes antigen as a peptide bound
  by a particular allelic variant of an MHC molecule, and will not
  recognize the same peptide bound to other MHC molecules.
This behavior of T cells is called MHC restriction. Most MHC alleles
  differ from one another by multiple amino acid substitutions, and
  these differences are focused on the peptide-binding site and adjacent
  regions that make direct contact with the T-cell receptor.
At least three properties of MHC molecules are affected by MHC
  polymorphism: the range of peptides bound; the conformation of the
  bound peptide; and the direct interaction of the MHC molecule with the
  T-cell receptor. Thus the highly polymorphic nature of the MHC has
  functional consequences, and the evolutionary selection for this
  polymorphism suggests that it is critical to the role of the MHC
  molecules in the immune response.

While a good explanation, this does not address the question.

@canadianer Apologies, misread the question. Editing the answer now.


text:
Before I move my arm the brain sends signals - what causes the brain to send signals?

Please tell me what causes the brain to send signals, how does the brain send signals?
can you tell me what happens between the point when you make an intention to pick up a glass of water, and before the brains sends signals to the body which excites the muscles.

So what happens at the moment when you make the intention to pick up a glass of water but before the brains sends signals after you reach to pick up a glass of water.

subquestion one seems too broad, but the remainder is interesting.

Action potential - I haven't read through the entire Wikipedia article so I can't vouch for its accuracy (not that my neurophysiology is good enough to critique it), but it's probably a good start.
Broadly speaking: the brain contains different regions that are each responsible for fairly specific tasks. In the case of picking up a glass of water we can, at a high level, describe the mechanism behind thirst. Your blood contains electrolytes in water; you can consider the electrolytes as being like cordial (reduce the water and you have a higher concentration of cordial / electrolytes). A sensing mechanism (beyond the scope of this answer) will trigger action potentials between the relevant areas of the brain (motor, memory, etc.) to result in the final movement.

satisfying answer. nice answer to the question. good attempt because this question I think is not asked before I think.

i think question is bizzare, so there is no need to judge any answers posted

question isn't bizarre, question is good, god wants mankind to learn more about his creation, you just don't know, you are not knowledgeable enough to know what questions are good or not. just be quiet

1) There is always a persistent sodium current which is slowly inactivating in comparison with the fast transient sodium current that occurs when a neuron is depolarized. The effects of this persistent sodium current brings the resting membrane potential near the threshold. Furthermore, neurons do indeed fire and reach depolarization state due to these fluctuations in membrane potential, but those action potentials will not always cause a depolarization of the post-synaptic neurons, since those neurons have inputs of convergence from inhibitory neurons that produce inhibitory post-synaptic potentials. There is no moment or situations where all of your neurons are quiet.
Further information about persistent sodium current can be read in French et al.,1990., "A Voltage-dependent Persistent Sodium Current in Mammalian Hippocampal Neurons"., J. Gen. Physiol., Vol 95;1139-1157 http://jgp.rupress.org/content/95/6/1139.full.pdf
2) The brain center which is thought to play an important role, not only in decision making, but also in behavioral control of the decision making dependent on the reward and outcome, is the prefrontal cortex. Except for its associative learning capabilities prefrontal cortex is thought to have neuronal connections with many part of other brain structures and it must first gather information and integrate the information before deciding what to do. In your question the reward is the glass of water, the emotional response you would get to drink that cold water would aid to the decision making, and the motoric movement is initiated by the subsequent firing of neurons when you see the glass of water and when you recall/remember the feeling to drink it. Prefrontal cortex is therefore activated and can thereafter send action potentials to motor cortex and then to your peripheral nervous system and muscles, so you can pick up the glass of water.
More about this here: http://ac.els-cdn.com/S0959438800001926/1-s2.0-S0959438800001926-main.pdf?_tid=83268f2a-eed1-11e4-ae1f-00000aab0f6c&acdnat=1430354614_ddc06d6aeae4543af28ebe02e29486cc


text:
Why do genes with closely related functions often reside on different chromosomes?
Why do genes with closely related products are so often positioned on different chromosomes?
To illustrate what I mean, here is an example from immunology:

the invariant region of MHC is on chromosome 5
the variant region of MHC is on chromosome 6
β2-microglobulin is on chromosome 15

These three gene products associate into a single protein-complex to present antigens. Why are these genes situated on different chromosomes? Wouldn't it make more sense to keep them associated into a localized region onto a single chromosome so that their transcription can be jointly regulated?
It is just an example; I get the impression that many multiprotein complexes are formed with products from different chromosomes.

I don't understand your question - you mean why associated gene products are located on different chromosomes?

probably, because it creates more variability, through random mutations and crosses you can enhance parts of same pathway independently. Chromosomes are mixed up during sexual reproduction as an additional mechanism of variability (together with crossing-over) during meiosis.

@AliceD Yes. Please edit my question if you think it needs clarification! My English is far from perfect.

Perhaps something like this?

Simply because it can (happen). Natural selection does not yield processes that are designed because there are no designers involved. Barring non-terrestrial involvement (cf. the pan-spermian hypothesis), as Stephen Jay Gould was fond of pointing out, natural selection can only work on what has come before. In other words, the raw material consists of what is currently available (for better or worse). All that matters is having more offspring than other individuals have in the next generation. That is what gets selected. It doesn't matter what we think about comparative efficiency.

The thing we must remember is that during evolution, there occurs many events that may result in genomic reshuffling.
Considering your example of MHC, when we look into the evolution of the complexes

The classical human MHC contains 224 genes, .... Antibody and T cell mediated immune responses against invading pathogens are initiated through MHC class I and class II molecules. These main components are not only missing from invertebrates, but are also not present in primitive jawless fish, such as hagfish and lamprey. MHC class I and II molecules do, however, exist in all jawed vertebrates, including the cartilaginous fish.

Now that tells us something in itself. If you observe the universal evolutionary tree, we can conclude that the hagfish and lamprey are most ancestral, especially compared to telostii. This is crucial when speaking in terms of evolution, as

this demonstrates that the separation of the MHC class I and class II loci is characteristic of teleost fish, which represent half of all vertebrates. Since the genes of the immune system were present in the common ancestor of tetrapods and teleosts, the differences in their genomic organisation may be the result of lineage-specific chromosomal events such as duplications, inversions, deletions and translocations.

You can read more about the MHCs here:
Sambrook, Jennifer G., Felipe Figueroa, and Stephan Beck. "A genome-wide survey of Major Histocompatibility Complex (MHC) genes and their paralogues in zebrafish." BMC genomics 6.1 (2005): 152.
And thats usually the reason for the major changes you see. Often other changes occur, due to transposons, which cause pseudogenes to form and/or neofunctionaliation to occur. You can read about them here:
Feschotte, Cédric, and Ellen J. Pritham. "DNA transposons and the evolution of eukaryotic genomes." Annual review of genetics 41 (2007): 331.
I am fairly certain, that this applies practically to majority of the genes, that are not linked strongly genetically (http://learn.genetics.utah.edu/content/pigeons/geneticlinkage/).

Can you give me some link about how this duplications, inversions, deletions and translocations affect the regulation of such genes? Are they activated by the same stimulus? I guess so, because they are duplicates at the beginning of separation.

Would you prefer me to answer here or in a different question? as you are asking more about functional divergence, and the evolutionary fate of diverged genes, and in the original question here you asked about linkage and genome wide chromosomal events

If you think it does worth a new question, then ofc. I can write a new one.

@inf3rno its upto you really. You can look up subfunctionalisation here (http://en.wikipedia.org/wiki/Subfunctionalization)

Thx, I'll read about it.


text:
Do human-ape hybrids exist?
Since humans and apes share up to 99% of their DNA, can they interbreed? For example, a horse and a donkey seem to be just as distantly related and produce offspring. Mules, however, are sterile. Would ape-human interbreds be sterile?

Human-ape hybrids are genetically impossible, because the two species have different numbers of chromosomes - humans have 23 pairs (46 total) while all great apes (orangutans, gorillas, and chimps) all have 24 pairs, or 48 total chromosomes. The egg would likely not get fertilized, due to differences in surface markers, but if by some chance the sperm penetrated the egg, the resulting cell would never* divide.

Welcome to Biology S.E.! If you have any question regarding the site, please visit The Help Center.

Although this question sounds easy to answer in the first place, it is not. The main problem between humans and the apes we are most closely related to is that we have 46 chromosomes, while the apes all have 48. At some point in the evolution of the humans the ancestral chromosomes 2 and 4 fused together to form our chromosome 2, leaving us with only 46 chromosomes (see reference 1).
This makes offsprings much more complicated, but not completely impossible. A good example for this are crosses between donkey and horses (donkeys have 64 chromosomes, horses 62) to get mules (male donkey crossed with a female horse) or hinnys (male horse crossed with a female donkey) which subsequently have 63 chromosomes and are infertile. There are even crosses possible between horses and zebras which even differ wider. Zebras have between 32 and 46 chromosomes (depending on the species) but still zebroids are possible. See reference 2 for some more details.
So far there has been no successfull attempt to produce such hybrids, although there have been some attempts to make them. Some information can be found in reference 3.
Besides this problems (which are also due to ethical restrictions), there is a study available that at least humans and chimpanzees interbred for at least 1.2 million years after diverging and still produced fertile off-springs. See references 4 (for a summary) and 5 (original paper) for details.
Based on this evidence, I would say it is possible for humans and apes to produces off-springs, however, this is relatively unlikely and they will probably be infertile.
References:

Origin of human chromosome 2: an ancestral telomere-telomere fusion.
The chromosomes of two horse x zebra hybrids; E. cahallus x E.
grevyi and E. hurchelli
Blasts from the past: The Soviet ape-man scandal
Human Ancestors May Have Interbred With Chimpanzees
Genetic evidence for complex speciation of humans and chimpanzees


text:
Recessive alleles at Hardy-Weinberg equilibrium
I've run into a question that I disagree with others on but I would like to receive the input of others. The question is:
If a population is at Hardy-Weinberg equilibrium, which of the following can be predicted for the recessive alleles in the population? 1) They will eventually disappear, 2) They will be selected against, 3) They will be maintained at the same frequency, 4) They will be expressed in the heterozygous condition, and 5) They will become dominant.
Some people said that the answer to this question was that the recessive alleles would be selected against, but I interpreted the question as having the answer that the allele frequency of the recessive alleles would not change and instead would be maintained at the same frequency.
My rationale for this was that Hardy-Weinberg equilibrium means there is random mating and basically no radical shifts in allele frequencies from outside sources, such as gene flow, natural selection, etc. I would think that the allele frequency would not change, but I may be incorrect.
Is my methodology correct?

In short: No, you're wrong. Hardy-Weinberg is nothing but a formula that link genotypes frequencies to allele frequencies (under random mating). Allele frequencies will change in response to selection so does the genotype frequencies. The only think that doesn't change is the relationship between allele frequency and genotype frequency. (the above assumes that selection occurs on survival, not on fecundity).

@Remi.b I think you're conflating Hardy-Weinberg frequencies with Hardy-Weinberg equilibrum. The former are exactly what you say, "nothing but a formula that link genotypes frequencies to allele frequencies (under random mating)". The latter imply stable maintenance of these frequencies via the term equilibrium.

Let's go through the possible answers. Which of the following could be predicted? Not (1), because we don't know whether selection favors or disfavors the recessive alleles. Not (2) for the same reason. Not (4) by definition. Not (5) because recessive alleles don't magically become dominant.
This leaves us with (3), which also seems correct: not only do we know that frequencies don't change under the Hardy-Weinberg assumptions, but also an equilibrium is by definition a state at which frequencies remain the same.
An aside: this question fairly clearly recalls G. Udny Yule's confusion about the fate of recessive alleles, which lead Punnett to enlist G. H. Hardy's help in deriving Hardy-Weinberg equilibrium. Yule expected recessive alleles to decline in frequency by virtue of their recessiveness; Hardy showed otherwise.


text:
GPCRs: Gi and Gs
GPCR = G-protein coupled receptor
Gi = G inhibitory alpha subunit
Gs = G stimulatory alpha subunit
Are there structural differences between Gi and Gs subunits (secondary structure)? Or is it just categorization by effect on cAMP level? (Gi inhibits cAMP production, while Gs stimulates cAMP production)

Adding some more background is recommended. A good start is to remove any unnecessary acronyms and supplying some background to what the physiological function of both these peptides is. And what effort, if any, you have put in looking up the structure of both subunits (crystallography etc).

@AliceD. This is perfectly clear if you know GPCRs.

@cagliari2005, I know what G-prot couples Rs are, I am just trying to prevent question closure. Otherwise it'll be tagged as homework.

Jenny, both subunits differ in amino acid sequence - so differences in primary structure are inherent. Can you elaborate what you are after exactly? Secondary and/or tertiary structure perhaps?

This is question of how the subunits are categorized. So is it the structure of subunits or effect on cAMP? Or is there a very high correlation between the structure and effect on cAMP that they are essentially the same method of categorization?

Also, I didn't know that there was the difference in the amino acid sequence. That helped me grasp the difference between the two subunits somewhat.

Gi and Gs have a structurally different sub unit in their alpha chain.

The receptors for PGE1 and adenosine interact with inhibitory Gi,
  which contains the same β and γ subunits as stimulatory Gs but a
  different α subunit (Giα). In response to binding of an inhibitory
  ligand to its receptor, the associated Gi protein releases its bound
  GDP and binds GTP; the active Giα · GTP complex then dissociates from
  Gβγ and inhibits (rather than stimulates) adenylyl cyclase.

Both β1- and β2-adrenergic receptors are coupled to G proteins (Gs), which activate adenylyl cyclase. In contrast, α1 and α2 receptors are coupled to two other G proteins, Gq and Gi, respectively. Gi inhibits adenylyl cyclase, and Gq stimulates phospholipase C to generate IP3 and DAG as second messengers.

Also this,

A comparison of chimeric receptor 1, which interacts with Gs, and
  chimeric receptor 3, which interacts with Gi, shows that the G protein
  specificity is determined primarily by the source of the
  cytosol-facing loop between α helices 5 and 6. A comparison of
  chimeras 1 and 2 indicates that α helix 7 plays a role in determining
  the ligand-binding . B. Kobilka et al., 1988, Science 240:1310; W. A.
  Catterall, 1989, Science 243:236.

I'd recommend reading through this:
http://www.ncbi.nlm.nih.gov/books/NBK21718/

So in summary, structure between 5th and 6th helix is different between Gs and Gi, and this leads to binding to adenylyl cyclase at different sites, one being stimulatory and one being inhibitory. And this means a very high correlation between structure and function. Thank you for your answer!


text:
Can we produce synthetic red blood cells lacking antigens?
I had an idea come to me during Biology class and I immediately asked my teacher, but she couldn't really answer the question, so I'll ask it here.
What are the limiting factors in the production of synthetic red blood cells with no antigens? I mean, we do have the human genome mapped, but am I naive to think that we have genetic technology capable of doing this?
If red blood cells are too complex to manufacture, is it feasible to manufacture much smaller particles of just hemoglobin inside small spheres of cell membrane and use that as a temporary replacement for red blood cells?
(I was at a medical research talk a while ago and one professor was explaining that there are many other proteins bound onto a red blood cell that aren't of the ABO or RH system. Normally this isn't a problem for recipients who only occasionally received transfusions but for people who need a long-term supply of blood, their bodies do get sensitized to the foreign proteins and will eventually start attacking the foreign red blood cells).

Actually there are such particles. It is estimated that about 20% of the hemoglobin (HGB hereafter) is in HGB vesicles (HbV hereafter) formed by RBCs. So sure, it is possible to use small particles instead of RBCs, but these vesicles have major and minor antigens on their surface. According to some of the articles they cause other complications too by blood transfusions and they are destroyed by the immune system within 3 to 7 days. So they don't solve the problem.

In Vivo Volume and Hemoglobin Dynamics of Human Red Blood Cells
Artificial Oxygen Carriers (Hemoglobin-Vesicles) as a Transfusion Alternative and for Oxygen Therapeutics
Red blood cell vesiculation in hereditary hemolytic anemia
The red cell revisited--matters of life and death.
Red blood cell microparticles and blood group antigens: an analysis by flow cytometry
Hemoglobin-Vesicles as Oxygen Carriers
Physiological Capacity of the Reticuloendothelial System for the Degradation of Hemoglobin Vesicles (Artificial Oxygen Carriers) after Massive Intravenous Doses by Daily Repeated Infusions for 14 Days

HGB vesicles without major and minor antigens are not a perfect solution either (I think), because the immune system tends to attack such things. For example by viral infections the MHC1 levels are low (in cells with nucleus) to avoid T cell response and the NK cells does not like that, so they destroy such cells. I am almost sure something similar would happen with this kind of vesicles as well. At least afaik. the immune system checks not just the presence of these antigens, but their composition as well. So if a RBC is under stress, then it changes the antigen composition on its surface and the leukocytes destroy it if necessary. According to some of the experiments PEG can cover HbV antigens and increase immune compatibility, so having less surface antigens seems to be a better choice than having more.

Development of a Synthetic Blood Substitute Utilizing Hemoglobin Vesicles
Biocompatibility of Hemoglobin Vesicles, a Cellular-Type Artificial Oxygen Carrier, on Blood Cells and Plasma Proteins In Vitro and In Vivo
Artificial Oxygen Carriers, Hemoglobin Vesicles and Albumin−Hemes, Based on Bioconjugate Chemistry
Hemoglobin Vesicles, Polyethylene Glycol (PEG)ylated Liposomes Developed as a Red Blood Cell Substitute, Do Not Induce the Accelerated Blood Clearance Phenomenon in Mice

HGB vesicles have another problem. The HGB inactivates in them without reduction (metHb formation). Only Fe2+ HGB can carry oxygen. This can be solved with methylene blue according to this study.

Red Blood Cells Donate Electrons to Methylene Blue Mediated Chemical Reduction of Methemoglobin Compartmentalized in Liposomes in Blood
Inhibition of methemoglobin formation in aqueous solutions under aerobic conditions by the addition of amino acids

We cannot use free HGB either, because it would decrease the NO levels and lead to endothelial dysfunction. I think to small particles would have the same effect because of increased surface.

Mechanisms of Slower Nitric Oxide Uptake by Red Blood Cells and Other Hemoglobin-containing Vesicles
Microparticles in stored red blood cells as potential mediators of transfusion complications
Removal of Cellular-Type Hemoglobin-Based Oxygen Carrier (Hemoglobin-Vesicles) From Blood Using Centrifugation and Ultrafiltration

According to other studies RHSA-heme (serum albumin bound to synthetic heme) is another option. It seems to be safe if you replace only 20% of blood volume (of rats). I think a complete transfusion is not safe, because it would reduce the NO levels as we already discussed. I have not found an experiment which does complete transfusion.

Safety evaluation of an artificial O2 carrier as a red blood cell substitute by blood biochemical tests and histopathology observations.
Exchange transfusion with synthetic oxygen-carrying plasma protein “albumin-heme” into an acute anemia rat model after seventy-percent hemodilution

So there is ongoing research in the topic. There is progress, but none of the current solutions is perfect I think.

Artificial blood substitutes are being researched and developed as alternatives for replacing RBCs for oxygen carrying capacity. Regular human blood has a shelf life of only 42 days which limits their utilization over more extended periods. This necessitates the development of blood substitutes which can be stored for longer duration. In addition, blood substitutes have universal compatibility, and therefore their application is not restricted by typing and cross-matching. Blood substitutes are extremely necessary in case of acute and chronic blood loss from injuries and accidents where a shortage of oxygen to cells affects the survival of patient by inflicting permanent damage to tissues.
Blood substitutes market is categorized into two segments viz. Perfluorocarbon-based oxygen carriers (PFBOC), and Hemoglobin-based oxygen carriers (HBOC). PFBOCs are based on inert components which replace hydrogen with fluorine. HBOCs consists of hemoglobin derived products sourced from humans blood, bovine blood, microorganisms and transgenic animals.

Artificial blood Substitute is an artificially developed substitute for red blood cells which is use for transporting oxygen and nutrients to the body cells and transporting back carbon dioxide, ammonia and other waste products away from cells.
Six potential application markets have been identified based on the possibility of replacing donor blood in critical medical treatments-
Injuries,
Cardiovascular diseases,
Malignant neoplasms,
Neonatal Conditions,
Organ transplants,
Maternal condition

Welcome - The question is on antigens in specific and hence your answer doesn't address the question. Further, your answer is not references or supported by credible web links. -1


text:
What is contiguous premise culling and dangerous contact culling?
I am reading this paper related to FMD (foot and mouth disease) epidemics which occurred in UK. It mentioned about terms like IP (infected premise culling), CP (contiguous premise) and DC (dangerous contact cull). IP is the mandatory slaughter of all livestock on an infected premise. But what is CP and DC?

Dangerous Contacts were defined as premises where animals have been in direct contact with infected animals or have, in any way, become exposed to infection
Contigous Premises are defined as a category of dangerous contacts where animals may have been exposed to infection on neighbouring infected premises

Tildesley, Michael J., et al. "The role of pre-emptive culling in the control of foot-and-mouth disease." Proceedings of the Royal Society B: Biological Sciences (2009): rspb20090427.

Oh great. This helped me a lot.