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What is the current molecular explanation of Mendel's pea cross?
With reference to the simplest Punnet square for Mendel's pea plant experiments it occurred to me that I could not connect the little I know about genetics to the little I know about molecules.
The mathematical model assumes that there are two factors (alleles) involved. With respect to Mendel's pea flower colors, to what do those alleles correspond at the molecular level? Genes--minimally it might be two codons, each with binary states so that a protein involved in the manufacture of color molecules changes at two specific amino acids.
Of course it is not so simple. But it must be true that there are two physical objects which in the aggregate have two binary states for this particular case. Do we know what they are, exactly, for Mendel's peas?
Thanks for any insight.

I think the following goes a long way. The language is confusing in on respect--the authors speak of the 'A gene' and a bit later of a G to A transition, and I assume the latter refers to bases.  http://www.ncbi.nlm.nih.gov/pubmed/20949001/

The article you have linked to does explain everything thoroughly, though in a somewhat complex way. I did not know how much genetics you actually know, so I tried to answer very thoroughly.
So the article states that the gene Mendel studied and that was responsible for the white color of the pea flower is ANTHOCYANIN1 (in the article it is also called - bHLH, that is the name of the protein family that ANTHOCYANIN1 belongs to). So, ANTHOCYANIN1 is a transcription factor - a molecule that activates the transcription (making of mRNA) of other genes, basically it activates other genes.
The white flowered peas have a mutation (Guanine to Adenine transition) in the sixed intron of the gene ANTHOCYANIN1. Introns are sequences of non-coding DNA, that does not encode amino acids, and is removed from the RNA transcript by a process called splicing. The mutation occurs at a binding site for the Spliceosome (a protein and RNA molecule) that splices the RNA, because of this the RNA transcript is not spliced correctly. The faulty RNA transcript for the gene ANTHOCYANIN1 contains 8 extra nucleotides and because the genetic code is a triplet, a frame shift occurs. When a frame shift occurs all of the codons bellow the frame shift sight get changed. In this case, this leads to a premature stop codon. The translation of the ANTHOCYANIN1 RNA get stopped before a full protein can get synthesized and a non-functional protein is made.
If ANTHOCYANIN1 does not function, no genes are activated and no pigment is synthesized.
To summarize - the white pea flower color is a consequence of a nucleotide mutation (Guanine to Adenine) in a intron sequence of the gene ANTHOCYANIN1, this leads to incorrect splicing of the ANTHOCYANIN1 RNA (a frame shift) and to the production of a shorter protein that is non-functional.

Regarding the mathematical model can we say, in short, that what Mendel knew simply as a/A involve mutant and non-mutant versions of the transcription factor? Thanks. +1

Yes Daniel you are correct, what he studied in truth was the mutant and non-mutant versions of the transcription factor, he just did not know it, nor understand it that deeply.

My apologies, I misread you original comment.

@canadianer: no problem, thanks. i deleted my responses.


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Could the Warburg effect be used to starve cancer cells in situ?
What is wrong with the following chain of reasoning?

Nearly all cancer cells rely on high rates of glucose uptake (upto 200 times more than normal cells). This is known as the the Warburg effect.
There is only one cell type in the human body that is obligated to use glucose - red blood cells (erythrocytes).
Starve cancer cells of their only energy source by inducing hypoglycaemia in the patient, preserving red blood cells using, for example, erythrocytapheresis or an oxygen-carrying substitute.

I understand that to completely eliminate a tumour such a regime would need to be in place for an extended period, but would like to know why such a treatment isn't feasible in theory?

As a type 1 diabetic for 39 years I can only say that hypoglycaemia is a life threatening  state which any of us tries to avoid  as much as possible.

Any untreated episode of  hypoglycaemia can easily lead to diabetic coma and irreversible   brain damage.
When encountering low blood sugar, the organism anyway  releases sugar stored in liver just for that case, so prolonged  artificially induced  hypoglycemia would place a lot (i imagine unsustainable) stress on liver. Not sure, but I suspect it would lead to liver failure.

The human body needs energy (ATP) for even the most basic function. I guess when you decrease glucose levels (which is broken down for ATP), you will be in affect taking away the ability of the body to function normally by depriving it of energy. This is my theory so I would be happy to if someone with more information on the topic could tell me if I am right or wrong.

I think Kelvin is suggesting the use of beta oxidation to yield ATP from fats.

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Why don't we breathe nitrogen when it makes up most of the air?
Why don't we breathe nitrogen while it makes most of the air?
Why do we always tend to breathe oxygen, not hydrogen and nitrogen?

I'd argue that we do "breathe" all those gases. Air that we inhale (at sea level) is about 78% N$_2$, 20.9% O$_2$, 1% argon, and smaller percentages of CO$_2$, neon, methane, etc. So all those gases are going into the lungs with every breath in.
We take up oxygen preferentially because we have hemoglobin to bind O$_2$. When hemoglobin binds the oxygen, it upsets the balance and pulls more oxygen across the alveolar membrane. This is aided by pulmonary circulation which carries the blood away. Here's a demo of the diffusion process.

Nitrogen dissolved in the blood and pressurized during an underwater dive can, during a return to the surface, bubble out of the blood, just like the release of pressure opening a bottle of a carbonated drink causes bubbling.  In human divers, it can causes the painful  and potentially lethal condition called decompression sickness or "the bends".

You seem to be saying that nitrogen does not get absorbed into the blood. Are you, in fact, saying that? I came here because I am trying to learn whether humans can survive with trace quantities or even no nitrogen in the atmosphere.

I would argue that your argumentation isn't correct. Saying we have hemogobin to transport oxygen is like saying we have amino acids to build proteins. Your answer describes how the oxygen gets transported but not what the actual goal of this transport is. This is mainly because  oxygen is extremely electronegative and therefore important to form water  during oxidative phosphorylation

Completely agree with @RickBeeloo,  this answer gets the causality all wrong. We don't breathe O2 because we have hemoglobin --- we have hemoglobin because we breathe O2!

Animals use oxygen as a chemical energy source because oxygen gas can react with many other compounds to form oxides, which releases energy and happen spontaneously.
Both carbon and nitrogen can be made to react with oxygen, but otherwise they are pretty inert.  So of all the gasses in the air present at over a fraction of a percent, oxygen is the only one we can use for energy.
Nitrogen gas itself (N2) is incredibly chemically inert; N2 requires energy input into it to react chemically.  Biometabolism relies upon a chemical release of energy.
If we had ammonia gas (NH3) in our air it would be a great redox source of energy... taking energy from the ammonia could produce N2.   N2 takes a lot of work put into it to get the nitrogen out for other uses.
Hydrogen (and sulfer) are both possible substitutes for oxygen in the role of redox energy source, but are normally pretty small components of our environment.  On another planet they might well be the basis of biometabolism.
Of course the fact that plants can use carbon dioxide to fix carbon is a different case of biology using a gas out of the air.  Its the defining quality of plants!
The energetics of using CO2 is endothermic - it requires energy input. They have to use sunlight to get the energy to utilize this energy and its very costly energetically.  Animals can afford to move and grow because they use oxygen while they eat plants.

I wouldn't call oxygen an "energy source". It's an electron acceptor.  But the rest of the first sentence, "because oxygen gas can react with many other compounds to form oxides, which releases energy" is spot on. +1

try doing without it for a few minutes and see what happens to your energy :) combustion engines, forest fires and thermite reactions could also be called 'electron transfer' reactions. People falling off of tall buildings could also be called 'release of potential energy events' but also i wouldn't expect the use of language to conform to freshman chemistry just because there is different language for the same thing.

@shigeta, superb answer. I know you tried to keep the answer simple for our benefit, but could you please edit the answer to include the relevant scientific concepts (an equation perhaps). What does inert mean in chemistry? Does it mean for example that a chemical reaction involving an inert element/compound has a higher activation energy? Gracias.

ok @AgentSmith i made an effort though discoursing into freshman chemistry is something i typically try to avoid

@shigeta, ok, arigato gozaimus. A quick question. What makes a molecule reactive as opposed to inert? Is it the electron configuration? Also endothermicity is a good explanation.

Sure.  @AgentSmith its about the electron configuration around the nucleus of a given charge.  this is one of the foundational bases of chemistry.  some chemicals react, others do not.  why is a pretty deep question... far beyond a single answer here. https://www.coursera.org/learn/intro-chemistry this course is free at the moment

Nitrogen is much less reactive than oxygen.  Indeed, if I haven't totally forgotten my long-ago chemistry courses, most chemical reactions involving N2 are energy-consuming.  Thus you get nitrogen compounds produced by lightning, in auto engines, and other places where there's a lot of energy to spare.
Oxygen reactions, OTOH, are energy-producing.  You might think instead of fire: most organic stuff will burn (if dried), but it only combines with the oxygen in the air, not the nitrogen.
PS: Indeed, many nitrogen compounds take so much energy to create that they are explosives.  Ammonium nitrate, nitroglycerin, trinitrotolulene (TNT), even the potassium nitrate (saltpeter) used to make gunpowder.

You can focus on the fact that dinitrogen (N₂) is very stable and is not a good electron acceptor. Many anaerobic organisms can use metal ions as electron acceptors instead of oxygen.

The bond in oxygen molecules is high energy, and ready to undergo an energy-yielding reaction with other molecules like sugar.
The bond in nitrogen not chemical useful to us...other organisms use energy to "fix" nitrogen to make energy rich nitrogen compounds that we can use.

The other answers seem to be missing the role of oxygen in oxidative phosphorylation, as an organism with aerobic metabolism we use oxygen for its electronegativity. Basically, as we break down glucose energy is released in the form of free electrons, these are "transported" for use in the oxidative phosphorylation to create new ATP which is our main form of energy storage. Oxygen eagerly accepts these free electrons at the last step of the oxidative phosphorylation and binds with H+ to form H2O. See here.
So without oxygen there would be an accumulation of electrons, stopping the oxidative phosphorylation and forcing us to break down glucose in the (less efficient) anaerobic manner.

There are two parts to this answer, and several answers have addressed one or both aspects but I figured I'd put it all in one place.
1) We use oxygen for a purpose that nitrogen is chemically useless for
2) While there is a different purpose we might want to use nitrogen for, it is something that is difficult to evolve (only bacteria have done it) and we can manage without.
Explanations:
1) We use oxygen because our metabolism uses it for energy. Our metabolism derives chemical energy from the breakdown of complex carbon molecules; this doesn't happen on its own and you need very reactive molecules to interact with those complex carbon molecules and break them down. All organisms do this step-by-step, using successive "electron acceptors" to basically strip electrons off of simpler-and-simpler molecules and thus break them down. Molecular oxygen is the most reactive molecule and greedy electron acceptor out there, and allows organisms that use it to get the most energy possible out of a given carbohydrate. That's why aerobic respiration is so useful, and that's what we use oxygen for. Molecular nitrogen has completely different chemical properties; it isn't that electronegative (i.e. greedy for electrons) at all. There are other molecules that can be used as electron acceptors, and are used in various forms of anaerobic respiration: nitrate, sulfate, carbon dioxide... but molecular nitrogen isn't one of them.
For various kinds of anaerobic respiration, see :
https://en.wikipedia.org/wiki/Microbial_metabolism
2) There IS a purpose for which one could use molecular nitrogen, which is to use it to build nitrogen-based molecules that our body depends on - like DNA, RNA and proteins, which basically do everything in a living organism. No organism uses molecular nitrogen as a source for these; it's much easier to use organic nitrogen compounds like nitrates and ammonia. It can seem silly that such compounds are so limiting, when nitrogen makes up most of the atmosphere! This is less of an issue for carnivores since we get all of our nitrogen needs from eating nitrogen-filled animals, but it's a huge issue for plants. The need for such compounds (and, to a lesser extent, phosphates) is why agriculture needs fertilizer. So why can very very few organisms break down molecular nitrogen ? Because it is a very stable molecule; if you've done chemistry you might know that the two nitrogen atoms in the nitrogen molecule are connected by a triple bond, which is very strong and hard to break. This may be a big reason why the metabolism to break that bond evolved only in bacteria, and all Eukaryotes get by using the bacteria themselves (nitrogen-fixing plants), absorbing nitrogen-filled organisms (carnivores, carnivorous plants - it's the reason they're carnivorous!) or getting by on the organic nitrogen that naturally occurs in the ground thanks to nitrogen-fixing bacteria.
https://en.wikipedia.org/wiki/Nitrogen_fixation
As an aside, the fertilizer humans make uses the Haber process, which converts molecular nitrogen in the atmosphere to ammonia. If you look at the Wikipedia page by the way you'll get an idea of how hard it is to break that triple bond, between the catalysts and the high temperatures and pressures... But through that process you could argue that humanity as a species does "breathe" nitrogen.
https://en.wikipedia.org/wiki/Haber_process
So basically, tl;dr:
1) we don't need to breathe nitrogen
2) if we did our bodies still wouldn't because it's really hard to do; no eukaryote does it, except maybe humans themselves but only through technology.

As others have pointed out, we do breathe atmospheric nitrogen but we cannot do anything useful with it.
The problem is that the triple-bonded N2 is very unreactive and almost all animals and plants cannot convert it to anything else. Humans do not have the ability to reduce it to NH3, for example, but is would be great if we could.
All forms of life need nitrogen. It is necessary to make protein and DNA, for example. It is also very plentiful. N2 constitutes about 78% of air by volume, but it is in a form (N2) not usable by most forms of life. And therein lies the problem: in order to use atmospheric nitrogen, it needs to be 'fixed', ie converted to a form available to 'normal' metabolic transformation.  This is usually taken to mean that N2 needs to be converted to NH3.  Very few forms of life have the ability to do this.  The 'fixation' of N2 is also a great industrial problem.
As outlined by Rozenn Keribin, the first artificial process to successfully 'fix' N2 is the Haber-Bosch process, which was developed in the early part of the 20th century, and uses a metal catalyst and high pressures to achieve the following transformation:

N2 + 3 H2 → 2 NH3

This process remains the main industrial source of NH3 today, and is a 'mainstay' of the fertilizer industry. During the First World War, it was also an source of NH3 for the production of ammunition by Germany. For his work in this area, Haber was awarded the 1918 Nobel prize in Chemistry, a (controversial) honour that has surely stood the test of time.
Biological N2 fixation is an amazing story, and I'll restrict the discussion to an amazing enzyme: nitrogenase. This enzyme catalyzes the ATP-dependent reduction of N2 to NH3
(I will not deal with  leguminous plants, which can also 'fix' N2 using a symbiotic relationship with bacteria in root nodules, as I do not know enough about it).

In nature, [the] ability to fix N2 is restricted to a small
  but diverse group of diazotrophic microorganisms that contain the enzyme nitrogenase (Burgess & Lowe, 1996)

One type of nitrogenase (that contains molybdenum) catalyzes the following reaction:

N2 + 8 H+ + 8 e- + 16 ATP → 2 NH3 + H2 + 16 ADP + 16 Pi

Let's analyze this one: that's an eight-electron reduction that uses 16 ATPs just to make two  NH3 from one N2 !
Nitrogenases may be classified into 3 general types depending on metal content: Molybdenum nitrogenase, vanadium nitrogenase and iron-only nitrogenase. (All forms contain iron).
Biological nitrogen fixation was discovered by Martinus Beijerinck and t Hermann Hellriegel.  In addition, Beijerinck discovered that tobacco mosaic disease was caused by a virus.  Neither received a Nobel prize.
Ref
Burgess, B,K. & Lowe, D. J. (1996) Mechanism of Molybdenum Nitrogenase
Chem. Rev. 96, 2983−3011

Basically when air fills our alveoli, by the process of diffusion, only oxygen in the air is taken into the blood stream while the other gases along with the waste CO2 is exhaled. So you do breathe in nitrogen, but it is exhaled as it is by the body. The whole process of the respiratory system is explained here with diagrams.

Nitrogen and CO2 are also taken in. All gases dissolve and diffuse across the alveolar membrane

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Are people genetically predisposed to being interested in specific fields/ideas? How does specialization occur?
I'm not sure if I formulated my question well, but I'm curious about a couple statements made by Steven Pinker and and James Heckman.
In this interview: http://www.youtube.com/watch?v=KJ9Ad6s8g7I&t=7m51s Steven Pinker says

"there'd be a wide variety of families I could have grown up with and
  had the same kinds of interests"

and in this interview with James Heckman, he says:

But anyway, Smith says people are basically born the same and at age 8 one can't really see much difference among them. But then starting at age 8, 9, 10, they pursue different fields, they specialize and they diverge. In his mind, the butcher and the lawyer and the journalist and the professor and the mechanic, all are basically the same person at age 8.
  This is wrong. IQ is basically formed by age 8, and there are huge differences in IQ among people. Smith was right that people specialize after 8, but they started specializing before 8.

Can anyone explain Heckman's statement that people "start specializing before 8"?
What do we know about genetic influence on interests? (Is this the right stackexchange to ask this on?)

I think the concept you are looking for is the one of heritability.
In short, heritability represents the part of the variance for a trait that is caused by the genetic variance only. For more information, you can refer to this, this, this or this post or to wiki.
This wikipedia article talks about the heritability of IQ in human. It has been measured to be around 0.7.
Of course, heritability in IQ is not the same as heritability of "interests". But I don't know about any measure concerning the heritability of "interests". Such measure will be highly dependent on how you classify interests together. Does a mathematician specialist of probability theory have the same interests than a mathematician specialist of non-linear algebra? Does a Mathematician have the same interests than a chemist? and of a engineer? and of an electrician? Does a butcher have the same interests than a backer? and of a waiter? and of a bricklayer? .. Does anyone who work in business have the same interests? The fewer groups you make, the higher will the correlation between parents and offsprings and the higher is the part of the genetic variance that explain the variance in interests choice.

I guess this is another nature vs nurture debate. IQ may be a heritable trait but the question is whether proclivities are also genetically heritable.

Have there been any "separated twin" studies on this? Although, speaking from informal experience, several of the twin sets I know are in completely different lines of work, if that's any measure of "interest."


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psychological database with sequenced DNA records
I'm looking for an epigenetic database which includes for each example the psychological history of the persons DNA. Right now I can only find DNA and epigenetic databases. Sadly none of the databases provide "thick data" (qualitative data eg. history of person) to the sequenced DNA.
I want to investigate the effects of psychology on epigenetic and vice versa.

I would be very surprised if such a thing exists. Apart from the privacy issues (OK, you can anonymize the data), there aren't to my knowledge any projects for such large scale sequencing of human samples. The closest I can think of is the 1000 genomes project but I doubt any psychological data will be included.

23andme, for example,  along with SNP data collects information on different traits (including behavioral) from their customers and publishes interesting results from time to time, but their database is not for public usage.

You might want to look at the Danish Data archive:
http://www.sa.dk/content/us/about_us/danish_data_archive
I have never used their data and I don't know what barriers there might be to accessing it, but the impression I got at a talk by Soren Brunak (http://ctbr.hunter.cuny.edu/Brunak), was that this was one of the most complete databases for studying relationships between people's DNA records and other health information that might be available about them.


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Hebbian theory "fire together" clarification
Donald Hebb states it as follows:

"Let us assume that the persistence or repetition of a reverberatory activity (or "trace") tends to induce lasting cellular changes that add to its stability.… When an axon of cell A is near enough to excite a cell B and repeatedly or persistently takes part in firing it, some growth process or metabolic change takes place in one or both cells such that A's efficiency, as one of the cells firing B, is increased."
  Or we can conclude in short: "Neurons that fire together, wire together".

As I understand it, this means that synapses that already exist become stronger between neurons.

Could new synapses form between neighboring neurons that "fire together", but are not necessarily directly connected through an axon?
And if so, what is the mechanism to direct the new synapse formation towards that other neighboring neuron that "fires together"?

Strictly stated, Hebb's rule applies only to existing synapses, and not to the formation of new synapses. (This answer applies to biological neurons, not to ANNs).
Synapse formation is a topic of active research. During development (and in fact continuously even during adulthood), many synapses are created and destroyed. It is not unreasonable to suspect that a similar form of rule is used to decide which synapses are removed and which should remain.
Synaptic connections between neurons show a good deal of specificity -- for example, in the projection from the retina to the optic tectum, synaptic connections are made only with target neurons at an appropriate retinotopic location. This happens because growing axons follow molecular gradients.
Within a cortical column, some possible connection pathways seem to be actively sought -- for example, axo-axonal cells connect specifically to the axon initial segments of target neurons. Neurons certainly have membrane molecules that could be used to identify target cell classes.
So there are probably a number of rules used to determine when a new synapse is made. However, I am not aware of a mechanism for a pre-synaptic neuron to detect how a putative post-synaptic parter is firing, without a synapse already being present. So it seems likely that some form of random process is involved to form new synapses with reasonable post-synaptic partners, after which some activity-dependent rule (like Hebb's) could be applied.

It probably depends on what stage of development the neurons are in and what region of the brain.  If there's not branching still going on, then probably not.  Hebbian learning is generally considered a concept of neuron connections strengthening (more synapses forming and dendritic spines growing larger) and not the initial formation, particularly in artificial neural networks, where a non-zero weight is already assigned to the neurons, and it's just a matter of strong vs. weak connections.

Keegan's answer is good I gave it an up vote. I want to offer a valid alternative.
Psychology may induce redundant pathways which trigger approximate simultaneous firing of neurons near or in completely different parts of the brain.
Emotionally intense memories can trigger emotions, basically hallucinations of the event, smells and touch based recollections. The pathways work in reverse as well actual sensory input triggering the memory. The more often you delve into your other memories the stronger your abilities to remember those events become it can be very vicious or pleasurable.

(-1). This answer could benefit from improved grammar and syntax. Additionally, it's difficult for me to understand the relevance with the question, even after reading it several times.

Hebb himself (Hebb 2002) actually thought that both the formation of new or the enlargement of pre-existing synaptic contacts (what he called "synaptic knobs") were the most likely possibilities. However, he did not exclude a role for metabolic processes, such as the alteration of intrinsic firing properties of the neuron that could lead to increased synchronicity or a change in the firing threshold, or a limited role for microscopic motility ("neurobiotaxis"). From his language, it is unclear if he had a concept of pre- and post-synaptic elements. Indeed, evidence for the existence of the synapse from electron microscopy were presented about a decade later after the publication of his book.
It is pretty straightforward how the strengthening of pre-existing synaptic contacts can contribute to the proposed model. However, one can also imagine that the postsynaptic element, most often dendritic spines in the neocortex, could actively reach an already active presynaptic bouton. Even if spines are formed completely independently of presynaptic activity, it is still reasonable to think that only those that find an active presynaptic partner will stabilise by forming a synapse. See my answer here for more details on this matter.
Except from the temporal coincidence that is explicitly posited in the famous postulate, Hebb also predicted that the spatial proximity of two neuronal processes could result in synaptic contacts forming or strengthening. The hypothesis of spatial synaptic clustering, as we may call it, is actively investigated with modern methodological tools (Harvey and Svoboda 2007) and it is thought to be important in learning (Fu et al. 2012).

References

Hebb, D. O. (2002). The Organization of Behavior. Routledge.
https://doi.org/10.4324/9781410612403
Harvey, C. D., & Svoboda, K. (2007). Locally dynamic synaptic
learning rules in pyramidal neuron dendrites. Nature, 450(7173),
1195–1200. https://doi.org/10.1038/nature06416
Fu, M., Yu, X., Lu, J., & Zuo, Y. (2012). Repetitive motor learning
induces coordinated formation of clustered dendritic spines in vivo.
Nature, 483(7387), 92–95. https://doi.org/10.1038/nature10844


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How are dental cavities different from body injuries?
I always had this question why dental cavities cause pain. I stumbled on this question on the reasons why dental cavities are painful. I have a followup question on how dental cavities are different from bodily injuries. I was under the impression that pain causes inflammation which in turn triggers something like mitosis that causes healing. Why does the same not happen with the dental cavities? Why are they not treated like the bodily injuries?

I disagree with some of these statements. Dental cavities are injuries and are treated like injuries warrent.
Unlike maybe trauma or cancer, dental cavities are a injury caused by decay of the enamel (the protective hard shell of the tooth). The decay is a result of the proliferation of bacteria, streptococcus mutants which releases an acid and breaks down the tooth.
When you have perforated enamel, other particles like food can get caught in the tooth and give rise to the growth of other bacteria. At this point you have a cavity.
Infection, the presence of certain toxins, and trauma all causes inflammation, a type of non specific immune reaction characterized by increased blood flow to the site of injury (which causes swelling, pain, redness).

Can you be specific on where you disagree?

You did not explain The increased blood flow and trauma happens to kickin healing processes in other parts of the body. Why does this not happen in the mouth?

@koya it does happen in the mouth. My disagreement was in reference to your mention that oral injuries did not induce inflammation. After re-reading your question I'm going to delete mention if that and edit some content.- I think I have a clearer idea what your asking.


text:
Can a neuron make a synapse onto itself?
I was wondering if a neuron can make a synapse to itself? I suspect that it would be extremely unusual for a neuron to do this. Anyway, has anyone seen even a single instance of this?
Is the process by which a neuron 'knows' not to make a synapse onto itself is known?

A synapse from a neuron unto itself is called an Autapse. Not a whole lot is known about them. Tamas et al. (1) give a summary:

Van der Loos and Glaser (1972)proposed the word “autapse” to describe
  a transmitter release site made by the axon of a neuron and its own
  somatodendritic domain. In addition to their original Golgi study in
  rabbit neocortex predicting the existence of autapses, possible
  autaptic contacts have been described in dog (Shkol’nik-Yarros, 1971)
  and rat (Peters and Proskauer, 1980; Preston et al., 1980) cerebral
  cortex, monkey neostriatum (DiFiglia et al., 1976), and cat spinal
  cord (Scheibel and Scheibel, 1971). (...)
  Although autapses formed in cell cultures have been used extensively
  to study the physiology of synaptic mechanisms (Segal, 1991; Pan et
  al., 1993;Shi and Rayport, 1994), few proposals have been made for the
  functional significance of inhibitory autaptic innervation in
  vivo(neostriatum, Park et al., 1980; Aplysia buccal ganglia,White and
  Gardner, 1981).

Thanks for the references. I'll probably wait for few more days before accepting it as answer. Let's see if someone can comment on why autapse are rare.

@dilawar it would also be interesting to know what function,if any is done by such neurons. If they do not have a significant role they would most likely be rare.

There isn't enough research out there to explain the role of autapses however having read a selection of the latest research I can perhaps explain some of the proposed theory. Autapses may self inhibit or self excite. In the latter, one of their roles is thought to be to make a rhythmic action potential. This allows the brain to have an action potential which fires rhythmically if needed. Autapses of this nature have been identified in Interneurones for this purpose of continual activity.
Then there is even less researched areas. Imagine you need a neurone to fire twice to certain neurones but once to others or other similar requirements. A mixture of autapses with self inhibition and self stimulation properties can achieve this elegantly in a short space.
Things like this however aren't required frequently. Usually interconnecting neurones is sufficient, however possibly in places of high rhythmic activity or fine control these autapses may be helpful.
http://www.sciencedirect.com/science/article/pii/S0960982203003634


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Could super-caffeinating somebody's bloodstream be dangerous?
I'm currently planning out an RPG based on Misfits. Basically young offenders get super powers. I want one of the villains to have a really lame power that they use to become incredibly dangerous. I thought about using a power to caffeinate drinks. If someone used that to super-caffeinate somebody's bloodstream, could that hurt or kill somebody? Or would it not cause any real damage?

In extreme doses, caffeine can - like almost any substance - cause death. Wikipedia has this to say on the subject:

Extreme overdose can result in death.[59][60] The median lethal dose
  (LD50) given orally is 192 milligrams per kilogram in rats. The LD50
  of caffeine in humans is dependent on individual sensitivity, but is
  estimated to be about 150 to 200 milligrams per kilogram of body mass
  or roughly 80 to 100 cups of coffee for an average adult.[61] Though
  achieving lethal dose of caffeine would be difficult with regular
  coffee, it is easier to reach high doses with caffeine pills, and the
  lethal dose can be lower in individuals whose ability to metabolize
  caffeine is impaired.

You may wish to consult the references mentioned in the Wikipedia article for further details (As we all know, one should not trust Wikipedia too much). Note that caffeine administrated directly to the bloodstream will be more dangerous than the same amounted ingested.
Information on caffeine toxicity can also be found at Medscape. I you need concrete examples, Holmgreen, Norden-Petterson and Ahlner have published case reports on four recent cases of coffeine-related fatalities. (3)
To cover all bases, it should be said that none of the information mentioned should be used to estimate a safe level of caffeine intake.


text:
Are hens and roosters the same species?
I know that one is a female chicken and the other is male chicken. Are the chickens laying eggs considered the same species as those that we use for poultry meat? Or, are they different sub-species, analogous to how there are multiple breeds of dogs?

Hi @fedslaur, I have made some corrections to your spelling/grammar to make it read more easily. I have made sure to keep the nature of your question.

The main difference between a rooster and a hen is that the former is male and the latter is female. Their appearance differs in several ways [1].
A rooster also known as a cockerel or cock, is a male gallinaceous bird. The term usually refers to a male chicken [2]. The hen or the chicken (Gallus gallus domesticus) is a domesticated fowl, a subspecies of the Red Junglefowl [3].
And yes, the chickens laying eggs could be the same as the chickens that we use for poultry meat.
References:

Anjus Chiedozie. Rooster Vs. Hen on eHow.com
Wikipedia. Rooster
Wikipedia. Chicken

There are probably different breeds that are commercially preferred for egg laying versus eating.

Actually, this is partially correct.  I disagree with the downvoting.  Yes hen = female, rooster = male of same species.  But although basically all chickens can be used for meat and for eggs, there are some breeds that are better for prolific egg-laying and some for fast growth of thick meat.  See here: https://www.extension.purdue.edu/extmedia/as/as-518.pdf

Yes, they are the same species. Meat birds and layers are the same species, they have just been bred differently to produce a certain result. (Along these lines, you may wish to picture a tomato, there are many different shapes and colors. However, they are all the same thing.).
As with humans, certain chickens have certain characteristics. And to an extent "personalities".
It does appear, based on this link, that chickens are a subspecies of Red Junglefowl. However, chickens themselves do not appear to have an subspecies within them. Sorry I had to use Wikipedia.


text:
Sequence alignment scoring
The following table is from Deonier's text Computational Gene Analysis at p. 152.
This is an exercise in global sequence alignment and scoring of alternative sequences.
The text proposed a solution (in parentheses). Setting aside the upper left hand portion of the table it seems there may be a better path.
It's more likely I  misunderstand the idea than that there is a typo.
$$\begin{array}{c | c | c | c | c | c | c |}- & -& T & G & G & T & G\\ \hline  - & (0 ) & -2 & -4 & -6  &-8  & -10 \\ \hline
A &(-2)  & -1 & -3 & -5 & -7 & -9 \\ \hline
T &-4 & (-1)  & -2 & -4 & -4 & -6  \\ \hline
C &-6 & -3  & (-2)  & -3 & -5 & -5  \\ \hline
G &-8 & -5 & -2 & (-1) & -3 & -4 \\ \hline
T &-10 & -7 & -4 &-3 & (0)  & (-2 )\\ \hline  \end{array}$$
Just looking at the upper left corner,
$$\begin{array}{c | c | c |} (0) & -2 & -4...\\ \hline -2 & (-1) & -3...\\ \hline  -4 & (-1) & -2...\\ \hline  -6 & -3 & (-2)...\\ \hline  \end{array}$$
which seems to give -7 versus -8 for the book's path. Below are the book's alignment and the one corresponding to my scoring, which may reveal my error.
$$\begin{array}{c | c | c | c | c | c | c |} A: & A & T & C & G & T & - \\ \hline
B: & - & T & G & G & T & G  \\ \hline
\end{array}$$
$$\begin{array}{c | c | c | c | c | c | c |}
A: & A & T & C & G & T & - \\ \hline
B: & T &  - & G & G & T & G  \\ \hline
 \end{array}$$
I had no trouble constructing the matrix just scoring it. it's a small point but I don't like to move on without understanding it.  Thanks for any assistance.
Edit: Both current answer seem clear on this but just for completeness: a match = 1; mismatch = -1; indel = -2.

If I am myself not mistaken, the table shows the paths of least resistance. There are many paths through this table and all of them are not shown only the ones that cost the least. You need to understand that a mismatch between the letters costs -1 (eg - AT), but an empty square  costs -2 (-A or -T). So your solution would cost = -1-3-4-3-2-4 which sums up too -17.
This is a full alignment table. The top value is going diagonal, the second value is going down and the third value is going right.

Could you explain how you get that -17? A gap costs between -2 and -10 depending on which one in the table in the OP. The score of the mismatch also changes. Where are your numbers coming from?

The score of a mismatch is always -2, only if you use more than one gap then it increases by -2 with every gap. That is why the top row is -2 (one gap); -4 (two gaps); -6 (three gaps) and so on.
I did explain how I got -17 = - 1 - 3 - 4 - 3 - 2 - 4. You just need to add the values of each place.

The problem is that you are using the T twice. Let's build the alignment manually, we have two sequences:
>seq1
ATCGT
>seq2
TGGTG

So, to build the alignment using your approach, we would take the first nt of seq1, the A and choose the highest scoring nt from seq2 to align it against. In your example, that would be the T (-1) which produces:
A
T

OK, now we move to the next nt of seq1, the T. Now, in your table, the highest score is indeed for TT but we have already used the T from seq2, we can't use it again! In your alignment, you used a -. The score for T- at position 2 is -4. This means that your alignment:
ATCGT-
T-GGTG

Has a score of:
$(AT)_{pos1} + (T-)_{pos2} + (CG)_{pos3} + (GG)_{pos4} + (TT)_{pos5} + (-G)_{pos6}$
Which is:
$-1-4-2-1-10 = -18 $
While the book's alignment is:
$(A-)_{pos1} + (TT)_{pos2} + (CG)_{pos3} + (GG)_{pos4} + (TT)_{pos5} + (-G)_{pos6}$
Which is:
$-2 -1 -2 -1 -10 = -16 $

@daniel in which case it is probably mistaken (my approach, not your text). Taking what you show out of context, I am simply using the score for each position. So, since T- has a score of -10 in your table, I am using that.

We agree about the alignments. Why is the second score -4 in my alignment? That might clarify for me.

If you are saying the -4 in my score is because it's -2 in the 2d position, then why isn't -1 in the 4th position -4? This might clarify.

@daniel the -4 in your score is because a T in seq1 aligned to a - in seq2 has a score of -4 in the table. The -1 is because TT has a score of -1 in the table. However, while I have actually worked with this kind of thing, I have never worked with it in depth and it was a few years ago now, I may well be wrong.


text:
Do insomniacs yawn?
According to wikipedia, the jury is still out on the function a yawn serves. The article referenced above however writes to say

Yawning most often occurs in adults immediately before and after sleep, during tedious activities and as a result of its infectious quality. It is commonly associated with tiredness, stress, overwork, lack of stimulation and boredom, though studies show it may be linked to the cooling of the brain

The first sentence there draws my attention. Given a yawn is almost definitely associated with sleep - being expected to occur immediately before, and after.
Does it follow that an insomniac does not yawn?
As a corollary, are there any known medical conditions which preclude the act of yawning? For instance, a comatose person probably does not yawn.

Anecdotally, YES insomniacs yawn. Especially when tired from not sleeping

Of course. As you quoted from Wikipedia:

It is commonly associated with tiredness, stress, overwork, lack of stimulation and boredom.

Insomniacs, because they can't get a good sleep, are more tired and stressed than the others.


text:
chimeric sequences
I understand that chimeric sequence identification is done in results of sequencing projects to remove them and improve the quality of the output. I am unsure as to how they show up during sequencing. Any explanation is appreciated.

Do you mean chimeric sequences that are artifacts of the sequencing process or actual bona fide chimeric transcripts that are present in vivo?

Yes, but you're contradicting yourself. Some chimeric sequences are very real and exist in vivo. Others are artifacts, mistakes introduced by the sequencing process. Which ones are you asking about?

Chimeric sequences show up in sequencing projects a lot and you always have to watch for them. They show up a lot for a couple of reasons.
Firstly, sequencers are not perfect and generate sequences with errors.  Also they produce a lot of data but often not quite enough.  There are usually thin spots in the sequence assembly - regions which are not covered very well.
When a sequencing error coincides with a gap in the sequencing, the two ends of a sequence alignment can align to two unrelated or distant segments of sequence, creating an alignment assembly which has two unrelated portions - a chimera.
This is especially the case in EST and RnaSeq runs where long scaffold sequences and higher coverage might not help as much. It does have an impact in Chromosomal sequencing as well.  There's some interest in how often contaminating DNA get included into sequencing output.

My understanding of chimeric sequences is that they are produced as the result of inserting two different cDNAs (usually from different species) into a backbone such as pUAST to make a protein that is partly from one species and partly from another species. Sometimes you want to do this because for example the ligand for a receptor in lets say Drosophila is very difficult to produce but the ligand for the mammalian receptor is easily available so what scientists do is that they attach the human cDNA corresponding to the extracellular side of the receptor to the Drosophila intercellular portion of the Drosophila receptor. Now you can intracellularly activate a Drosophila receptor using a human ligand for a receptor. Now I have never seen/heard of chimeric in vivo sequences and that just doesn't seem possible but what I imagine can happen when viewing sequencing data for a species that are not fully sequences is that the search engines says a particular sequence is from a different species that you have sequenced. This is because the database will try to find the closest match to the sequence. NCBI BLAST for example can do this but usually it gives you a percentage sequence matching/probability. Otherwise I'm not sure what you mean by the word sequencing projects. Could you provide an example/reference?


text:
Amino acid profile of GPCRs

You are studying cellular signalling through a newly identified GPCR.
   Specifically you’re working on a pair of newly identified GPCRs,
  GPCR-A and GPCR-B. Each binds the same small ligand, but activates different
  heterotrimeric G-proteins that act on adenylyl cyclase.
  Your grad student mentor explains that both the receptors and the
  Gα and Gβγ subunits of the heterotrimeric G-proteins are membrane associated.  You examine the sequences of the seven predicted
  transmembrane α-helices of GPCR-B. You’re surprised to find that there are
  hydrophilic amino acid residues in these helices. How can you explain this
  observation?

This was an MIT quiz question.I have my guesses. But I wanted to know the correct answer.
Well, since GPCRs are transmembrane proteins, normally the transmembrane helices have higher hydrophobic amino acids or only hydrophobic, non-polar aa . Here it says they saw some polar residues. Well my guess is that, since there are two GPCRs a and b that bind to the same ligand, it could be that one activates a stimulatory G protein and the other an inhibitory G protein Gi . So probably the polar amino acids which are in the transmembrane alpha helical segment of the stimulatory GPCR is slightly displaced and is in the intracellular region of the inhibitory GPCR (Gpcr that activates inhibitory G protein ). To be in the intracellular region, it has to be hydrophilic.
This is all I can think of.
Any help with this question is much appreciated. It is not a homework question for me. I don't go to MIT. I just wanted to reinforce my concepts.

Polar amino acids in this case stabilize the helical structure within the apolar milieu of the membrane by making intra- and inter-helical connections. Thus the side chains of polar amino acids turn to one another while apolars face the apolar membrane. This would be definitely supported if you could find alternating apolar - polar segments in the sequence of helices.

Thanks for the answer. You mean to say that the helices are closely packed that the polar residues are found where they contact each other and the apolar residues are probably more denser on the helices at the two extreme ends where they make contacts with the apolar milieu of the lipid bilayer that is the membrane.

Is this the only way around in this question ? Are there any other possibilities ? Could it be that one of the helices with the polar residues protrude into the cytosol to make contacts with the G-protein ?


text:
Metapopulation structure - book recommendations
What book would you recommend me to study:

the dynamics of metapopulations,
the structure of metapopulations,
the evolution in structured metapopulations?

I am not looking for an introduction but for a book that offers good and extensive mathematical formulations.

Probably the best source to start would be Ilkka Hanksi's work, you can find a full list here: http://www.helsinki.fi/science/metapop/People/IlkkaPub2.htm.  The seminal work would be "Ecology, Genetics and Evolution of Metapopulations"  It gives a strong mathematical treatment

I was indeed thinking about "Ecology, Genetics and Evolution of Metapopulations". Thank you!


text:
How does a blunt force stimulate histamine to develop early stages of inflammation?
I know that viruses and sharp forces can stimulate mast cells by cut or by a virus infecting them and then release histamine. How can blunt force do this and cause inflammation? It doesn't have the above process. And how will the macrophages, neutrophils and plasma cells  react to this type of inflammation when there is no bacteria or viruses to swallow and create antibodies for?

An brunt force (trauma) may destroy cells and tissues by mechanical action. It simply squashes them.
Cells contain different kinds of chemical substances in specific cellular organelles. The most important in this context are enzymes from lysozyme.
Once enzymes are released (by squashing the cell) they induce irritating reactions to other cells and activate specific receptors found on immunitary system cells. This is how non-infectious inflammation occurs.
Cell components act as inflammatory mediators responsible for the clinical signs of inflammation. Here are some examples  [Wikipedia]:

Lysosome granules from destroyed cells
NO (Nitric oxide) from endothelial cells and some neurons

Other inflammatory mediators are produced by macrophages, neutrophiles and plasma cells, thus leading to a chain reaction, in which immunitary system cells activate one by another.
Macrophages have enough to 'swallow': all the destroyed cells which must be removed from the tissue.
Antibodies are produced because altered cell structures are considered non-self and gain antigen properties.
Source: Wikipedia, Inflammation


text:
How does chromosome cross-over occur?
I have heard that during meiosis, homologous chromosomes from each parent "cross-over", which enables the off-spring to inherit some alleles from the mother and some alleles from the father.  The picture below illustrates this "cross-over", but of course this must occur at multiple sites, rather than just the one shown in the picture.

Now my question is what causes the chromosomes to align perfectly during cross-over so that the loci of a particular gene will substitute for the corresponding loci on the homologous chromosome, as opposed to being substituted with a completely random locus?  Does each gene have a unique non coding sequence before it specifying what gene it is to enable this process to occur?

You might enjoy reading  the section on crossing over from Bruce Alberts' The Cell. I love that book as it has answers to many beautiful questions that may arise regarding cell biology.

Quite simply, because chromosome pairing is sequence specific. Holliday Junctions, which are the functional structures of a cross-over, occur through a process called "strand invasion," during which a region of one chromosome physically base-pairs with that of another.  Thus one locus cannot pair with a random locus, as there is generally insufficient sequence complimentarity between two random regions to form a functional Holliday Junction.  One interesting consequence of this mechanism is gene duplication and deletion in repetitious regions of the chromosome.  For example, genes with large repeated regions, such as the gene responsible for Huntington's disease, can expand and contract during homologous recombination due to strand invasion occurring at non-equivalent, but still homologous, sites.  Wikipedia does a nice job going over homologous recombination.  I also recommend looking over the relevant sections in Molecular Biology of the Cell, available on the PubMed Bookshelf.

Most of the time sequence differences between alleles are quite small.  Two genes with large changes between them are not alleles, they're homologs.  Alleles tend to have one or a few Single Nucleotide Polymorphisms (SNPs) that distinguish them.  For example, the gene that causes sickle cell anemia, differs from the wild type allele by only a single base change. http://www.nature.com/scitable/topicpage/genetic-mutation-441.  These very small changes are irrelevant in the context of a 10 Kb cross over.


text:
Does anyone know good software for producing tanglegrams?
I'm trying to look at relationships between parasite and host phylogenetic trees. I have done a bit of searching for software with which to do this, and I have tried using Dendroscope and TreeMap, but can't get to grips with them.
I want to produce something along the lines of this;

Treemap and Dendroscope are the only ones that I know of. Can you start small? Search for examples like: http://ib.berkeley.edu/courses/ib200b/ib200b_2009/Labs/15%20Biogeography/15%20Biogeography%20and%20Treemap.pdf and try to work through.

I think that I may have underestimated the complexity of the matter. That run through is very useful, however it is the very earliest stage that I am struggling with. I have two phylogenetic trees (one host and one parasite). Both are in newick format. In this manual it says "This file contains two trees,
one for the host and one for the parasite, and a description of which hosts are associated
with which parasites.". I think the lack of description of association is the problem. I assumed the software would take the associations from the information in the trees? I'm not an expert!

how to use dendroscope3 for making phylogenetic tree?

The word "software" is uncountable in English so cannot take the indefinite article. I have corrected this in the question.

Dendroscope
Using Dendroscope, I opened the provided example file trees.new. This opens a new window with 16 trees in it.

Shift click on the first two trees (Tree1 and Tree2).
Choose Algorithms $\rightarrow$ Tanglegram...
This will compute the tanglegram and open a new window.

At this point, I get:

There is nothing special in the trees.new file, just 16 Newick trees. So it looks like all you need is to have your trees in the same file or use File $\rightarrow$ Add from file.
I think that the tricky part is that your trees have to have the same tip labels, so that they can be lined up optimally. So in your example, Phalacrocorax pygmaeus and Pectinopygus excornis must have been named the same in the original Nexus file and then modified to produce the final figure.
TreeMap 3
TreeMap requires some preliminary setup. Basically you create a Nexus file manually. Using the 4taxonmatch file from the examples, you can get the basic layout. You have a HOST block and a PARASITE block. Within each one of those is a TREE block, which contains the Newick formatted tree.
The RANGE block inside the DISTRIBUTION block contains the mapping table. Here p maps to u, etc. This is the connection between host and parasite.
#NEXUS
BEGIN HOST;
TREE * Host1 = (u, (v, (w, x)));
ENDBLOCK;

BEGIN PARASITE;
TREE * Para1 = (p, (q, (r, s)));
ENDBLOCK;

BEGIN DISTRIBUTION;
RANGE
    p: u,
    q: v,
    r: w,
    s: x
;
END;

In contrast, you get the correctly labelled tree directly. See below.

Brillian,it was the tip labels in Dendroscope. I understand how these work now, thank you!

I have to confess that I know nothing about phylogenetics and the associated software but according to the abstract of this article it seems that they used BEAST to map coalescence of co-evolving hosts and parasites.
Also this article is probably of highest interest to you as it compares the efficiency of different software to construct tanglegrams

That makes two of us! I shall try and use dendoscope again with that article in mind. Thank you!

You can try the R package dendextend. The function tanglegram can do the trick.  Several associated functions are also available for getting plots with minimum entanglements such as untangle_step_rotate_2side.

Jane 4 (software for cophylogeny reconcilation) has a tanglegram viewer with an interactive editor.  (https://www.cs.hmc.edu/~hadas/jane/)

I recommend mesquite, which I've used to create phylogeny trees with.
There are some intricacies with using it, but there is plenty of documentation on its webpage!
https://www.mesquiteproject.org/


text:
Seeing strange things in light
I have noticed that if you look directly at tubelight (I have only white ones in my home) and close your eyes little, you see little random shaped colourless things sometimes with slow speed and sometimes with falling down.
They are shaped like circles with something in between and in chains of random length.
My father has also seen them. So, I am sure I am not imagining things. What the hell are they?

They're inside your eyes ;)

Oh, John Rennie's answered that. My bad, didn't see!

Almost everyone has these and they are harmless in small numbers. If you have a sudden increase in the number of floaters then that is symptomatic of potentially serious problems and you should consult an eyecare professional.

It's been suggested that this is off topic here and belongs on [biology.SE].

This was an enigma to me from my birth to yet.

Those are floaters. These are objects floating in the vitreous humour that fills the eyeball. They typically look like:

Thanks. Up until now, I knew that it were white blood cells.. :)

@SachinShekhar They're a variety of stuff. Protein structures, cell debris, etc.

Wikipedia says in old age.Is it normal for a 15 year old kid to see them?

@Awesome: Have you tried Googling to find out? Given that this is a physics site I doubt there are many experts on eye health hereabouts.

Oh... my bad... happens when you study too much chemistry ... Thanks.

@Awesome: I've seen them ever since I was a little kid, so I don't think it's abnormal.

I've seen them since a young age too so probably nothing to worry about. (Sorry this was supposed to be a response to the existing answer, I can't see how to move it.)

@Awesome I can recall being fascinated by this when I was still in my cot - probably about 3 years old. I recall quivverring my eyes to make them move around! I'm now 50 and everything sight wise still works well!

In https://en.wikipedia.org/wiki/Blue_field_entoptic_phenomenon this phenomenon is explained with white blood cells in your retina.


text:
Why do so many people have group O blood?
Please forgive me in case my question wouldn't make much sense. I was reading about ABO blood groups on Wikipedia, where I learnt that O is a recessive allele, and that it seems the A allele predates the O allele. My question is, therefore, how is it possible that almost half of the human population is group O?
For instance, I would expect (quite naively I reckon), if only alleles A and O existed, that around 75% of the population should be A, and 25% should be O.

You are wondering because O is recessive and A is older?

Exactly. Unless there were an evolutionary advantage to having group O (which I could find no evidence of by searching the web), it would appear logical to me that there should be more people with group A, for both of these reasons.

There are many different variants of O (all loss-of-function) indicating that this mutation has arisen many times in the human population. The prevalence of O is indeed taken as evidence of balancing selection. Various pathogens use the A or B antigens as receptors. The cited paper presents evidence about the phylogeny of the ABO gene in human populations and reports that there is clear evidence of balancing selection.

We propose several hypotheses for the cause of [balancing selection], which most likely involved interactions with multiple pathogens at different geographic regions and timescales.
Calafell et al (2008) Evolutionary dynamics of the human ABO gene. Human Genetics 124: 123-135


text:
Why do cockroaches burst from soapy water?
(careful, disturbing!)
I was experimenting with some stray cockroaches that ended up falling in my bath tub overnight (there is currently an infestation undergoing in my apartment building) and I found out that they are very easily killed by simply soaking them in soapy water.
I read that soap blocks some pores in insects' bodies which leads to suffocation, which appears to be the cause of death for my test cockroaches. But what I don't get is why about a half of them died with their innards bursting from their tail end. The water wasn't too hot to make them boil. Is it that they suffocate so hard that attempting to breathe they blow out their insides? Or is it the soap's reaction with the cockroach's bodily materials? Or is something else causing this?
I remember watching a documentary on injecting various insects with hydrogen peroxide which caused much more dramatic explosions, but it's not like I was injecting cockroaches, I just sprinkled them with soap water.

But they did fall inside the bath tub right?

As far as I am aware, cockroaches don't burst from being sprayed with soapy water (water + some liquid dish detergent). We previously had many cockroaches in our apartment (some came back after a year of nothing!), and we regularly sprayed the cockroaches with soapy water plus some vineger (more as a disinfectant/cleaner) and they never burst. We've killed at least 30 using this method.
Having said that, what you likely witnessed was the egg sacs dislodging from the back of the female cockroach. As you didn't mention what species of cockroach you were dealing with, I am assuming you had German cockroaches as they seem to be the most common type in non-tropical/hot areas.
According to a number of biology sites, German cockroaches are particularly difficult to control and eradicate is because they carry their egg sacs with them until they are ready to hatch. At which point they drop the sac.
If you are able to catch a few that seem especially big, you will notice that they have a sac at their back.
If you don't have German cockroaches, I have not idea why they would burst...

What you saw was simply female cockroaches expelling their many eggs as they approached death.
We have German cockroaches here in Australia. I am always astonished at how quickly they spread and equally how easy to is to kill them. While there are many poisons on the Australian market for spraying them, which generally work, often quite slowly, any water which is marginally hotter than what is comfortable to keep your hand in will kill a cockroach in a matter of 10 seconds. If cockroaches are silly enough to be around the kitchen sink, shower or any basin they are very quickly dead meat. Pouring boiling water on them would kill them in seconds.
Many insects will quickly die if exposed to hot water.
I don't like sprays because they indiscriminately kill all insects, good and bad. We have encouraged huntsman spiders in all of the houses we have lived, as they are excellent roaches and fly killers.
But short of flooding everywhere with hot water which isn't a useful plan in most instances, sticky roach baits, which are placed in strategic positions to attract and kill roaches, are the best way to kill (only) roaches over time. They ensure that the roaches get stuck in the bait, and lay their eggs in the bait, thus keeping roach reproduction down.

Cockroach abdomen burst out when it sinks in soapy water. A white color thing burst out from the body which are not eggs.They lay only one big egg which will be in brown color. Cockroach lack hemoglobin(red pigmentation) in their blood. White color busting out is actually blood. So even male cockroach burst out when it is in soapy water. May be due to some soap reactions with blood it burst i guess.

Can you add some references please?


text:
How does a person get AIDS?
I am inquisitive to know about how a person contracts AIDS.
Among the common masses it's still the belief that having sex with multiple partners causes the disease but that is not the case when read online that it can come only from persons carrying the virus.
So, if a person (male or female) is carrying the virus (HIV positive) does it mean that he/she is suffering from the disease or the person may be carrying the HIV disease and still be free from AIDS. If so how did this chain reaction of spreading the virus start?
Also is it true that immune systems of some rare people in this world can fight with this disease.

You read right: it can only come from people already infected through:

sexual contact
contact with an infected person's body fluids (blood transfusions), although not all fluids carry HIV (saliva, tears)
from mother to child (pregnancy, breast feeding)

Having unprotected sex with multiple partners statistically increases the risk of stumbling upon someone infected.
A person carrying the HIV virus may not show symptoms of AIDS, because the HIV infection passes through a stage of clinical and symptomatic latency (the asymptomatic HIV or chronic HIV) which can last up 20 years (average of 8 years) when only uncommon symptoms like fever and weight loss show up.
Where it started? It is believed that HIV originated in non-human primates in West-central Africa and were transferred to humans in the early 20th century. The virus adapted and became strong, because the virus from primates is typically suppressed by the human immune system within weeks of infection.
HIV is a retrovirus that primarily infects components of the human immune system such as CD4+ T cells, macrophages and dendritic cells. It directly and indirectly destroys CD4+ T cells.
So it destroys the cells reponsible of its removal from the human body. Hard to believe that there are people whose immune can really destroy the virus. A virus lives inside the cell it parasite, so the immune cells must destroy one the other. Also the virus infects and kills them (the good ones). However, as MattDMo suggested an infected person may take antiretroviral drugs and the disease progression can be slowed down.
Source: Wikipedia - HIV, AIDS

It is not entirely correct that a "person carrying the HIV virus is suffering from AIDS." HIV (Human Immunodeficiency Virus Type 1) is the virus that causes the disease known as AIDS (Acquired Immune Deficiency Syndrome). People can be carrying the virus and yet not displaying any of the symptoms of AIDS, at various timepoints from the point of infection, not just in the very beginning. It is much more scientifically/medically correct to refer to one's status as HIV-positive or HIV-negative, thanks to the amazing anti-viral drugs now on the market.

@MattDMo you should edit it to improve the se trusts you enough to give you editing privileges for that reason and your comment has +4

Also there are people who are immune to HIV due to a genetic difference. http://en.wikipedia.org/wiki/Stephen_Crohn

Being HIV+ and having AIDS are slightly different terminologies:
If the virus is detectable in an individual by existing medical techniques he/she is called HIV+.
A HIV+ person is said to have progressed to AIDS only when the CD4+ T-lymphocyte count drops below 200 cells per ml of blood.
Cornelius has nicely summarized the infection routes so I wont touch on that.

Also is it true that immune systems of some rare people in this world
  can fight with this disease.

Yes. In some people the progression from HIV+ to AIDS is very slow and they practically lead a normal life. Such individuals are called long term non progressors (LTNP). Some genetic reasons for having an LTNP phenotype is summarized in the link, however, this topic is still under active research.
Some individuals just don't acquire HIV. This is because they lack the CCR5 chemokine receptor which is essential for HIV entry into the cells. Deleting this receptor is also being considered to cure AIDS via a stem cell therapy.

Simple transplants wont work because the virus may infect the transplanted cells. In case of transplant from a CCR5-$\Delta$ individual there is a risk of immune complications such as GVHD. Transplanting CCR5-$\Delta$ HSC (either obtained from bone marrow or iPSC and then engineered) would be a solution but it is also quite difficult.

uh let me get you a link it does work i dont remember how though

http://en.wikipedia.org/wiki/Gero_H%C3%BCtter

Agreed it does work when you transplant a CCR5-$\Delta$ HSC to a patient but there may be risk of GVHD. Plus you may not find suitable donors every time.

what about if it is done by CRISPR as done by chinese scientist "https://www.bbc.com/news/world-asia-china-46368731"

Cornelius covers Primary Infection and some of Dissemination.
Wysiwyg covers some reasons when HIV cannot proceeds to AIDS.
Little however is discussed yet exactly about the Pathogenesis - how HIV proceeds into AIDS.
There are many stages:

Primary infection
Dissemination of virus to lymphoid organs
Latency
Increased HIV expression
Constitutional symptoms
AIDS
opportunistic diseases (etc pneumocystis pneumonia - P. jirovecii for human; HIV-induced thrombocytopenia; ...)
death

Cornelius nicely mentions that HIV infects CD4+ T lymphocytes, macrophages and dendritic cells.
In other words, HIV infects CD4+ T lymphocytes and the major Antigen Presenting Cells (APC).
Also monocytes are infected.
These infected cells play a major role in dissemination and pathogenesis of HIV infection.
Antigen presentation couples innate and adaptive immune system.
Any attack on those cells will be difficult to control:

where I left NK cells only to innate immunity because they do not participate in antigen presentation.
Innate and adaptive immune systems are visualised on the plane.
You have then humoral immunity working around that plane as circles.
I emphasize with that the local nature of humoral immune system and how it extends the cell-mediated immune system.
Any attack on the heart of this system i.e. antigen presentation will also risk the humoral immunity and thus cause fast progression of the disease.
These APCs act as reservoirs for HIV virus in the body during latent period and after the latent period.
However, there is very active replication of the virus also during the latent period in these reservoirs.
The virus replicates actively in lymphatic system.
This is why you see steady level of HIV virus in blood during first eight years, see Figure below [Fitzpatrick's Color Atlas and Synopsis of Clinical Dermatology, 7e > Section 27. Viral Diseases of Skin and Mucosa].

The structure of lymph nodes is disrupted eventually.
There is a degeneration and loss of virus holding function.
Virus leaks into the blood which can be seen as increased viral load at about 7-8 years after infection when constitutional symptoms start.
This amount of virus is very large that is released into circulation.
There is a rise in viremia.
Now the infection becomes T-tropic (proliferates and replicates actively on CD4+ T lymphocytes), while it was M-tropic (proliferates and replicates actively on APCs in lymphatic circulation) until the start of AIDS.
Actually, these APCs play a major role in trapping the virus, until their architecture changes.
Some antiviral drugs work on these CD4+ cells i.e. at least macrophages coupled with MHC II complexes.
There is still much unknown in the pathogenesis of HIV:

role of dendritic cells in M-tropic phase
role of dendritic cells in T-tropic phase and restricting the functioning of HAART (Highly Active Antiretroviral Therapy) therapy.

and there exist no antiretroviral drug which can target the major antigen presenting cells or use another way - to stop viral replication completely.
Cornelius writes HIV virus kills CD4+ cells.
It is better to say HIV virus decreases CD4+ cell count.
Killing is just one mechanism.
The mechanisms are

HIV can induce apoptosis of CD4+ cells
lysis of CD4+ cells
killing (natural killers, macrophages)
networks (CD4+ cells will bind to other CD4+ cells so cells cannot work)
gp120 antigenic - which attach to CD4+ antibodies

which decreases CD4+ cell count.
Sources

Thomas, C. F, et al. Pneumocystis Pneumonia. The New England Journal of Medicine. 2004.
Fitzpatrick's Color Atlas and Synopsis of Clinical Dermatology, 7e > Section 27. Viral Diseases of Skin and Mucosa.
My class notes 2014-2016.


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Biological meaning/interpretation of clustering coefficience
I have been looking for some time to find an answer to the following question. I would be grateful for any help/advice or directions.
I work very frequently with large number of proteins and assess their importance in a biological network. Traditionally there are two methods used to visualise proteins in a network and withdraw conclusions purely on network architecture bases, before one looks at the top hits in details using databases. One is degree and the other is clustering coefficience.
Degree refers to a node being connected to edges. The higher the degree, the more nodes are connected to a given node. Traditionally people interpret nodes with high degree as being biologically important, so called hubs. Since hubs are so highly connected it means that a failure of a biological hub has catastrophic consequences since the functions of many proteins are related/dependent on hubs.
However what confuses me is the biological meaning of clustering coefficient of a node in a given network. I’m aware that clustering coefficience refers to the tendency of a nodes neighbours to connect to each other; however, I was unsure as to what it means biologically and whether that means a node with a high clustering coefficience is more “important” than a node with low clustering coefficience. This just seems unlikely to me because hub proteins, are considered important proteins; however, hubs usually have low clustering coefficience but that doesn’t mean they are less important since they are highly connected (high degree). Therefore to put it in plain english, why do people use clustering coeffience in biological networks and what biological information is it providing them?
So I would appreciate any explanation/advice and references you could provide that would help me understand the biological meaning/interpretation of clustering coefficience.

First of all, I find this an interesting question.
In short:

Clustering coefficience is widely used
It is widely accepted that hub genes are more essential than poorly connected genes
but research is not always interested in the hub genes / proteins / molecules (for example most metabolic pathways involve water)

Answering your question, why people would want to use this kind of method:
If you would take a random model (pathway) most of the lines will be equally distributed between the nodes. This is not the case for most biological networks. Because of this, the global clustering coeffiecence can be used to see if a network could be biological. Clustering coeffiecence can also be used to find out about more specific nodes. For example if a protein has a relationship with two other proteins (binding, regulation, etc.), the two other proteins are also more likely to have a relationship with each other (similar to a social network).
References:
http://en.wikipedia.org/wiki/Clustering_coefficient
http://www.biomedcentral.com/1752-0509/6/34
http://www.pnas.org/content/99/12/7821.full.pdf+html

Yes, the part about clustering coefficient of a specific node answers my question! I also though perhaps a node with a high clustering co-efficient shows a somewhat redundancy of that node in a sub-cluster of a network since if its connection with its immediate neighbours is terminated, that nodes neighbours would still remain connected. Would that be a correct interpretation too? Many thanks for the references!

I think that depends on what the nodes represent. In the case of hub genes I don't think redundant is the correct word (as water is obviously necessary for metabolism).


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Why are hybrids infertile?
Let's take a quote from Wikipedia about zebroids.

Donkeys are closely related to zebras and both animals belong to the horse family. These zebra donkey hybrids are very rare. In South Africa, they occur where zebras and donkeys are found in proximity to each other. Like mules, however, they are generally genetically unable to breed, due to an odd number of chromosomes disrupting meiosis.

First, if I understand meiosis, the resulting cells don't actually end up with half the number of chromosomes, but closer to a full set of halves of chromosomes. How is the meiotic process disrupted?
Then,

A donkey has 62 chromosomes; the zebra has between 32 and 46 chromosomes.

Apparently this difference doesn't obstruct producing (infertile) offspring. How comes the process of recombination of such vastly different number of chromosomes in gametes is viable? What happens to chromosomes that don't find their 'pair'?
And then,

Horses have 64 chromosomes, while most zebroids end up with 54 chromosomes.

54 is an even number. How comes zebroids can't just normally produce fertile offspring with other zebroids of the same number of chromosomes?

A critical step in meiosis is the formation of tetrads. In diploid organisms like donkeys, they have a paternal version and a maternal version of each chromosome. Two chromosomes 2, for instance. During prophase 1, these two "matching" or homologous chromosomes form a tetrad and cross over, swapping alelles. There is no recombination and no tetrad formation in mitosis, which is used for growth and daily living.

How is the meiotic process disrupted?

In a hybrid, there are no matching maternal and paternal chromosomes. In the zebroid testes or ovary, a lonely donkey chromosome 2 is wandering around, looking for another donkey chromosome 2, and there isn't a homologous chromosome. This mucks up Prophase 1, and the first division pulls crazy numbers of chromosomes to each daughter cell, and the gametes from this division are likely full of extra chromosomes and missing some critical ones.

Apparently this difference doesn't obstruct producing (infertile) offspring. How comes the process of recombination of such vastly
  different number of chromosomes in gametes is viable?

An embryo needs a solid set of genes to grow up, but chromosomes don't have to be homologous for mitosis, and organisms use mitosis for growth and living, not meiosis. As long as the crazy mis-matched chromosomes in a zebroid have everything needed for a healthy organism, the hybrid will be healthy. It isn't until the zebroid starts to make gametes via meiosis that a problem occurs, as the homologues ONLY form tetrads in making eggs and sperm. The inability to recombine only occurs in the making of gametes.

54 is an even number. How comes zebroids can't just normally produce
  fertile offspring with other zebroids of the same number of
  chromosomes?

Because even chromosome number doesn't help if they are not each homologous with another chromosome.

I am a little bit out of practice but i researched the genetics of the horse tribe during the 1990s at the start of the Internet.
Male hybrids of the diverse equine species are all infertile.
However, a fairly large number of fertile female mules have been observed for over a century and much genetic research has been done to them, both in the West as in China. A few fertile female hinnies have also been proven.
With zebroids only one fertile mare, a zebra-horse mix, is known and sadly her remains as that of her foal have not been subjected to serious research.
That donkeys are closer related to zebras as horses is not generally accepted.
There exist three species of zebras -and possibly one recently extinct species, the Quagga- but all three species have interbred and at least a few of the female hybrids have produced foals, in the wild even!

Please reference your response!

If you think about the complexity of successful reproduction -- sperm recognizing egg, entering egg, the intricate choreography of cell division and differentiation -- it's staggering that any two individuals of the same species ever successfully interbreed, and it's obvious that enormous selective pressure is needed to maintain this perfect compatibility.  It's much less surprising that genetic drift would randomly lose one or more of the thousands of adaptations that are needed to guarantee compatibility.
So random drift is probably the reason for most genetic incompatibility, but in cases where closely-related species come into contact (whether through sympatric speciation or through changes in the range of one or both), there's also positive selection that will actively prevent cross-species interfertility. Hybrids are almost certainly going to be less well adapted to either parental niche than are purebreds, and so investing energy into developing hybrids is likely to be much less evolutionarily successful than putting the same energy into purebreds.


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Saliva test for Toxoplasma gondii?
I am trying to find some reliable gene kit by which you can rapidly test Toxoplasma gondii.
I am not sure if it exists.
I have an intuition that some tests done during 90s-00s on this species had high false negatives.
Which genes should you detect to find Toxoplasma gondii in a gene kit?

rRNA sequence would also be good.

All research on saliva tests I've found involve antibody detection which, as you suspected, can produce false negatives depending on the disease process or the presence of immune disfunction (such as due to AIDS). Thus, if you can isolate T. gondii gDNA from the saliva, a genetic assay may be more sensitive. However, Amato Neto et al. report:

In 26 patients with AIDS, including six with tomographical evidence suggesting cerebral abscess caused by Toxoplasma gondii, no parasites were found in the saliva by the use of the mouse inoculation model. This trial [suggests] that the search for Toxoplasma gondii in the saliva is not an alternative method for the diagnosis of toxoplasmosis in patients with AIDS.

So perhaps the most difficult aspect of generating a gene based saliva test is actually isolating the parasite from the saliva. I was unable to find other isolation attempts, but my research was very brief.
As for which genes to detect, studies involving human blood samples have found that PCR amplification of B1 paralogs provides a sensitive and selective method for detecting T. gondii. Burg et al found that there are about 35 copies of the B1 gene in T. gondii and also state that:

Because of its repetitive nature, the B1 gene is an attractive target for detecting T. gondii parasites through amplification of B1-specific DNA.

They were able to amplify and detect the gene from crude cell lysate as well as from purified DNA samples containing a 1:10 000 ratio of parasite to leukocyte. Furthermore, they could not detect the gene when assaying other organisms. Ho-Yen et al. later attempted PCR amplification of the same genes in human blood from patients with suspected toxoplasmosis and found that:

PCR can be reliably used on human blood samples. For a reference laboratory, this is a valuable addition to its array of diagnostic tests, and provides a more rapid assay than animal culture.

Jones et al. compared detection of the B1 genes with P30 and 18S rRNA genes in aqueous humour. They were able to detect 50 fg of gDNA using the B1 assay, which is equivalent to a single parasite. They concluded that:

The B1 PCR protocol appears to be the most sensitive protocol in the detection of T. gondii DNA and has been successful in identification of T. gondii DNA in ocular fluids and retinal sections.

Good and clear meta-analysis about the current situation for the saliva test of Toxoplasma gondii!


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Identifying internal structures of dissected fish
Note : Images displayed below might be disturbing to some people.
I have dissected a fish for the first time ! I have some idea of what some of the structures might be but I am not sure and so would like your help.
1.Here is the fish I dissected. Are the white structures (towards the dorsal surface) muscles ? They are beautifully arranged.

2.I want to know what the yellow coloured structure (towards the ventral side) is. I guess it's the intestine. It looks "noodly". Here is a close up.

3.I have pointed at two different parts in the following images. I want to know whether they are part of the same structure - ie swim bladder or whether they are two different structures altogether. When I poked one of the parts the other part increased in size ,so I guess it's one structure but I just wanna make sure.

Since I can't actually look at and handle the yellow structures, it is difficult for me to provide any information on them.

As far as the white structures you mention on the first picture, I believe those are most likely muscles.
As for your third question. That does appear to be all one structure; and yes, going on that assumption, the entire structure would be the swim bladder.

Thanks! You can see the white structure very well in the second picture. I am pretty sure the yellow stuff isn't fat. I am actually confused between calling it intestine or pyloric seca.

A swim bladder in two parts is a common thing. At least I remember having seen at least in some of the few fish dissection I've made.


text:
What type of insect is this?
ery bug 1]1
What insect are these? Found them indoors. No wings, just crawling on the walls.

Where was the photo taken (geographically), at what time of the year, and how large are they (can you include a scale bar in the photo)? All will be useful for answering this question.

Looks like a termite; male; after loss of wings.

This answer could be improved by explaining why you think so - for example find a picture of a male termite with its wings and explain what body parts you compare with the insect in the photo to reach that conclusion.

Thick waist, straight antennae, head position are all consistent with a male termite.

Edit your answer to include that and provide a reference or picture for the question author to check up themselves and I would say this is a perfectly sufficient answer :)


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Identifying internal structure of dissected prawn
Note: Some of the images might be disturbing.
I have dissected prawn for the first time. Would like your help in identifying some structures
.

This is the dissection of the posterior part of the prawn. What is this blackish structure in the middle ? This structure becomes whitish farther down. Then, it forms a small sac like structure and then becomes thin again. This whole structure appeared just after I cut the exoskeleton. It is directly above the muscles.

I think that this is it's alimentary canal and the black area has digested food in it. The sac like structure might be the rectum.

It is, indeed, the alimentary canal. It is actually this canal that it's important for one to remove when "de-veining" shrimp, rather than the vein itself, which lies immediately dorsal to the digestive tract.

In the future, I might suggest doing a little more research prior to asking the stack exchange, as frequent users of the site do like to see evidence of effort on the part of the user to find their own answers. A quick search for "alimentary canal prawn" or "arthropod anatomy" would likely have turned up your answer.


text:
Any forms of pneumonia that can be caught?
I am aware of the fact that there are several different types of pneumonia.

However, I am wondering if any of these types of pneumonia are contagious from person to person.
Is this possible?

Pneumonia caused by bacteria or viruses is contagious.

@canadianer Thanks, I would appreciate a longer answer, but that does answer my question:)

Please refer to the "How contagious are different types of pneumonia" part in this article. Hope that clears your question.

Pneumonia means inflammation of lungs- especially alveoli.
There can be many causes of it including infectious agents, autoimmune condition and  chemical irritants. Pneumonitis is a more accurate word for lung inflammation, the causes of which includes the abovementioned agents; Pneumonia in common usage refers to the condition due to infectious agents such as bacteria, viruses and fungi.
In almost all the cases the infectious agents are airborne in the form of aerosols (spread by cough) and infect the respiratory tract directly. Some cases of fungal pneumonia (Pneumocystis, Penicillium) are observed more commonly in immunocompromised individuals, such as AIDS patients, and dissemination happens via spores.
As you can intuitively figure out the infectivity is different for different pathogens.


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Identifying structures from anterior end of dissected prawn
Note: This image might be disturbing.
I want to know what the red and the black structures (directly posterior to the red structure) are. I guess it's the heart.

are you sure about the antero-posterior axis in this picture ?
BTW, The image is not that disturbing but i think it is not a very good dissection :P

I guess you got your antero-posterior axis wrong. If I am correct then anterior is right and posterior is left in your image. In that case the black structure should be the cerebral ganglion and the red should be the heart. See the image below.

Aren't eyes of a prawn located at the anterior end ? If so, the red is towards the anterior end and the black towards the posterior. (I am not talking about the two black structures ie eyes. I am taking about the "black" to the left of the heart in the picture which would be posterior to the heart in prawns.

eyes are in the anterior but i cant see the eyes in your picture

see this picture. this is another species of shrimp but you can clearly see eyes anterior to the cerebral ganglion. also it seems that you have dissected on the ventral surface; eyes are present on the dorsal surface.

I have dissected the dorsal surface and the 2 black structures are definitely eyes.

No.. The two dark things in the right of this pictures are the eyes/

Sorry for the bad dissection + bad orientation of the photo.

let us continue this discussion in chat


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Polarized epithelium and localization of ion channels
I'm trying to learn more about polarized epithelial cells of the gut. I am familiar with classic brush border transporters localized to the apical memebrane to facilitate nutrient absorption. I am wondering though, where are ion channels located? I would guess basolaterally since they would be exposed to the extracellular space. I would appreciate a primary reference showing the location of voltage-gated channels in particular as I could not find them myself.

Well, that's a first for me. I wouldn't have guessed gut cells would have voltage-gated channels.
This article describes voltage-gated sodium channels on both the luminal and basolateral membranes:
Barshack, I., Levite, M., Lang, A., Fudim, E., Picard, O., Ben Horin, S., & Chowers, Y. (2008). Functional voltage-gated sodium channels are expressed in human intestinal epithelial cells. Digestion, 77(2), 108-117.
http://www.ncbi.nlm.nih.gov/pubmed/18391489

Thanks for the suggested article. I'm not able to get it through my institution, do you have a copy, or can you quote the relevant results?

Check your email, Leonardo.


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About stem cells and Cancer
Do stem cells have an apoptosis mechanism and , if they do could this be used to repair the  cell self-destruction pathways in a cancer cell?

No but they can be used as part of a gene therapy to induce cellular death in cancer.
TRAIL-secreting mesenchymal stem cells promote apoptosis in heat-shock-treated liver cancer cells and inhibit tumor growth in nude mice

Liver cancer is one of the top six leading causes of cancer-related death. Radiofrequency ablation (RFA) is an important means of treating liver cancer. Residual cancer after RFA is the most frequent cause of recurrence in cases of liver cancer. The main difference between residual cancer cells and ordinary liver cancer cells is that residual cancer cells experience heat shock. The secretable form of trimeric human tumor necrosis factor-related apoptosis-inducing ligand (stTRAIL) induces apoptosis in a variety of human cancers but not in normal tissues. It has shown potent cancer-selective killing activity and has drawn considerable attention as a possible cancer therapy. In the present work, the therapeutic potential of this stTRAIL-based gene therapy was evaluated in hepatocellular carcinoma subjected to RFA. Rat bone marrow mesenchymal stem cells (BM-MSCs) were isolated and transduced with a lentiviral vector encoding stTRAIL (stTRAIL-MSCs, T-MSCs). Cells treated with heat treatment at 43 °C for 45 min served as simulated residual cancer cells. After treatment with T-MSCs, apoptosis in heat-shock-treated liver cancer cells increased significantly, and caspase-3 was upregulated. When T-MSCs were subcutaneously injected into nude mice, they localized to the tumors and inhibited tumor growth, significantly increasing survival. Collectively, the results of the present study indicate that BM-MSC can provide a steady source of stTRAIL and may be suitable for use in the prevention of the recurrence of hepatocellular carcinoma after RFA with secretable trimeric TRAIL.

If cancer cells are susceptible to heat-shock  but normal cells are not ( if I'm correct) does this mean cancer cells exist on the 'fringe' of cellular stability? If a certain disease or virus attacked liver cells would it affect any cancerous liver cells first?

@user128932 yes cancer cells before they are exposed and adapt to treatments are very unstable. Chemotherapy exploits this.

If one used beams of microwaves that intersect at a point where a tumor is so the intersection point is very hot yet all the other part of the beams that don't intersect are not hot ; could this destabilize the tumor without hurting surrounding cells ?

@user128932 i'm sorry i dont know...i'm not really a fan of any radiation as a treatment and haven't studied it my focus is chems.

The point of narrow beams of microwaves that intersect at a tumor would be to reduce non-tumor cell death and decrease side effects.