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An over-simplified model of cell division and its relation to stem cells
I am a mathematician, and I decided to try to model cell division with math and see what conclusions came out of it. I had some questions concerning stem cells that came up in the model.
In an extremely simplified model of cell division, each cell decides what cells it will divide into with no output from the outside workd, including from neighboring cells. I also assume the time frame is small enough that cells do not die, and that there are only finitely many 'programs' telling different cells how to divide.
Given these assumptions, I came to the conclusion that one of two things could happen:
1. The number of cells grows exponentially, or
2. Most cells will never divide into other cells.
In fact, if growth is going to remain constant (e.g. 300,000,000 cells per month, every month in a sample), then eventually there will be two kinds of cells:
1. Normal cells, which never divide, and
2. 'Starter cells', which divide into normal cells but NEVER create other starter cells. The number of starter cells is eventually constant.
I hypothesized that these starter cells would eventually be far outnumbered and become a very small part if the body proportionally. I hypothesized that hair follicles, nail roots, growth plates, and bone marrow contained starter cells. I further hypothesized that these are adult stem cells.

Question 1: Is this what stem cells are? Are they the cells that divide to create other, non-dividing cells?

After this, I realized that if the starter cells die, they would not be replaced under my model, because no cell is allowed to divide into new starter cells. I hypothesized that stem cell transplants fail because the host body kills off stem cells one by one and they can it be replaced. I also hypothesized that in the host, outside signals like hormones (which weren't allowed in my model) tell the body to create new stem cells as needed.

Question 2: Do stem cell transplants fail because isolated stem cells do not replicate themselves?

Finally, I noted above that the alternative to a bounded amount of stem cells is exponential growth, where stem cells divide into stem cells.

Question 3: Do embryo stem cells divide into other stem cells exponentially? Is this why embryo stem cells are easier to work with?

Thanks for your time. Even answers like "no, this is obviously wrong because ..." would be appreciated.

You have a few misconceptions about stem cells, I will try to explain where they are.
First of all, cells are not independent. They influence each other with signals and secreted messenger substances. If you look at a human embryo the state of totipotency (where all cells can differentiate into each cell type of the body) ends after 3-4 days when the blastocyte has developed. This structure already has a differentiation into a inner cell mass (embryoblast) and a outer cell layer (tropoblast).
If all cells would simply divide on their own, this would rather look like bacteria dividing in culture media, but not as a forming, multicellular organism.
From these few cells in the beginning all cell types of the body have to develop (around 200, if I remember the number correctly). To reach this, the pluripotent stem cells need to proliferate and differentiate (develop into more specialized cell types) quite a lot. So embryonic stem cells do proliferate. Adult stem cells are not proliferating at the same rate a embryonic, but they still do. A good example are the melanocyte stem cells (which are already pretty specialized as they can only further differentiate into melanocytes) which replenish the melanocyte population of the hair bulb at the beginning of each hair cycle. Differentiated cells can divide as well, when necessary, think only about wound healing.
Question 2: Stem cells (especially adult stem cells) need very defined living conditions. This includes specific signalling molecules (Oct or nanog are examples for that) to stay stem cells. If this signalling is missing (and it does in the normal human body) then these cells either differentiate or (more likely) die.
The only stem cell transplant which takes place regulary is the transfer of hematopoietic stem cells to leukemia patients. There the problem is to keep the immune system from atacking these cells as foreign.


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Is a neurostimulation implant for the soft-palate component of obstructive sleep apnea plausible?
There are currently ongoing clinical trials for neurostimulation implants designed to keep the tongue from blocking the airway in obstructive sleep apnea.  The nerves for this are in the neck and surgically accessible.
Where are the nerves that control the soft-palate, and would it be plausible to implant a similar device for them (given years of development obviously)?

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2 blue eyed children
My husband had light brown eyes. His father had hazel and his mother, light brown as well. His younger brother however, has blue eyes. Both my children have blue eyes. Is this possible? I thought once the recessive gene was used in my first child, his dominant brown gene would take over?

What is your eye color?

I think this - "I thought once the recessive gene was used in my first child, his dominant brown gene would take over?" is where you are going wrong.

There is some chance for that. Look at this chart with some probabilities:

Its from this webpage, which also gives some background information.
There is also an online calculation tool available, which takes the grandparents into account as well. It can be found here.

I think this color chart is dependent upon the heritage of the individual. (the population in genetic speak). there are no blue eyed people in some populations.  The mutation is only 10,000 years old or so. http://scienceblog.com/15361/all-blue-eyed-humans-have-common-ancestor/

I know. Its a mutation in the OCA2 gene, which is thought to come up from the black sea. See the answer in this topic for the reference.

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Bioinformatics : Drawbacks of using ORA(Overlap Analysis)
What do you think are the potential drawbacks/weakness of using ORA to explain distinction between two phenotypes.
I identified a few which were the dependencies of DE and the statistical method used to filter the starting DE list.
Any other weakness?
Thanks

ORA = over-representation analysis; DE = differential expression.

Like Liam said, this sort of analysis is dependent on the database you use, which may not be adequate for what you are trying to accomplish. And as far as I know, these databases are at the gene, not isoform, level. So if a change in two conditions is a result of a change in which isoform is expressed, rather than the amount of expression, you will not detect it.
Also it treats genes as equals that are independent of each other but thats usually not the case. For example if p53, at the top of a pathway, is expressed differently,  that has much stronger implications than if a gene at the bottom of the pathway was expressed differently. Additionally, it treats each pathway as independent of each other, but again that is usually not that case and there usually is some overlap between pathways.
You can read more here http://www.ploscompbiol.org/article/info%3Adoi%2F10.1371%2Fjournal.pcbi.1002375

It really depends on the specific methods you're using. If you're using a pathway-based methodology, I'd strongly recommend reading Khatri et al (2012) (1), which provides a good overview.
The main issue that's not touched on in that work is that pathway-based methods are highly dependent on the pathway definitions used, and the contents of the pathways are not always what you might expect in terms of their topology (a good example is KEGG's Neuroactive ligand-receptor interaction (2), which contains a huge number of events that look like 'single ligand binds to receptor', with no downstream events).


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How does a stonefish get oxygen out of water?
It is said that the stonefish (Synanceia) is able to stay out of the water for up to 24 hours. I wonder how they get oxygen from the air. Could someone explain this?

Interestingly all people seem to write down this number without reference. I found one reference from 1961 (Endean, R. (1961) A study of the distribution, habitat, behaviour, venom apparatus and venom of the stonefish.
Austr. J. Marine Freshwater Res. 12: 177-190.) which I am currently trying to track down. This paper has been cited a number of times in connection with the survival out of water.

Two things to add the the answer from @Chris.
We are used to the idea that fish extract oxygen from water using gills. When such a fish is transferred into air we imagine that it can no longer breathe. However fish do in fact obtain a significant proportion of their oxygen through their skin. Furthermore, as long as the gills remain moist it should be possible to obtain some oxygen by direct diffusion from the air into the layer of water surrounding the gills.
According to Rombough PJ (1998) Partitioning of oxygen uptake between the gills and skin in fish larvae: a novel method for estimating cutaneous oxygen uptake. J Expt. Biol. 201: 1763 - 1769

Adults of water-breathing fish typically obtain 10–20 % of their oxygen across the skin, but values as high as 30 % have been reported (Feder and Burggren, 1985).

The cited paper is: Feder, M.E. and Burggren WW (1985) Cutaneous gas exchange in vertebrates: design, patterns, control and implications. Biol. Rev. 60: 1-45. Table 1 of this paper presents measurements for the contribution of cutaneous respiration for a number of species including, for example, the European plaice (Pleuronectes platessa) which apparently can obtain 27 % of its oxygen through its skin.
There are, of course many fish, which are designated as air-breathing e.g. the European eel (Anguilla vulgaris). Table 2 of Feder & Burggren presents data acomparing the contribution of skin and gills for various air-breathing fish in water and in air. In the eel this goes from (skin/gills) 12%/88% in water to 33%/67% in air at 15 °C.
I don't know if stone-fish are designated as 'air-breathing' but it is clear that as long as they are in a moist environment many fish can obtain significant amounts of oxygen from the surrounding air. @Chris suggests that the fish may "turn down their metabolism" under these circumstances. The very fact that the fish is no longer swimming presumably reduces oxygen requirement considerably.

I have been trying to find an answer to this question, but until now, no one seems to have really analyzed why this is possible. The only hint I found comes from this paper:

A study of the distribution, habitat, behaviour, venom apparatus and
venom of the stonefish.

They state:

At periods of low water, stone-fish are often left partially exposed
  by the retreating tide. At such times they may be surrounded only by a
  small quantity of water which fills the depression in which each lies
  and the main mass of water may be a considerable distance away. They
  can survive long periods (at least 24 hours) out of water providing
  their surroundings are kept moist.

Obviously the fish only needs minimal moisture to get enough oxygen. I would further speculate that the fish turns down its metabolism during this time to minimize the need for oxygen. This paper is widely cited as a source for this survival time, but there seems to be no follow up on it. What is widely analyzed is the toxin of the stonefish.


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cerebral edema and blood pressure, pulse
What happens to blood pressure in cerebral edema; does systolic and diastolic rise equally? So the pulse actually slows down? Can't find anything about that, please help

Can you rephrase your question please? Is your question on whether blood pressure decreases when you have cerebral edema?

In cerebral oedema the observations (blood pressure, pulse, respiratory rate etc.) can be all over the place. They can depend on the cause e.g. infectious more likely to have raised pulse (tachycardia) with lower blood pressure (shock) but with the anxiety there might be raised blood pressure. Then with the vomiting, a symptom of cerebral oedema, this could lead to dehydration which leads to lower blood pressure or movement of fluid from the blood to the brain because it is oedematous could also drop the blood pressure. With the cerebral oedema affecting different structures, particularly the brain stem in coning (brain swells, pushes brain out through the big hole at the bottom where all the nerves come out particularly affecting respiratory rate) the respiratory rate could be low. It could also be high due to structures getting less oxygen causing the body to push the sympathetic nervous system to increase heart rate and respiratory rate.
In conclusion, things can be completely over the place but usually blood pressure is low and there's reflex tachycardia for the reasons explained above. For these reasons, to diagnose cerebral oedema we usually use the characteristic symptoms of nausea, vomiting, faintness and other features in a patient we know is at risk because of the signs and symptoms of the original disease or cause of the cerebral oedema e.g. the cancer, trauma or infection.


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Any relevant knowledge/studies about voluntary goose bumps
I'm not entirely sure how normal this is, but since I was a child, I've been able to produce myself voluntarily a "chill" sensation that seems to start on my head and traverse the rest of my body, being least intense in the feet. Looking around the internet and forums, looks like other people but not everybody also describe this ability. However, unlike other people's reports, I don't see "goose bumps" on my skin, at least there aren't any visibly; it's just the sensation.
Does anybody know if there are any relevant studies or knowledge out there about "voluntary goose bumps"? Is there even a proper name for that?

Related question: Getting goosebumps at will

Recent studies prove that this involuntary phenomenon must be untrue. Obviously this is false, in order for research like this to take place people need to spend money. It would be interesting if we could create a crowd sourcing account maybe on kick starter to find ways to bring money into the research. I wish I had more information for you, I've been able to do it as long as. When you go to the dentist, just curious, you don't happen to have two bones underneath your tongue that is an anomaly as well? I've been trying to think of correlations for years. I can get the medical terms, if you like. Find me on Facebook Chris Azzy

What you wrote is much more of a comment than an actual answer. Your statement of "Recent studies..." should reference the studies.


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Start studying mathematical biology from basics
I am really passionate about theoretical and quantitative biology and I would like to build my future career around this topic.
I've just got my bachelor's degree in biology (ecology) but scince I've had only one math class through the years, my math skills are very poor, so I have problems in understanding even simpe models. My main interests are population dynamics, adaptive dynamics and game theoretical models of social conflicts.
I would like to improve my skills, but I have just no idea where/how to start. Could you give me some advice about textbooks or online resources?
I have almost no knowledge in the field of math, I am interested in resources for complete beginners. And I would also appreciate any suggestions about skills/topics I should master if I am interested in these biological phenomena.
Thank you!

There is one book that will perfectly suits your needs:
A biologist's guide to Mathematical Modeling in Ecology and Evolution, by Sally Otto
It is a very good book that is very easy to understand and in the meantime goes pretty far (It ends with the use of diffusion equation in Evolutionary Biology). I highly recommend it.
It covers:

How to create a model
Function approximation
Find general solution with $n$ variables for discrete and continuous model
Stability analysis
Find equilibrium
Analyzing cyclic behavior
Gives very good introduction in linear algebra and probability theory
Class structured population
Stochastic modeling (birth-death processes and diffusion approximations)
Transformations
All examples are from the field of ecology and evolution and the author derives many of the most important equations in ecology and evolution.

Online ressources
Also I think that Khan Academy is a very good and easy source of information for improving your math skills but it takes quite a bit of time to go through all these lectures.
For a good and complete introduction to probability theory, I'd recommend this MIT Opencourseware but again, it takes time to go through all these videos.
For further recommendations in population genetics, you should have a look to this post.
If you are interested in theoretical biology, you may also want to learn about programming (if you don't already know much about it). $R$ is used for data analysis purposes, $Mathematica$ or $Matlab$ for deal with mathematical modeling and $Python$, $Java$ or $C++$ for individual-based simulations.
Note: A bit less than 2 years ago, I had the same interests than you and had to face the same issues than you.

Thank you so much for your answer. It is most helpful. May I ask, if these resources were enough for you to get on well in this field?

@Alana Well..At the moment I just finished my Master degree and am starting my PhD (in theoretical population genetics at UBC, Vancouver) in early September. It is a bit hard to compare myself with specialist in this field but anyway these references allowed me to learn a lot and helped me to be creative and develop my own research projects. I feel I should still learn more about mathematics. I learned to program with online tutorials.

I edited my other answer here to add a new important reference. Wish you all the best in your readings and self education! Don't hesitate to ask further questions.

Thank you so much! Your answer really helped me a lot. I'll have only one more question: what programming language do you use? I've read aboutthe ones you recommended, but I've only used R so far.

I mostly use R (data analysis and some very simple simulation), Mathematica (for mathematical modeling) and Python (for Individual-based simulation (Object-oriented programming) ).

I can program in Java but I prefer Python and I know nothing about C++. Python has the advantage to be very easy to learn and to be good-looking as it uses much less special characters such as curly brackets than many other languages. You may be able to start simulating some fairly complex population (individual-based simulation) with Python after only 1 or 2 days of reading tutorials (The tutorial I used was in french, I am afraid I can't suggest you a given tutorial but you will probably find recommendation on other SE sites).

Thank you so much! I couldn't decide so far, what language to learn. I started practicing Java and C but both seemed complicated. I've just a find a nice Python tutorial at codacademy, and I think it is just for me. Thank you again, it was a great help for me! :)

My pleasure $\ddot \smile$


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Location of nucleotide synthesis and transport
I couldn't find this question directly asked so I thought I would ask it
In Fundamentals of Biochemistry 3e (Voet et al), it has a small small little comment about pyrimidine synthesis:
(In a diagram showing UMP synthesis)
"In the eukaryotic enzyme, which contains FMN and nonheme Fe, is located on the outer surface of the inner mitochondrial membrane where quinones supply its oxidizing power. The other five enzymes of pyrimidine biosynthesis are cytosolic in animal cells."
So it seems for the most part pyrimidine synthesis occurs in the cytosol??
When the book talks about purine synthesis no mention is made of where this is actually happening in the cell.
Also, if nucleotides are being made in the cytosol, I suspect there must be some kind of membrane protein that allows nucleotides to cross the nuclear and mitochondrial membranes... what are they??
I'm a visual person, and knowing where and how these things are happening in the cell helps me understand it better than just following what's happening after each synthesis step.
Thanks!

Correct, all but one step in pyrimidine synthesis occurs in the cytosol, and purine synthesis occurs in the cytosol only.
Nucleotides freely diffuse through nuclear pores but are actively transported through mitochondrial membranes via embedded membrane transport proteins (i.e. ATP-ADP translocators, GTP transporters, and pyrimidine nucleotide transporters).
http://themedicalbiochemistrypage.org/nucleotide-metabolism.php

I should add that nucleotides can also pass through nuclear and mitochondrial membranes as cofactors for some proteins.


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Why is the author citation of Polypodium porosum (C. Presl) Mett.?
I would like to understand what constitutes a valid taxonomic description of a species in botany and by chance I encountered this example (which I otherwise know nothing about).
Either
Pyrrosia porosa (C.Presl) Hovenkamp
or
Polypodium porosum (C. Presl) Mett.
Ignoring the issue which one of the above genus attribution is better, my question is why the publication of C. Presl is the base when he only refers to the species by pointing to Polypodium porosum Wall.. However, that publication is considered invalid and was published again by Mettenheimer (Tropicos seems to point to Band 1 in error). However, why is the citation Polypodium porosum (C. Presl) Mett. and not Polypodium porosum Wall. ex Mett. or Pyrrosia porosa (Wall ex Mett.) Hovenkamp? And why the synonym is Niphobolus porosus C.Presl and not ... I do not know what it would be when he just points to a name used in an invalid publication.

As you state, the designation from Wallich is not a valid name, and I don't think it was even effectively published (the work appears to be just a hand-written manuscript, not even an "indelible autograph" [International Code of Nomenclature for algae, fungi, and plants. Article 30.6-30.6]). It does, however, indicate a specimen, #266.
Carl Presl both effectively and validly published Niphobolus porosus when he both pointed to a specimen (the one from Wallich) and provided a description on page 200.

Fasiculi vasorum in stipite duro tres, teretes, minuti, juxta se aut in triangulum positi, medio seu posteriore minore, in N. poruso quator teretes aequales.

[For Niphobolus generally:] Three bundles of hard, rounded stem, small, placed near each other or in a triangle, in the middle or smaller posterior, in N. porusus four round smooth ones.

Normally, this would lead to a citation of "Niphobolus porosus Wall. ex C. Presl", except in this case Wallich used the designation Polypodium porosus and Presl is using Niphobolus porosum. Since they're not the same combination, Wallich doesn't get credit (Article 46.4). Article 46, Example 27 states:

When publishing Andropogon drummondii, Steudel (Syn. Pl. Glumac. 1: 393. 1854) attributed the name to “Nees. (mpt. sub: Sorghum.)”. This reference to the unpublished binary designation “Sorghum drummondii Nees” is not ascription of A. drummondii to Nees, and the name is cited as A. drummondii Steud., not A. drummondii “Nees ex Steud.”

The combinations from Mettenius and Hovenkamp, therefore, use Niphobolus porosum C. Presl as the basionym.

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Why is too much glucose harmful?
I learned the citric acid cycle in biotechnology school and how cells work; about ADP and ATP and how the Cellular respiration (C6H12O6 + 6O2 -> 6CO2+6H2O) works.
I am interested in understanding why exactly too much glucose is harmful, e.g. when having diabetes.
What happens inside the cells so that the organs get damaged over time? Why can't the cells not simply "ignore" the needless glucose or convert it into energy?

High intracellular glucose.
Affects: all cells that do not depend on insulin to take in glucose. Examples: neurons [1], kidney cells, retina cells.
Causes: high extracellular glucose (in most cases hyperglycemia)
Effects: promoting necrotic cell death through $H_2O_2$ (peroxide) formation, which may participate in the development of diabetic vasculopathies and associated disease [2].

High extracellular glucose.
Affects: extracellular matrix, cardiac muscle
Causes: lack of / low levels of insulin, insulin resistance
Effects: enhances collagen production thus affecting kidney by thickening glomerular basal membrane [3, 4]. It promotes cardiomyocyte metabolic stress and altered glucose handling [5]. It is also a potential mechanism involved in cardiac glycogen accumulation [5].

Diabetes mellitus involves:

high extracellular glucose, leading to:
high intracellular glucose in cells that do not depend on insulin to uptake glucose;
low intracellular glucose in cells that depend on insulin (muscle and fat tissue).

References:

David R. Tomlinson and Natalie J. Gardiner. Glucose neurotoxicity (2008). Available from http://didattica.uniroma2.it/assets/uploads/corsi/140868/Glucose_Neurotoxicity_-NATURE_Reviews-Neuro,_Jan_2008.pdf (accessed 27.07.2014)
RnCeus.com. Glucose Homeostasis (2012). Available from http://www.rnceus.com/dmeds/glucose.html (accessed 27.07.2014)
Takeuchi A, Throckmorton DC, Brogden AP, Yoshizawa N, Rasmussen H, Kashgarian M. Periodic high extracellular glucose enhances production of collagens III and IV by mesangial cells. Am. J. Physiol. 1995 Jan;268(1 Pt 2):F13-9. PubMed PMID: 7840239.
Ayo SH, Radnik RA, Garoni JA, Glass WF, Kreisberg JI. High glucose causes an increase in extracellular matrix proteins in cultured mesangial cells. Am. J. Pathol. 1990 Jun;136(6):1339-48. PubMed PMID: 2356864.
Kimberley M. Mellor , Upasna Varma , David I. Stapleton , Lea M. D. Delbridge. Cardiomyocyte glycophagy is regulated by insulin and exposure to high extracellular glucose. American Journal of Physiology - Heart and Circulatory PhysiologyPublished 15 April 2014Vol. 306no. H1240-H1245DOI: 10.1152/ajpheart.00059.2014

An excellent answer - it really should be accepted.

The glucose can react with proteins, damaging them.  This is called glycation.  Note that glucose is the preferred body fuel and has a 10 fold lower ability to cause glycation than fructose.
http://en.wikipedia.org/wiki/Glycation

Perhaps worth adding that the level of glycated haemoglobin is used as a way of monitoring how well diabetes is being controlled over the long term.

Protein is also insulinogenic, so presumably the body tries to keep it under some level in the blood. Would the same things happen with excess amino acids as you've mentioned?

Too much glucose leads to the formation of advanced glycated end products, which deposit in tissues like glomerulus and cause disease like diabetic nephropathy.
Also glucose is osmotically active, so when it starts appearing in urine (because of its high levels in blood), it leads to polyuria, following which the lost water is recovered from body tissues, leading to dehydration and increased thirst.

Glucose transports from the blood into the cells via facilitated diffusion. This means that glucose goes from higher concentrations (in the blood) to lower concentration (in the cell). Therefore, if you have super high glucose concentrations in the blood, you will have a ton of glucose in the cells. Glucose will oxidize by itself, thus it will contribute a lot to the oxidative stress experienced by the cell.
To answer your question of why they cannot "ignore" it, it is because it simply goes down its concentration gradient via facilitated diffusion.
To answer your question of why they can't convert it to energy, well they can, but too much metabolism of glucose will also generate an excess of reactive oxygen species.
In conclusion, high glucose in cells generates a lot of oxidative stress, which of course, is bad.

This answer has things backwards. In diabetes the failure of the insulin response to high blood sugar means that the glucose carriers are not recruited to the cell membranes. This results in a decreased capacity for glucose uptake and so blood sugar stays high. Also, glucose does not "oxidise itself".

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What is wrong with this analogy: Individuals are to alleles what governments are to individuals
I'm an amateur when it comes to genetics, I'm hoping to learn something from the corrections. I am taking epigenetics into account (kind of); all 3 entities are susceptible to external physical influences.
Kind regards,
Frank

In this analogy, what is a gene?

Alleles are passed down (to individuals) and created by individuals (although not fully under their control). But individuals are not passed out or created by the governments (I suppose), although individuals are influenced by the governments and they can influence governments, whereas individuals can not necessarily influence the allele of the gene they already have unless you take epi-genetics into account. Also, the creation of an allele is not entirely influenced by individuals due to independent assortment and chromosomal crossover, but individuals can more or less influence governments.


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What can myelination tell you about the evolution of sensory receptors?
I am reading Avi Chaudhuri's Fundamentals of Sensory Perception and wondering if the information given about the somatosensory system could tell us anything about the way it evolved.
It seems (at least naively) reasonable to assume that nerves became larger and more myelinated as time went on. The types of somatosensory nerve fibre are (in order from least to most myelinated):
C < A-delta < A-beta < A-alpha
This gives an ordering on receptors of:
warm receptors < cold receptors < nociceptors < tactile mechanoreceptors < proprioceptors
My question is then: was this the order in which these receptors evolved? If not, can myelination still give us useful information about the evolutionary history of the nervous system?
P.S. Meta question: is this question better suited for the Bio or Cog Sci stack exchange? I asked it here since it seemed to be more about evolution than neurons.

I think it's definitely on-topic here and would be welcomed on CogSci as well.  The evolution aspect is probably better addressed here, as you have already observed.

Interesting question. I will dissect your question into its assumptions before giving my view on the overall question.
1) ..that nerves became larger.. : Why should there be a general tendency for nerves to increase in size during the course of evolution when there is no need to?
2) ...that nerves became more myelinated...: A general tendency towards more myelination is not the case. Myelination is definitely a trait that has been acquired later in evolution, but "the more the better" does not apply. Imagine an electrical conductor - to insulate it a bit of plastic is enough. Adding more after that doesn't make a substantial difference.
3) ...the order in which these receptors evolved...: myleine sheaths are made up of glial cells that wrap themselves around axons of neurons. Myeline makes neural transduction more efficient and faster. Hence, the amount of myelination tells you something about the efficiency and speed of transduction of the nerve (Hartline (2007)). For example, longer axons tend to be myelinated, short ones not. That, in turn, will have certain evolutionary benefits for the host, as more efficient communications means less energy required, lesser loss of information, and increased processing speeds. The amount of myelin hence tells you something about the importance of efficient communication of that sensory system. However, it does not tell you anything about when this receptor evolved.
Hence, the relation between myelination and receptor evolution is remote at best. In terms of evolution, amounts of myelination may tell you something about the evolutionary pressure placed on faster and more efficient workings of the receptor systems.


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How are HSPs identified in UCLUST
I am new in Bioinformatics and recently studying UCLUST algorithm by Robert Edgar(2010). It is a fast sequence searching and clustering algorithm. The algorithm is heuristic based. I studied that first, this algorithm finds unique common words(k-mers) between a query sequence and a target sequence.(one of the sequences from sequence database). If there are enough common k-mers between a target sequence and a database sequence then it is selected for the alignment in the next step, otherwise skipped. All such sequences having enough common k-mers are selected. Target sequences are compared in order of decreasing common k-mers.
In next step, HSPs (High Scoring Segment Pairs) are identified. For this purpose, exact matching words between a query sequence and a target sequence (one of the sequences selected in the previous step) are found. I AM CONFUSED AT THIS POINT. Is it necessary that these matching words(between the query sequence and the target sequence) be at same positions ?
Kindly if some one explains with an example, will be very help full.
Any guidance will highly be appreciated.


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What is the biological principle of this "holotropic breathwork" technique?
Holotropic breathwork is a non-drug technique developed by Stanislav Grof used in psychotherapy. The therapy as a whole is usually called holotropic breathwork (at least by Grof himself) and will most probably rely on a range of effects. However, I am mainly concerned about the core technique, which leads to hallucination and a changed state of conciousness (i.e. being half concious and having a distorted perception of time).
As quick googling does not reveal any specific information of the technique, I will describe a demonstration of an amateur enactment of something which was stated to be based on the same principle as holotropic breathwork. (I consider the respective people very irresponsible to have done this without trained assistance, it is probably very dangerous, do NOT try at home!)
A person squats curled near a wall and breaths as quickly and as heavily as possible for a few minutes. After that they quickly stand up in front of the wall and another person pushes them quickly in the chest and presses them strongly against the wall behind them. The pushed person collapses completely, their muscles relaxed, they even don't have the time to close eyes and you can see their eyeballs rolling around freely. They are in this state for about 15 seconds and then wake up reporting vivid hallucinations. Some of the people said that their perception e.g. of sources of light and surfaces were altered for another several hours.
So, what is the biological basis of this collapse and hallucinations? (It would be perhaps good to also comment on the possible risks.)

I think this is mostly caused by hyperventilation. The excessive breathing disturbs the balance between CO$_{2}$ and oxygen in our lungs. This will cause respiratory alkalosis (the blood pH, which is normally strictly regulated, gets higher), which can cause dizziness, headaches and fainting.
The shift in pH can also disturb the eclectrolyte balance, especially the concentration of the free dissolved calcium, as it binds to negatively charged plasma proteins (which release protons into the blood due to the higher pH). This can lead to craps and spasms.
I would be very careful not playing around here, as this can have some severe consequences.

It makes sense that the high levels of oxygen may cause fainting, but what is the mechanism of the hallucinations? Somebody told me that the procedure causes a sudden peak of adrenaline which overwhelms the receptors, but I cannot find any reference.

Pressing on the chest changes the concentration of dissolved gasses in the blood stream. Your brain reacts due to excessive oxygen in the blood. This is oxygen toxicity.
Why the brain generates vivid imagery when unconscious is a big topic. There's a theory that correlates dreams with a lack of cognitive stimulation. This is called autostimulation and may function as pseudo-learning when external stimulation is low. For children it's thought this helps them learn when they can't communicate. We may dream less as we age because adults are highly stimulated.
I hypothesize dreaming while knocked unconscious has side effects which mimic dreaming.


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Dataset of microscopic images before and after staining?
I am looking for a freely distributed dataset of microscopic images. I am hoping to find a dataset that would feature histological images before and after staining (e.g. H&E or some other standard one, preferably). I have been searching through various databases, but I cannot find a proper set. I hope the sample size to be at least about 100. Suggestions?

What do you mean, "before and after staining"? An image taken before staining won't show anything...

Oh, I must have understood something incorrectly. Well, I hope I can have access to the "raw" data, as well as the processed versions.

There should be very minimal processing for scientific images - otherwise you are not looking at true results.

Do you have a particular species in mind? are you looking for something like this? (http://www.virtualflybrain.org/site/stacks/index.htm)

Virtual fly brain (http://www.virtualflybrain.org/site/stacks/index.htm) is an excellent database of fly (Drosophila) brain sections, which can be electronically processed/annotated/highlighted on the fly to show different areas of the fly brain as an overlay on top of the original images.
Alternatively, you can use BrainTrap (http://fruitfly.inf.ed.ac.uk/braintrap/) for the expression of proteins in the fly (Drosophila) brain using brain sections. Another database which has silver stains of Drosophila brain sections is the flybrain (http://flybrain.neurobio.arizona.edu/Flybrain/html/atlas/) database. This database also contains 3D models of different fly brain structures and much more!
I'm sure there are many many similar databases, but these are the ones I knew of, which are widely used in the Drosophila community.


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Microscope scale bar
In some microscopic images, there is a bar scale at one of the corners or near a specific object. How are they added to the images? Does the slide have some markers, or are they digitally added? If so, how are they computed? I am planning to buy a microscope and wondering is there something I should look for. Thanks for any help!

There are two common ways to generate a scale bar:

Measure it.  You can take a picture of an object with known spacing such as a grid target and then measure the size of each pixel.
Compute it.  If you know the magnification of your objective, and the magnification of any relay optics after the object but before your camera, you can compute the total optical magnification.  Then using the pixel size on your camera, you can get the actual pixel size.  For example, suppose you have a camera with 7.4 micron pixels, a 20x objective, and a 0.5x adapter lens before your camera, then you would have a pixel size in your image of 7.4/20/0.5 = 0.74 microns.

It depends on the type of microscope you want to buy. Most microscopes come with a slide with precise measurement bars on them and you select the objective and if it is connected to some sort of camera and comes with a software then you can calibrate the scale bar for a particular objective using the software it comes with. Otherwise if you know the pixel per micron for each objective, then once you acquired your images, you can draw a scale bar using a software like Image-J. In terms of what microscope to buy and what to look for, it depends on the application so you need to clarify the question. I have answered a question similar to this here (What to look for when buying a light microscope?).


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Do bees make honey from fallen fruit?
I know bees make honey from nectar, and I know they drink the juice of fallen fruit, but do they actually make honey from fruit, or do they only eat from it for themselves?

Well, they do, but I'm still looking for scientific backup. They also make honey from maple syrup, corn syrup, sugarwater, molasses, etc.


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How do genes get passed from one hive to another?
In hive species, like honeybees, how do genes propagate from one hive to another?
If the queen only mates with drones from the same hive, and queens and drones are born to the hive they end up mating in, I'd expect that each hive would end up like its own little species, a tiny gene pool with no outside influence.  But since honeybees haven't broken into myriad local species, there must be some gap in my understanding here.

See https://en.wikipedia.org/wiki/Nuptial_flight


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Is cysteine deficiency possible?
Is there such a thing as cysteine deficiency in humans or other mammals?
What effects would such a deficiency have?
As I understand it, most cysteine for humans comes from dietary sources, though it can be biosynthesized in humans.

Cysteine deficiencies are possible, and one cause is the genetic disorder homocystinuria. Cysteine can be produced from methionine through a homocysteine intermediate, and defective genes for the enzymes involved can prevent proper cysteine production and cause a buildup of homocysteine. Patients have to eat a very carefully controlled diet with very low amounts of protein. This prevents homocysteine buildup by avoiding methionine exposure, but also requires that the patient take vitamin B6 and  B12 supplements and betaine. They might need to take cysteine supplements as well. The symptoms affect many organ systems, including the brain, nerves, and blood vessels, with about 25% of patients dying due to blood clots by age 30.


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Can pheromones in perfume be formulated to cause agitation?
I generally don't care for female perfume. I have very sensitive olfactory receptors and in general, I just find perfume overwhelming.
A couple weeks ago, my wife of almost 14 years and I were shopping. As has happened many times before, she asked me to smell a perfume (Play it Rock by Playboy) to see if I liked it. Shockingly, on first whiff, though still overwhelming, I quite liked it. So she bought it.
Now, when she wears it, I do find the aroma pleasing, however I find myself getting quite agitated, depressed and even overcome with jealousy and paranoia.
Obviously, there are lots of psychological factors in play :

Perfume's primary purpose is to arouse and attract men
She almost only uses it when there are going to be other men around
It is playboy, subtly indicating the promotion of promiscuity

However my internal reactions are so intense I can't help but conclude there something more physiological triggering/intensifying them.

Could the perfume's pheromones be slightly misformulated to cause
this reaction?
Would the same pheromones that arouse a man also inherently trigger the fear of the arousal of others?
Is it possible that my pheromone "sense" is also heightened like my sense of smell, causing an abnormal reaction specifically in me?

Note : I can't find official documentation that the playboy perfumes apply pheromonology (Yes, I did just make up that word), but I have found them listed by other sources in sections of perfumes that do, but Playboy perfumes seem to be priced drastically less than the rest of the pheromoned perfumes.

You are really getting at psychology here as opposed to the biological question(s). As written, it's really too general. There is no way to answer a question about your specifically or anyone else.

@kmm - This question presents a scenario in which the sample group (me) is far too specialized to draw a conclusion. Thus, presenting some, specifically physiological (biological), hypotheses is seeking response from the biology community. You state that this is getting at psychology, which is true, however it's specifically the biological causes of psychological response.  I'd also like to note that ALL psychology boils down to biology.

The point is that your question is too broad as written, about your specific experiences rather than general phenomena. If you have a specific biological question about pheromones and behavior, then feel free to edit your question.

Insects generate and respond to pheromones. But despite what sci-fi TV might have told you, there is no evidence that humans make or respond to pheromones like that.  Humans don't have that good sense of smell, for one thing.
The fact that you know it's a Playboy brand of perfume is affecting you?  That's obviously not chemical, is psychological.
Also, historically, perfume was used just as much to mask unpleasant odors as it was to attract anyone.  When men go through puberty, their sweat changes odor.  That's not to attract other men.
If this perfume is affecting you emotionally it's psychological, not chemical.

Thank you! Your response shows notable intellect though you may have skimmed through my question a bit too hastily.
First, I was specifically highlighting the purely psychological components to consider. However, the experienced result seemed to outweigh the sum of their potential.
Second, perfume's primary purpose WAS for masking odor. I'd submit that WAS to prevent repulsion, thus attract. It's current iteration is simply more direct.
Finally, by simplest definition pheromones are chemicals released that affect an animal's own species. This definition leaves little room for human exemption.


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How do I get a brighter DNA bands
I've been trying to a good contrast for my DNA bands, however I haven't been so successful. I've been running the ladders only to make sure I get a good contrast before further experimentation.
I created the gel using 70mL 1X TAE buffer, 0.84g of agarose (so about 1.2% gel), and 28ul EtBr.
I set the electrophoresis box at 90V for about 1 hour hoping to get a better gel but the results came out looking the same as if I had ran it at 110V.
I've attached a picture of my gel. It was taken with a DSLR, no flash, 20 seconds exposure time.
Any tips would help. Thanks

That is a lot of EtBr. You are using about 30x more than what most people do! You're potentially exposing yourself to a higher amount of a dangerous chemical than usual.

What's the typical amount? My graduate TA told me to run 10uL per 25mL for the gel.

EtBr is a powder that can be made to solutions of different concentrations. So volumes don't make much sense unless the stock concentration is mentioned. Final concentration of EtBr in the gel should be 0.5$\mu g/ml$

EtBr needs to be detected with UV light. Then: What is the concentration of you EtBr solution? @Superbest EtBr is not as dangerous as many people think. Yes, it is an intercalating agent (as most DNA dyes are) but it is not the monster that many people make it.

@Chris Yes. However, I've heard a nice analogy - "it's kind of like smoking a cigarette". I, personally, don't smoke.

I normally use 1-2 ul (depending on whether my gut tells me I have a lot of DNA, or a little that day) in a 70 ml 1% gel (which is probably 60-65 ml after boiling in the microwave). I have no trouble whatsoever seeing ladders and DNA samples of down to 100 ug in wells not much bigger than about 4 mm.
Here are the factors that you can manipulate to alter the brightness:

Amount of EtBr. More is brighter. (However, you already use a lot - using less may even be better because it would reduce background while still saturating the DNA with EtBr)
Amount of DNA. More is brighter. To avoid guesswork, use a ladder and consult the instructions in its manual or spec sheet. They usually have an example picture of a gel, and say exactly how they obtained it.
You messed up. Do other people in the lab get good gels? Ask them to do the protocol with you.
Sample preparation. Are you using a loading dye in the correct amount? Is the DNA diffusing out of the wells? Are you spilling a lot of it when you load?
Band width. Obviously if you load the same amount of DNA in a well 4 times as wide, it will be 4 times fainter.
Strength of UV light. Many illuminators have a knob to adjust the intensity, people turn it down to avoid damaging DNA when gel-purifying restriction fragments. You can also play with intensity, gamma and exposure in a geldoc machine.
Quality of EtBr. I've never actually had this happen, but your stock may be bad for some reason. Ask another lab for a ul or two to easily control for this.
Quality of DNA. Obviously, your sample must actually have DNA in it, and not be degraded. You can check amount and purity easily with a spectrophotometer, but it will not tell you if the DNA has been digested into its component nucleotides (that is usually checked with a gel).
Amount of gel. The crucial variable is obviously not total amount of EtBr, but concentration. Less gel, brighter bands - but you seem to be using a standard gel amount.
Quality of gel. Again, never had this happen, but try making the gel with someone else's reagents.

I can see that you have a ladder in the middle, so at least some DNA is definitely there.
Also, keep in mind that off-the-shelf cameras are not good at imaging the EtBr fluorescence, because the wavelength is a bit unusual. The nice pictures you see in papers are taken with a specialized geldoc machine or a camera with an appropriate filter.

Thanks. As far as taking the picture, I am using a blue transilluminator from io rodeo: link

@leonardo, the pictures with less exposure time look a lot brighter. Here's a picture taken (of the same gel) at .6s exposure time. link. Also, is there another illumination solution that is inexpensive that I can try?

Since this answer was accepted, let me clarify: Looks like the problem is that the wrong illuminator was used. The linked device produces blue light, for use with CYBR Green. For EtBr, you need UV. Probably the signal you did get was from UV bleeding from the blue LEDs of the device.


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Can protein precipitate out in alcohol during DNA extraction?
In common lab sessions to extract DNA from strawberry or cheek cells, will there be protein contaminating the DNA extract in alcohol? If so, how can we prevent protein from precipitating out of the solution?

Yes, Ethanol can precipitate proteins during a DNA precipitation as well, although Acetone will be more efficient. Usually you do a proteinase K digest or a proteinase K digest followed by a Phenol/Chloroform extraction to avoid this problem. I was usually doing the later, I can post my protocol if you are interested.

A proteinase eg.proteinase K is usually added when extracting dna.


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Do trees have no set lifespan and
"quite"immortal?
Many trees survive centuries and die only in disasters like
storms and lightnings or infections. So do they have no set
life span? Are they exceptionally resistant to genetic
mutations and have very less cell cycle regulations which
keep them 'forever young'?

List of oldest trees(wiki), list of long living organisms (wiki) and some impressive lifespan in animals

There are certain annual(eg.peas) and biennial plants(eg.carrot) also which die at fixed times.
But for perennial plants :
From this

Trees endure as long as they do basically because they're
  nonhierarchical organisms. In animals, all vital functions are
  controlled by the central nervous system, the guiding element of which
  is the brain. When the brain dies, so does the animal. By contrast,
  vital functions in trees are decentralized. A large part of the tree
  can die, and indeed routinely does die, without killing off the tree
  as a whole. Most of a mature tree is dead except for a few layers
  under the bark.....
All trees die eventually, of course. Four thousand years is old
  compared to the life spans of gossamer creatures like ourselves, but
  in the context of geologic time it's the blink of an eye. As they get
  older trees become more susceptible to disease, pests, and other
  perils, and inevitably these take their toll.

@user44289 Hi! You are welcome. If you think this has answered your question, you can accept it by clicking the green checkmark !

Sure! It is amazing they don't have a set limit of their lifespan.

@user44289 Yes, I agree ! Plants are pretty amazing!


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What is this discarded exoskeleton from?
This morning I was looking round the garden and found this sticking out of a pit in patch of soil, next to the wall of the house (in a trough sort of thing). I came to the conclusion it must be part of an insects exoskeleton that was discarded or part of a pupae. Can anybody identify what this belongs to? My location is in the south-west (Wiltshire region) of Great Britain. I'm just interested in what exactly I've found!

I can't be certain, but it is probably the pupal shell of a crane fly (daddy longlegs, Tipula palidosa). Here is an image to compare, and you can find lots more with a Google image search.
In the UK at least, these are colloquially referred to as leatherjackets and if you find one in soil before the adult has emerged it will often twitch.

I think it's a moth: http://www.uksafari.com/buried_treasure.htm

I very much doubt this specimen and the photo you refer to are tipulid pupae. They look more like this one


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Why does low temperature make RuBP, GP and TP concentrations fall in Calvin cycle?
In my A level revision guide and places on the internet it states that at low temperatures levels of RuBP, GP and TP all fall. However I don't quite understand how this is the case, because as far as I can see, a reduction in temperature would give the molecules less kinetic energy and reduce the rate of reaction of the enzymes and so there would be no change to relative concentrations, because everything is slower all equally. Could anybody explain to me why all three decrease in concentration at low temperatures?

Enzymes don't universally reduce their catalytic ability when the ambient temperature is lower. Some will be affected more than others. You could probably look up the KM values with relation to temperature if you're curious.

Note that reaction rates depend exponentially on temperature as per Arrhenius equation. So the change won't be linear. Moreover the activation energies for different reactions will be different. $\k=Ae^{-E_a/{RT}} \\frac{k_1}{k_2}=e^{-E_aR(\frac{1}{T1} - \frac{1}{T2})}\\$

@MCM so, if the enzyme to convert TP into the respiratory substrates works faster than all the other enzymes, and given that Carbon Dioxide will diffuse slower in lower temperatures (hence less input), all the levels of intermediates should decrease?

@WYSIWYG that's an interesting equation, I will look into it, I love a bit of exponential decay from physics!

@J_mie6 I missed it then but after a while looked at this question again. The answer to your question requires the model parameters and other reactions. Can you provide the link to the source where you read this?

@WYSIWYG The OCR A level biology textbook I think


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Do ants or other insects sleep, and if so why?
I was thinking yesterday about insects (as there was a spider in the house, and I couldn't help but think of anything else, even though they aren't insects), and I started to wonder if ants sleep?
After thinking about it for a while I decided that they might sleep, but then what would be the purpose of sleeping for them? My limited understanding of the need of sleep is that it is used for the brain to compartmentalise the events of the day and allow memories to be formed. But ants don't really have to think about much during the day, given that they act more as a collective than an individual. Or in the case of other insects, they have simpler more instinctive brains which rely on taxis, reflexes and kineses.
So, do ants and other insects sleep (or do they have a different type of sleep to us) and what would the purpose of it be for them?

related: http://biology.stackexchange.com/questions/19176/where-do-butterflies-sleep

What happened to the purpose of sleep as a mechanism of physical relaxation? After a hard day's work, they would need to relax.

"act more as a collective than an individual" That's just perspective, same can be said for humans.

@Jonathan Yeah I completely agree, I meant more of a collective intelligence. Badly worded :p

Sleep can have many uses, and may have different uses for different species. NIH claims that sleep may be used also to help remove toxins from the brain, which would be beneficial for ants, too.

Do amoebas and other single cellular organisms sleep?

Wow, this is a really interesting topic. I had no idea arthropods required sleep. Perhaps the purpose of sleep is more than just the consolidation of memories - and some insects do, in fact, have memories - including neural repair and rejuvenation. Maybe the neural systems have to be turned off for maintenance to be effective.

A quick search on Web of Science yields "Polyphasic Wake/Sleep Episodes in the Fire Ant, Solenopsis Invicta" (Cassill et al., 2009, @Mike Taylor found an accessable copy here) as one of the first hits.
The main points from the abstract:

Yes, ants sleep.
indicators of deep sleep:

ants are non-responsive to contact by other ants and antennae are folded
rapid antennal movement (RAM sleep)

Queens have about 92 sleep episodes per day, each 6 minutes long.
Queens synchronize their wake/sleep cycles.
Workers have about 253 sleep episodes per day, each 1.1 minutes long.
"Activity episodes were unaffected by light/dark periods."

If you study the paper you might find more information in its introduction or in the references regarding why ants sleep, although there doesn't seem to be scientific consens. The abstract only says that the shorter total sleeping time of the workers is likely related to them being disposable.

Interesting, a queen gets 9 hours of sleep, a worker only 4.5 hours...

@tohecz: also queens sleeps are much longer & less interrupted -> more quality sleep time.

Are there animals that don't need sleep?

The short answer is apparently yes.  Studies on sleep in insects date back to papers published by Phil and Nellie Rau in 1916 and 1938. Hussaini et al. (2003) showed that sleep does affect memory formation in honey bees. They showed that retention of extinction learning is significantly reduced in bees that were sleep-deprived.  More about sleep in honeybees can be found in this paper by Eban-Rothschild and Block (2012).
I did not find anything on sleeping in ants after a brief Google Scholar search but ants and bees are both hymenopterans, so it's reasonable to hypothesize that many of the effects of sleep (and sleep deprivation) found in bees could also apply to ants. The Eban-Rothschild and Block paper linked above has some comparisons of circadian rhythms between ants and bees before discussing sleep as a function of circadian rhythms.


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What types of light can't a plant photosynthesize in?
I have a plant on my desk, and it got me to wondering: Can my plant use the light from my monitors to photosynthesize? If so, what light (apart from green light, to a degree) can't plants use to perform photosynthesis?
I know that plants have the photosynthetic pigments to absorb many different wavelengths of light (primarily red and blue) but would there be certain types of light it can't use?
(The specific plant by the way is Schlumbergera truncata)

possible duplicate of What does "chlorophyll photosynthesis peak" mean in relation to photon wavelength?

The other is a duplicate of this, not the other way round?

Chlorophyll can use a quite broad range of light for photosynthesis, the only range where it is not working is approximately between 500 and 620nm. See this adsorption spectrum of chlorophyll (from the Wikipedia article on Chlorophyll):

The lack of chlorophyll to absorb light between 500 and 620nm (roughly) results in the green color of leafs, because this light is reflected.
Besides the wavelength also the energy of the light is important, so plants will grow better in sunlight than in the light of your monitor. This link about the maximum effectiveness of photosynthesis is also interesting.

I like this image because it also shows why chlorophyll is green.

Would I be right to assume, then, that the monitor's red and blue pixels would be useful for the plant, while the green would not? (granted, a monitor produces so much less light than the sun that having it nearby isn't doing much for the plant...just theoretical)

Theoretical, yes. And this is what special growth lamps for plants do. They leave out parts of the spectrum. The Wikipedia article I linked contains a photo of such an installation.

"Besides the wavelength also the energy of the light is important" - wavelength defines the energy of light and vice versa. What you wanted to say was the intensity of light field.

It might also be of use to know that plants 'use' certain wavelengths of light as a sort of sensory input, in addition to providing the photosynth energy . The same can be said for light-dark cycles. Plants know when winter is coming as the days get shorter. https://today.duke.edu/2015/07/plantlightsensors                Phytochrome https://en.wikipedia.org/wiki/Phytochrome      Phototropism  https://en.wikipedia.org/wiki/Phototropism


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If all B cells are present at birth, why should the primary response to an infection take longer than the secondary response?
When learning about the immune response, my teacher mentioned that all the bodies B cells are present at birth, and there is one to counter every disease. But if this is the case, why should the primary response take a long time?
As far as I know, the primary response involves the non-specific response followed by the specific response, where APCs cause the activation of T cells resulting in clonal selection and expansion of T and B cells. The B cells then differentiate into plasma cells and produce antibodies. It results in the memory cells being produced, which can quickly reengage the specific response the next time the pathogen enters.
Why doesn't the body just make memory cells to begin with? As if it has already encountered every possible pathogen. I presume it is just a lack of specificity in the A level teaching, but I am curious to know what I am missing here.
Thanks,
Jamie

These so called virgin B-cells (becase they never had contact with their antigen) which are present in your body only have random B-cell receptors (when secreted, these are the antibodies), mostly of a relatively low binding affinity. These B-cells undergo division, re-arrangement and somatic hypermutation of the B-cell receptor and clonal selection. Only cells producing high-affinity antibodies survive this selection process and build later the pool for the memory cells and the plasma cells. It is like in the image below (from here):

Using this approach we have a big pool of low affinity antibodies (which somewhat fit). These are then used as the basis for the elaboration of a population of high affinity (perfectly fitting) antibodies, which target only the pathogen. And the antibodies are available relatively fast.

Ah, that explains it perfectly!

This is a great question, Jamie. And Chris gave an excellent answer above, describing how antibodies go through 'germinal center reactions' that improve the affinity of responding cells. However, Jamie actually brings up several concepts that are worth discussing and there is another important element to the immune response that Chris touches on, but could be elaborated.

Where do naive B Cells come from? When are they produced?
How many unique B Cells do we have?
What happens to cells during an immune reaction?
How do naive and memory B Cells (among other post-exposure cellular subsets) compare?

Briefly,
(1)  B Cells arise from progenitor cells living in the bone marrow. They are produced continuously throughout the life of the organism - or at least until 'old age' when hematopoiesis is qualitatively and quantitatively compromised(Gerstein and Cancro, among others address this problem).
(2) How many? That's a good question. The number of cells seems to be dependent upon the mass of the organism (indirectly through a cytokine called BLyS). There are a lot of subtleties governing the number and 'quality' of our cells that BLyS concentration seems to regulate, but, for the most part, we can assume that each B Cell (like each T Cell) reacts to a different target (epitope). The reason I bring up the BLyS thing is that it shows us that 'space' is limited, and the body is making decisions all the time about what cells to keep and what cells to discard.
(3) During an immune reaction, some small subset of cells 'sees' its target via it's B Cell Receptor (this is a surface-bound version of the antibodies that this cell will make later). Most cells will remain blind to the infection / whatever. The ones that do see their target expand (multiply), while those that don't, don't. This is Burnett's Clonal Expansion Theory (probably best explained by Wikipedia) and it states that we have only a small number of cells that are useful for each immune reaction, but these can divide and activate rapidly to participate in the response. When the infection is over, most cells die, but some subsets will remain, these are memory cells and their relatives (e.g. long-lived plasma cells). Imagine that for every unique B Cell you had before, now you have 100 memory cells (I'm making up that number) that are capable of responding to the same target.
Although I'm sure there are differences between these memory cells and naive cells, it's easiest to ignore that part and just think that now you will be starting with 100x the number of cells you had prior to the primary response.
So, to get to your basic question: why not just start with the memory cells? It's a question of space. Your immune system provides you with a broad repertoire because it has no idea what it's going to see during your life. But once it sees something once, it is ready for a second showing. (i.e. It is reasonable to think that if you have micro-organism X in your neck of the woods, you may come into contact with it more than once, so after that first time, you are now better prepared with more cells that already demonstrated that they were helpful once before. )


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Earwax versus Mucus
Something I have wondered for a while is why have two different primary defense mediums, ie earwax and mucus, that perform the same function?
As far as I know, mucus and earwax are both part of the primary defense of an organism against disease and foreign particles, by trapping any pathogens or dust that enters the body.
My question is; Why does the body use earwax for ears and mucus for the lining of other entrances to the body, why not have mucus in the ears or earwax everywhere else? is there an advantage to have each medium in their respective places?

Unique and interesting question.  It's hard to give a firm "why," but we can discuss the ways that the ear and other "holes" differ.
Mucous membranes line every tract into/out of the human body.  Technically the ear is not a point of entry, as the tympanic membrane makes the external auditory canal a sort of blind pouch.  The skin lining the ear is keratinzed skin.  Most skin has keratin and is difficult to permeate.  But mucous membranes are moist, thin, usually highly vascular, and generally easier to permeate.  Disease often takes hold or gains entry at mucous membranes (respiratory infections, GI infections, etc). That is why mucus is so critical as it is protective and acts as a barrier and flushing-system.
Mucus requires some form of circulation, as it is a fluid.  Once produced, usually at least some of the fluid is reabsorbed, and the remaining material is passed along until it exits the body.  In the lungs, cilia bring it up to the throat and it is swallowed into the GI tract.  In the nose, it drains down the back of the throat and is swallowed.  In the eye, the fluid (which has mucus components to it) drains into a small tract that runs into the nasal passageway, which drains along with the other nasal mucus.  Obviously saliva, which also has mucus components, is swallowed (2 liters a day of it, actually).  In the genito-urinary tract, there is both reabsorption of some of the fluid components, but mainly flushing outwards when urinating.  The GI tract reabsorbs almost all water components and the remnants pass with stool.
Mucus is produced by mucus glands.  Cerumen (ear wax) is produced by sebaceous (oil) glands and apocrine (sweat) glands, but is primarily composed of shed skin cells from the ear canal.  Sebaceous and apocrine glands are all over most of our exposed skin (except palms etc) so it stands to reason that they would be present in our ears as well.
Cerumen exits the ear several ways: all skin on the body sheds the top layers as new skin grows from underneath, and in the ear, the skin cells also migrate with a directionality from the tympanic membrane outwards.  Head movements (like chewing) help dislodge things stuck to the walls.
I'll put in my plug here about NOT using cotton swabs (aka Q-tips) to clear your ears.  It generally just pushes the wax deeper, except for the tiny bit you manage to get out.  I've cleaned out tons of wax-impacted ear canals from people who use Qtips on themselves or their kids!!
If the ear were to use a mucous membrane system, the lower viscosity fluid would have to go somewhere.  We would be weeping mucus from our ears unless there were a drainage system into the sinus passageways.  The body conserves liquid, so we couldn't afford the constant fluid loss otherwise. The middle ear has a canal - the eustachean tube - which leads into the nasal sinus (although primarily to equalize pressure).  But the external ear does not, so it's probably a good thing that we don't have mucous membranes in our ears.

Wow fantastic answer! That helps a lot! Out of curiousity, what should we use to clean our ears?

Ears mostly clean themselves, especially after you stop shoving it deeper inside with Q-tips.  But I completely understand the desire to "help it along."
This is gathered from recommendations from doctors in Audiology, Pediatrics, Family Medicine, and Emergency medicine - whom I have personally talked with about the topic.

In the shower, you can tilt your head to the side and let warm water and shampoo suds run into your ear.  Switch sides.  Then go back to the first ear, and tilt your head to drain the sudsy water.  Then let it fill with clear warm water again, tilt and drain, and repeat until no soap is left in the ear.  Soap residue also can be itchy and irritate.  If you do this regularly, there won't be an accumulation of lots of wax.

If you really need more help, you can use a little vinegar (25% solution) in warm water and let it soak in there several minutes before rinsing in the shower.  If it's to the point it's affecting your hearing or painful, call a primary care doctor, urgent care, or otorhinolaryngologist (ENT = Ear Nose and Throat specialist physician) and they can remove it for you.  There's a wax-softening solution that can be purchased at the pharmacy (not sure if it's prescription), but it's best to avoid anything medicated unless you're symptomatic (hearing loss, pain) - make sure you ask a doc/pharmacist.

Important note: if you've had surgery on your ear, especially eardrum (tubes etc included) don't do anything without asking your doctor.


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How is the transcription direction of RNA polymerase determined?
When transcription factors attach to the DNA strand - How do they know in which direction they have to initialize the transcription by rna polymerase? Is it always read in the same direction anyway? What about those 'promoters'? Do they influence the transcription direction?

Do you mean by direction which of the two DNA strands is transcribed? Or do you mean whether the polymerase goes from 5' to 3', or from 3' to 5' on a single strand?

@MadScientist Although the first question is also interesting, the second one is the one which I am interested in at the moment.

Transcription always proceeds in the direction 5' (5-prime) to 3' (3-prime) on the coding strand of DNA. Binding of both transcription factors and RNA polymerase to DNA depends on sequence motifs in the DNA. Transcription always happens in the same direction with respect to the chemical structure of the coding DNA strand, while the transcription direction with respect to the structure of the chromosome depends on which strand the coding sequence is found on (and thus which strand is defined as the coding strand for that gene).

Just to clarify, RNAP moves relative to the template strand from 3' to 5'. The transcript is polymerized from 5' to 3' and has the same sequence as the coding strand (except U instead of T).

Thanks, good point. The whole process is described, with figures, in an NCBI online book here: http://www.ncbi.nlm.nih.gov/books/NBK22085/

Glad to hear that. You can also communicate that an answer is useful by clicking the checkmark next to the answer, "accepting" it.

I don't think transcription always goes $5' \rightarrow 3'$ wrt to coding strand. See https://en.wikipedia.org/wiki/Promoter_%28genetics%29#Bidirectional_promoters_.28mammalian.29

In that instance there are two coding strands, so the transcription still goes the same way with respect to each coding strand.

What about in negative-sense ssRNA in viruses?

I think the more important thing to understand here is how these enzymes "know" what to do. I find it fascinating that the polymerase can actually move backward to perform error corrections. How do they know do do that? Is there some kind of biological software in an enzyme that tells them how to do these things?

user38945 "is right". Seriously: Any "promoter" is just a grain of sand in the strand, it's true that there are - right or left, from "that" promoter  - some nucleotides that define "its" direction, i.e. its directing.  (With my maths, two of them would suffice (as Polymerase is one trick pony, does from '3 to '5, always does it.))


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Can paralogous genes be under negative selection?
I have just aligned 9 paralogous genes from human, uploaded them into MEGA and calculated  negative selection. Can there be negative selection acting in between paralogous genes? Or how should I interpret this result?


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How does a Na+/H+ antiporter drive osmosis in this "osmotic motor"?
This recent paper in Cell describes a cancer cell using osmotic pressure to move in confined spaces. The cell preferentially inserts Na+/H+ antiporters in the leading membrane. I want someone to double-check my osmosis before I make students reason it out:

The normal Na+/K+ pumps cause an increase in Na+ ions outside the cell, but little change in osmotic pressure across the membrane.
Increased Na+/H+ antiporters will allow Na+ in while pushing H+ out at the "front" end of the traveling cell.
While this causes little net solute change, it increases water flow into the cell via aquaporins (?? this part I find mysterious)
Na+ continues to be pumped out of the cell by the Na+/K+ pump at the "back" end of the cell
Water follows the Na+ through aquaporins out the "back" of the cell, moving the cell forward

I don't feel convinced that moving ions around like this is causing osmotic gradients. Can anyone convince me?

Why don't you think that moving ions builds up osmotic gradients?

Because the same number of ions cross in and out - Na+ in, H+, out.

This means you are not building up apotential across the membrane (which would happen if you only transport ions in one direction), but you build up osmotic gradients. This is the reason why glucose is phosphorylated when it has been taken up by cells to remove it from the glucose gradient.

Sorry, I still don't understand how water flow can be triggered if there is not a net change in solute molecule number across the membrane... can you tell me more?

But how does an antiporter exchanging 1 solute for another build up an osmotic gradient Chris?

Since posting, I did some more research using background refs from the intro (who knew?).
The trick seems to be that when protons are pumped out, the cell regenerates them from water in order to maintain pH. So the solute concentration DOES increase inside the cell with more Na/H transport.

Thanks for the clarification, I was expecting something along the lines of that, but I had no idea about the specifics.

@Adrienne Can you make your comment into an answer (it is perfectly ok to anwer your own questions)?

Sure.
Typing more until this counts as a comment.....

Since posting, I did some more research using background refs from the intro (who knew?). The trick seems to be that when protons are pumped out, the cell regenerates them from water in order to maintain pH. So the solute concentration DOES increase inside the cell with more Na/H transport.


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Does the most common definition of "allele" include a change in phenotype?
I'm prepping an activity for my biology students on cystic fibrosis. There are about 2000 different mutations of the CFTR gene that cause CF. Since the final phenotype is pretty much the same, can I still claim that all these mutations represent different alleles?
I like to point out that genes tend to have more than two alleles - it's something that students really struggle with. But if every allele needs to have a different phenotype based on the standard definition, then this isn't ideal.
Thanks for the help.

I agree with the answer given by @Bez. The problem arises because the term "allele" was coined in an era when the only way to observe (or infer) the existence of different forms of a gene was through the associated change in phenotype (i.e. genes were not observable directly). Now that we can document single base changes via sequencing, the link to observable phenotype has been completely severed, but the idea of alleles as alternative forms of a single gene is still useful.

Yes, allele is an alternative form of the same gene which can be produced through any variations/mutations of a gene, such as deletion, segmental duplications, inversions, insertions through transposons, even a SNP or point mutation (http://en.wikipedia.org/wiki/Allele) and as correctly stated many alleles do not produce any observable/discernable phenotypic variation. A gene can have many alleles in a given population, but do not confuse allele with gene homologues (which I suspect what you were alluding to above in the second paragraph), which are similar versions of a gene such as RIN1, RIN2 and RIN3 (http://homepage.usask.ca/~ctl271/857/def_homolog.shtml).


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Is it theoretically possible to treat filaggrin deficiency with a dietary supplement?
http://f1000.com/prime/reports/m/3/2/

"Filaggrin is a highly abundant protein expressed in the uppermost part of the epidermis that is critical to the formation and hydration of the stratum corneum—the outermost dead cell layers responsible for the barrier function of the skin. Filaggrin deficiency leads to a 'leaky' skin barrier that allows higher than normal water loss (explaining the dry, scaly skin), as well as allowing entry of allergens through the epidermis where they trigger inflammatory and allergic immune responses (atopic eczema and allergies)."

Not that such a supplement exists, but is it biologically possible to treat filaggrin deficiency with something taken orally?

THe cause of the deficiency has to be ascertained before thinking about therapy. FOr e.g it could be because of improper diet or it could be because of a mutation.

It may be possible to upregulate the filaggrin gene in skin cells. https://www.ncbi.nlm.nih.gov/pubmed/24055295

Direct replacement of a protein through oral supplementation is extremely unlikely. Our digestive tract is designed to break down proteins into their constituent amino acids.
In the stomach pepsin breaks proteins into polypeptides which then pass into the small intestine. At this point (second part of duodenum) multiple enzymes (proteases) enter having been released from the pancreas in response to eating. These enzymes further reduced the polypeptides into smaller components such as you end up with component parts of the original protein.
These component parts are then transported across the intestine into the blood through cells lining the intestinal lumen (enterocytes). Enterocytes also have proteolytic action on long chains of amino acids.
As a result of this process, the original structure of the ingested protein is destroyed. However you do end up with the constituent amino acids. If your fillagrin or any other protein deficiency is as a result of lack of nutrients then in response your body may be able to synthesise the required protein. If on the other hand your deficiency is due to a gene defect, despite having the building blocks for the protien you will continue be deficient.

I highly doubt it. Filaggrin is a human protein which is expressed in the skin and stored as profilaggrin. The profilaggrin has a molecular weight of about 350 kDa (which is rather big) and is cut into smaller units of filaggrin, which then crosslinks kreatin fibers of the epidermal keratinocytes. This enhances the durability of the skin. Mutations in the filaggrin gene have been associated with dry skin and excema. See here for more information:"Filaggrin - revisited."
To supplement the profilaggrin, you would have to bring this rather large protein into the skin. You could think about making a cream with the smaller filaggrin in it to promote crosslinking of the upper skin. The question here would be how effective such a treatment ist and how deep the crosslinking would be.

Yes, according to this study 4g of histdine administered daily does the trick: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5634381

Welcome and thanks for your answer. Link-only answers are discouraged. It's great to link a research paper, but try to extract the answer and underlying proof from the paper and synthesize your answer, preferably with other sources as well. As of now, acknowledging the post is referenced, it still is a question comment rather than an answer.


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Could an annual plant be genetically modified to be a perennial?
My chives, asparagus, oregano, and rhubarb come back every year like clockwork.  Suppose I want my bok choy to join the party - is there an "I'll be seeing you next year!" gene that can be modified to be turned on to be like my hardy chives, or is it more complicated than that?

It is definitely more complicated than that.

@Chris But they just need a rhizome system to store nutrients for the winter right?

the plant's genes are all adapted in countless ways to optmize the out come for the annuals for their current lifestyle.  it would take a lot of effort, re-engineering many aspects of the plant's genome.  In the end you would have a very different plant if you could do it.  it sounds almost like a manhattan project of plant biology in scale.

Researchers at Ghent University have made a discovery that downregulation of the proteins CONSTANS 1 (SOC1) and FRUITFULL (FUL) lead to the development of many perennial traits in annual plants (in the study Arabidopsis thaliana is used) (reference).
The CONSTANS gene controls flowering in Arabidopsis thaliana (reference).
FRUITFULL (FUL) is an MADS box gene that functions early in controlling flowering time, meristem identity and cauline leaf morphology and later in carpel and fruit development in Arabidopsis thaliana (reference).
The process is complicated and would need many genes to be manipulated but this research proves that it is possible. Another article of interest.


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Could light/occasional smoking strengthen the lungs?
Here's my thought process, correct me where I'm wrong.  It seems the human body has thresholds.
Examples: You lift too much weight, and the muscles and tendons risk serious injury, but otherwise they tend to rebuild stronger to handle more weight.  Too much sun can lead to sunburn or worse, but moderate UVB exposure can lead to melanogenesis and increase protection to UV damage.
Do the lungs behave in a similar manner where a small amount of smoking might actually strengthen your lungs before reaching the threshold where you're causing severe damage?  My guess is the answer is "probably/somewhat" but that there haven't been any studies since it'd be difficult to analyze and quantify, but maybe somebody has an answer based on theory.

From your examples only the first is really true. Exercise leads to better physical abilities (within some boundaries).
Sunlight on the other hand is always potentially dangerous, depending on the dose. But the damages accumulate over the years which finally lead to the so called senile lentigos (others call them aging spots) occuring in sun exposed skin from the age of 50.
And the same is true for cigarette smoke. Here you expose yourself to a nasty cocktail of potentially harmful to cancerogenous substances (tar, polycyclic aromatic hydrocarbons, benzene, nicotine and much more). These do potential harm to your lungs depending on the dose (meaning how many cigarettes you smoke a day), but there is nothing like a harmless amount. Your lungs will eventually recover from this (tar takes the longest to be removed), but it is definitely not good.

Out of the womb, a person might be extremely prone to sunburn, but wouldn't 15 years of moderate exposure increase the overexposure threshold?  Maybe my usage of the word "strengthen" is inappropriate, I mean more along the lines of increasing the threshold until damage.  From my admittedly limited perspective, the human body seems to increase it's ability to withstand when exposed to harm, so long as the harmful factors are not prolonged and recovery time is allowed.

Sun exposure is difficult, since we need it to some degree to produce vitamin D. Nevertheless it can be pretty harmful, even in "small doses". The other problem are the harmful factors itself. There are a lot of things where the body can adapt and recover, like for drinking alcohol (which is also cytotoxic). For other substances which are cancerogenous this is not true. There every hit can be the fatal one which develops into a malignancy. Of course the dose plays a role here, too. But this is the reason why I can't consider smoking harmless.


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biologically speaking, what's the difference between sleeping and just resting?
I can lay down in a rested position with my mind at ease, but no matter how relaxed I am or for how long i do it, it seems I'll still need sleep eventually.  What's the difference - what is occurring during sleep that can't occur now matter how relaxed or rested you are?
And if you know of any studies that have been done to try and mimic the benefits of sleep in a waking state - ie during some type of meditation or whatnot - I'd consider that relevant and interesting to know.

I wish i could give a one word answer: brain-activity..

@WYSIWYG As that would be the epitome of "vague", I'm glad you can't. :)

haha sorry but it is the brain activity that is different between sleep and just physical rest.. al you need is details :P

@WYSIWYG you bring up an interesting point actually because I had thought something similar - that your brain must be takin a rest, but then I thought to myself: dreaming has to be pretty brain-intensive, no?  we're often creating scenarios that frequently don't even follow the same rules of existence as our waking world.  It seems to go far beyond normal waking reverie; isn't that taxing on the brain?

@coburne Personally when I dream during my sleep, I think I am not refreshed and I feel weariness.

Difference between rest and sleep
There are many factors which describe the difference between rest and sleep.
Rest
Rest occurs with conscious breathing. This allows the autonomic nervous system (ANS) to rest. The autonomic nervous system belongs to the peripheral nervous system. ANS controls many organs and muscles in the body.
In most situations, people do not know about the workings of the ANS since it functions in an involuntary, reflexive manner. For instance, we hardly notice if blood vessels change size.
This is the same case when our heart beats faster. There are some people who can control some of the functions in the body and can know the heart rate or blood pressure.
Sleep
Sleep it is a natural state of rest for mind and body. It happens in cyclic pattern. This can be one of the reasons to describe the difference between rest and sleep. There are four stages of sleep.
In the first stage of sleep, there is low-frequency, low-amplitude $\theta$ waves. This stage last several minutes before you enters into the next stage of sleep. In stage 2 of sleep, you brain moves into low frequency. In the third stage of sleep, you receive more high-amplitude $\delta$ waves.
During stage 4, the delta waves account for more of your brain activity and then they return back to stage 1.
Resting is more like being couch potatoes.
Rest is important for health and sleep is a necessary factor. You need both for your physical and mental activity to create energy. When the energy level goes down and wastes increase, there is tiredness and body needs rest. When you take rest, energy is restored. All the waste in the body gets extinguished. Rest and sleep are dependent upon each individual’s ability to relax. If an individual is tensed, he cannot be in the state of rest. Rest is taken to counteract fatigue.
Source:
[1] http://www.theatlantic.com/health/archive/2012/09/when-you-cant-sleep-how-good-is-lying-in-bed-with-your-eyes-closed/262484/
[2] http://insomnia.ygoy.com/difference-between-rest-and-sleep/

+1 for Resting is more like being couch potatoes.. Just kidding. This is a pretty good answer.

REST is not a deep sensation. We define various types of waves that are drawn using electroencephalogram.

$\alpha$ waves:

Awake but resting position.
Frequency: 8-13 Hz.
They originate from occipital region

$\beta$ waves:

Alert wide awake person.
They originate from frontal region.
Frequency about 14-30 Hz.

$\theta$ waves:

They occur under stress and in case one is drowsy.
Frequency about 4-7 Hz.

$\delta$ waves:

These originate when person is in deep sleep.
Frequency about 1-3 Hz.

does the lower frequency correspond to lower ionic activity by all neurons, or the same ionic activity per neuron, but fewer active neurons; ie, if I'm at a football game and everybody is screaming, decibel levels are high, but everybody talking at once might have the same lower decibel leval as 90% of people completely quiet and 10% of the people screaming.


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How does Oedipus complex fit in the evolutionary theory?
This is somthing that really makes me curious. How is posible that trough a  evolution process the best posible candidate is the one that falls in love whith his progenitor?

Can you provide (biological) scientific evidence that the Oedipus complex is real and not just a psychological theory?

It doesn't.  The Oedipus complex is one of Freud's theories to explain human behavior, not something that is endorsed by the fields of psychology or psychiatry.  Freud had a lot of interesting theories, some of which remain core concepts in psychology, and some of which have been marginalized or rejected.
There are some professionals who feel it has merits for consideration, to one degree or another, but if you look at publications by the APA (American Psychological Association) and Psych.org (American Psychiatric Association), you won't see in their practice guidelines.
APA: http://psycnet.apa.org/journals/pst/32/4/535/
Wikipedia: http://en.wikipedia.org/wiki/Oedipus_complex#Criticism

If you're asking how might it fit with evolution if it were to be true, that's more of a philosophical question - which perhaps is the better angle from which to approach the question.
In "survival of the fittest" - "fittest" is better described as "those who most successfully reproduce and produce offspring that are also highly successful in reproducing."
Reproducing with one's immediate family results frequently in severe birth defects, the opposite of "fit."  Those who want to reproduce with their mother but don't, and reject all other mates, will not reproduce.  Not "fit."  The only possibility similar to the oedipal complex is that males choose mates that are like their mothers.
What is true is that we often marry someone similar to our parent - but it is not a result of an actual oedipal complex.  Freud wrote the oedipal complex in part to try to explain this phenomenon.  But there are better explanations - we are attracted to that with which we are most familiar, to that which makes us feel comfortable, to that which makes us feel warm and fuzzy.  Our definition of beauty is largely shaped by family faces - because that is what you are surrounded with as your mind develops.  Etc etc.


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How long can human tissue last without blood?
I've heard it said various times that the body's tissues will begin to necrotize after being cut off from the blood supply for only a few minutes, but that can't be true.
A few years ago, I woke up one morning and apparently I'd been sleeping just right so that the main artery to my left arm was totally pinched closed, because it was completely numb.  Not just "arm's fallen asleep", either; I had no mental control over the entire arm and no feeling in it.  I could lift it up with my right hand, and it would fall back down immediately when I let go of it, and I didn't feel anything when it landed on the mattress.  It kind of freaked me out at first, but in just a few minutes I felt the "pins and needles" feeling of circulation returning, and it was 100% back to normal within less than an hour.
Given that I had presumably been sleeping on it like that for several hours, and yet I somehow didn't end up with a dead, useless arm that needed to be amputated, I know from personal experience that tissue doesn't die within a few minutes.  So how long does it really take?

Your supposition is incorrect. A limb or other body part goes numb because a nerve is blocked, not because the blood supply is cut off. If you had truly completely cut off either the subclavian or brachial artery for that long, your arm would be deep purple.

It depends on the tissue type and on the circumstances. Brain cells start to die after 5 minutes, while heart cells die after 2 hours without oxygen. You can slow down the process by cooling down the body.

In medical school, we called this Saturday Night Palsy (or Honeymoon Palsy) - key emphasis on palsy - a nerve injury, not an arterial blockage.

@anongoodnurse "Saturday Night Palsy (or Honeymoon Palsy)" is that because it is generally alcohol that suppresses your CNS so that you do not move or change position in your sleep? Or does it have to do with someone else sleeping on your body part and it going numb from nerve compression? Serious question.

@AMR - Both, actually. Seriously. The inebriate falls asleep in a bad position and stays that way; the honeymooners snuggle, her head on his arm usually.

It sounds more like your put pressure on your nerves rather than cutting blood supply. Your arm didn't turn purple or black.

@MasonWheeler, Maybe you reduced the blood supply by 90% or even 99% but not 100.0%?

As EMT (Emergency Medical Technician) instructors will tell you now, when wearing a tourniquet, you have about four hours to get the injury to a vascular surgeon and get it cared for appropriately. The rule therefore is four hours. However, the common thread I see in most sources is that about an hour and a half is the longest you want to go without blood flow to a limb.
As far as what happened to you, it sounds more like the limb simply fell asleep. When a limb falls asleep, it is getting the nerve pinched off for a time as well as loosing some blood flow. However, this is not a complete loss and so your arm is able to survive because it is still receiving enough oxygen and other nutrients to sustain its existence (as well as having toxins and CO2 pumped away from it).
I had a very difficult time finding any concrete, scientific information on this subject overall.
So, if you would like more information about this, please visit the following links. The first is a WikiPedia link on Limb Infarctions (or an embolism in a limb). The second is from Mental Floss on Why Limbs Fall Asleep. The third is a somewhat random article on someone's personal experience on Sleeping on their arm.
So, in summary: although I could find no solid evidence on how long a limb can live without its blood supply, it appears to be about 2-4 hours (some sources say 5-8); however, I would like to add that your case appears to be a severe case of an asleep limb, you were/are likely in no danger. Also, if your arm indeed did have circulation completely cut off, it would have turned pale, then blue and later a livid red and purple as the blood began to pool; you then would begin to experience the effects of the limb dying i.e. necrosis, gangrene.

The Mental Floss article says that it involves circulation being cut off as well as the nerve being pinched.

@MasonWheeler Oh dear... Thanks for pointing that out, I shall change that when I get the opportunity.