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How does an axon "know" it's not connecting to its own neuron?
I recently read about an experiment where they removed the dendrites and axons from rat neurons and placed them on a grid. After a while they started reconnecting and were able to learn things.
Since I'm trying to create a model simulating this, I'd like to know (as much as is needed to make it look at least a little bit realistic) how they reconnected. As far as I know some molecules are secreted attracting or repelling axon growth cones.
I think I can model that part, but the problem is that the axons can easily grow back to where they came from, so how do the axons in a brain 'know' they are not growing back to the neuron they originated from.

Grid is a 2D thing. I think this is a probabilistic problem. Brain is 3D thing. Probability is less there for the reconnection of axons.

Can you give us citations on the study you mentioned?

@Memming http://neural.bme.ufl.edu/page13/assets/NeuroFlght2.pdf, http://edition.cnn.com/2004/TECH/11/02/brain.dish/

@Lennart_96 that study was done with dissociated cortical culture; they formed random connections. (I happened to work with both authors, and did some modeling study myself, but not on the neurodevelopment side.)

@Memming Wow, that's pretty awesome. Do you mean by random that the axons just started growing in all directions or that there is no possible way to predict which neurons will connect?

@Lennart_96 I'm not a particular expert on neurodevelopment, but it seemed to me that they pretty much grew in many random directions. There were no extracellular matrix or chemicals that would give an overall structural guide to the neurons (though there were glia multiplying simultaneously).

If I understand correctly, based on neural simulation papers, sometimes neurons do connect to themselves, and this is supposedly an important type of connection. I'm not an expert as of yet so you should of course double check this.

I think I can partially answer you question. As far as I'm aware, there are many surface receptor molecules such as ephrins that are responsible for axonal guidance and dendritic repulsion in developing organisms such as flies (Drosophila). As you can tell this is extremely crucial since its important for neurons to spread their dendrites and axons as far as possible, evenly spaced out with axons bifurcating (separating) correctly and not sticking together. This is for example important in the Drosophila brain for axonal projections into different lobes.
One such surface receptor, which helps achieving the above is Dscam (Down syndrome cell adhesion molecule) (schmucker et al 2000 Cell). Dscam gene is expressed in over 38000 isoforms (through complex alternative splicing of Dscam mRNA) in flies. It is the homophilic binding and subsequent repulsion of Dscam protein isoforms that enables an intrinsic self-recognition for repulsion of same-cell axon. As far as I understand it, if a number of similar Dscam isoforms are present on axons or dendrites of a neuron, this is self recognised and the dendrites and axons get repelled from one another. This is the molecular pathway that ensures sister dendrites are not adhered together or become concentrated in one area.
In the absence of Dscam or when Dscam protein isoform diversity is removed flies die during larval stages and the early embryonic axonal patterning of the fly nervous system is clearly disrupted. In the absence of Dscam protein, Bolwig's axons exhibit frequent axon pathfinding errors at a specific intermediate target. Most of these processes are conserved in mammals.
For further information please look at Schmucker & chen, 2009 Genes and Dev

In cases of severe head injury where a large portion of neurons and their connections get shredded. I don't think a neuron would be very choosy  when presented with quite a few axons and lots of intracellular fluid
There are coup and the contra coup (p silent) brain injuries that occur because the brain bounces back and forth in the skull. The contra coup, other side contusion (bruise) is usually worse. A lot of axonal injury occurs in the brain stem and since the basics of life (breathing centers) a severe injury to the brain stem can cause not surviving the injury.
Probably speed of healing I is the priority. I forgot which journal it was in but those with a college education were 60% more likely to have a good recovery while those with just a high school diploma have only 10-20% chance of having a good recovery. It's a similar ranking when it comes to neuronal connections.
Thank you for answering my curiosities on how indeed does one heal from Diffuse Axonal Injury (DAI) on a molecular basis. I was a 1sr yr. radiology resident when I had a severe TBI or Traumatic Brain Injury. TBI is the fancy way of saying brain damaged. But now we know victims of severe head injury can recover and even grow new neurons until old age.

nice answer!  some references would really help tho ;)


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What's a replicate line?
The methods section inside a paper I'm reading make mention of replicate lines.
Example: "We founded 10 replicate lines from a single clone". This is in the context of experimental evolution and artificial selection of Chlamydomonas in a laboratory.
Can you please explain to me what a replicate line is?
Here's a reference to the paper:
Collins, S., Sültemeyer, D., & Bell, G. (2006). Rewinding the tape: selection of algae adapted to high $CO_2$ at current and Pleistocene levels of $CO_2$. Evolution 60, 7, 1392-401. DOI: 10.1111/j.0014-3820.2006.tb01218.x

It would certainly be easier to answer if we had a link to this article.

Or even a mention of what experiment they did, some context around the quote, anything really. Please [edit] your question to add more information, in the meantime I am voting to close as unclear.

Good point. I added a reference, and some clarification of the context.

In the context of experimental evolution, replicate lines are simply separate experimental (or control) lines the are established from the founder population at the beginning of the experiment. In this paper, the authors must have established 10 separate experimental lines that then evolved in different carbon dioxide levels. For example, 10 separate aliquots of algae are drawn from the same source population and then separately subjected to the agent of selection. These replicate lines should remain separate and not be mixed or crossed.
Replicate lines are useful in experimental evolution for a few reasons. Because you are studying a population that is experiencing a selection pressure, you expect that genetic changes are in response to that pressure. However, changes can also occur due to drift. Replicate lines (and a consistent response to selection among them) is important to ensure that changes are a response to selection rather than to some other force (drift, mutation). Some drift is bound to happen when the lines are founded, because you are selecting a subset of the population, which is actually a good thing. Each line gets a random subset of genes which then evolve together. This potentially allows discovery of different genetic pathways to the same adaptive response.
The background and lots of examples are in Garland and Rose, Experimental Evolution (UC Press, 2009).

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Will sperm cells exhibit chemotaxis towards sucrose?
I was wondering if sperm cells will exhibit chemotaxis towards sucrose? One of my friends told me that sperm cells die in presence of salts. So I guess sperms will move away from salt. Can someone give me any reference related to this area.

UPDATE (Answer for why sucrose?):
So I should have made things more clear. I was thinking to do an experiment by taking some sperm cells and its effects on sugar and salt and then to see it under a foldscope microscope. Since I am not a biologist, I wanted some guidance. The common available substances which came to my mind was sugar and salt.

If you google "sperm chemotaxis sucrose" you learn some things of interest. Notably, wikipedia's article on sperm chemotaxis indicates that the important chemoattractants for sperm (the things that attract sperm via chemotaxis) are various signaling molecules given off the by the egg.
It is not clear why you would necessarily think that sucrose would attract sperm or that salt would repel them. In the first case (sucrose), it is not obvious why sperm would expect to see sucrose. If I remember correctly, sucrose is actually pretty rare in animal physiology except as an energy source in plants that animals eat; and sucrose is largely broken down into monosaccharides before it even leaves the small intestine, so it's not like it's circulating in the body. For instance, a lab protocol for studying animal sperm chemotaxis suggests adding sucrose as a densifying agent that doesn't interfere with chemotaxis, suggesting that sperm are pretty independent of sucrose. In the second case (salt), it is not obvious that sperm would necessarily avoid the things that kill them. Those things may be correlated with doing their job! Most sperm cells are expected to die in the human reproductive strategy.
In plain terms: there are huge numbers of sperm which are competing really hard with each other to find and fertilize an egg, not to find sucrose or to avoid salt. The chemotaxis that sperm exhibit will tend to help them accomplish this goal. So it seems (according to wikipedia) that they follow the signals that say 'egg', not the ones that say 'sugar'.
Update:
Sorry, only just saw update on Q. Thanks for the clarification- sounds like fun! I've been curious about the foldscopes.
If what you want is to do an experiment, then I think you've actually got a great start with knowing first that salt interferes with their motility. That is a control experiment, e.g. the very first thing you should do, to make sure that the world works the way other people say it should. (First rule of experimental science: never trust anyone!). Look up a protocol which suggests a sperm-inhibitory concentration of salt (ideally kosher salt, not table salt which has a bunch of other stuff like iodine in it). Put sperm in that concentration of salt and then also in a medium where they should show chemotaxis (the protocol I linked to could be helpful here). See if you can reproduce the salt inhibition, ideally in a medium that is otherwise identical to the medium that allows chemotaxis.
Next, try other stuff. Unfortunately, chemoattractants are probably proteins/small molecules you can't buy at the supermarket. But you could try to get creative. I can't ethically recommend that you try to find a human source, because that gets weird pretty quick, though it is the obvious suggestion (I assume you are talking about human sperm). Potentially there is an animal source for such things which isn't too expensive.
However, you could say to hell with chemoattractants and chemotaxis, and try to just understand sperm motility. You could try other osmotic shocks, with simple cheap chemicals like glycine. It looks like there is some literature that calcium ions affect sperm motility. Or you could play with pH, using vinegar or lye, or temperature. I bet that all of those affect sperm motility (probably for the worse). Or you could try the effects of various weird hippie herbs from the health food store. It sounds like you are just looking for an easy, fun experiment, and if that's your goal then I suggest you try a bunch of things and see what happens. That way you're more likely to find something interesting.
If what you want is a more elaborate experiment, then I think it is worth your time to sit down and try to read up on how sperm work, and then design an experiment that really clearly tests a hypothesis. I am not an expert here, but the Yoshida article I link to looks like it has a good literature review.
Hope that helps.

Please see the update for why sucrose?

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Why majority of synthesized mRNAs are halted at Nuclear Pore Complex?
I was reading about mRNA export process. I came to know that only 36% of synthesized mRNA transport events at Nuclear Pore Complexes(NPC) of the nuclear membrane get successful in crossing to the cytoplasm. I have heard that transcription machinery is a highly accurate one and so why would NPCs want to regulate mRNA transport like this?

Is NPC acting as a quality checker? Are there any errors mRNAs facing in between the transcription and meeting NPCs? (Please share related literature, if you find some.)
Any other hypothesis someone would want to share?

I think this is so specific that you might want to consider contacting the authors directly, they've probably been thinking about this since their paper in 2013 found the same fraction of mRNAs unable to cross the NPC

One thought, upon re-reading. It says 36% of events are successful. This doesn't mean that 64% of mRNPs never cross, it just means that out of every 100 attempts to cross, 36% are sucessful. Perhaps most of the 64% that failed simply try again later and succeed?

@Thymine my bad. Should I delete the question?

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What is the biological relevance of RIPPLE phase in membranes?
I was reading about ripple phase in bilayer lipid membranes which is described here as a meta-stable state between lamellar tilted crystalline and lamellar fluid state. It is also known that ripple phase exists just below the phase transition temperature $T_m$. The figure below is from this article.

I have 2 questions here:
1) Is ripple phase a stationary structure or does it propagate in space as a travelling wave? (Since they have crystalline structures inbuilt will the fluidy defect propagate?)
2) Secondly and more importantly will ripple phase gets exhibited above transition temperature $T_m$ if the lipid interacts with some molecules like protein etc?
UPDATED QUESTION:
What can be the possible biological significance of Ripple phase in membranes? Will formation of ripple in membrane initiate any relevant processes, since membrane curvature itself is changing? I will be really helpful for any resources related to this.
I am citing an experimental biological work related to Hsp12 protein interaction with DMPG membrane in yeast which reports ripple phenomenon well above the usual transition temperature. Paper here.

NOTE: I was initially confused about whether to post this in biology.SE or physics.SE. I got more tags here. So posting it here.

Mmmm odd. Anyway, this post is indeed Bio, physics and also chemistry related. What I would do is go to the respective sites, enter their chat and ask if it's on topic there. Cross posting is not OK, so I'd reckon if Physics accepts it, I can either migrate or you can repost and delete it here. Physical might be your best bet, but Chemistry might as well.

@AliceD I have modified the question a little bit and given a bounty. Do you want to have a look now?

@dexterdev Halo dexterdev. I am very interested in this question and cant find any answers online. Please contact me if found out the answer.

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Can an infectious diseases come from a plant?
Coronavirus, HIV, 1918 Flu, etc. They all come from animals. Do any infectious diseases (in humans) come from plants? More specifically, are there viruses that infect plants that can mutate to infect humans?

Could you please clarify your question. Are you asking whether plants can be vectors for infectious agents such as E. coli O103, which only infects animals, or are you asking whether there are viruses that infect plants which can mutate and infect humans?

Edited question. The second part: are there viruses that infect plants which can mutate and infect humans?

Thank you for your clarification. It seem that my interpretation of the question was the correct one.

Question

“Are there viruses that infect plants that can mutate to infect
  humans?”

Answer
None appear to have been reported so far. It is difficult to provide supporting evidence for an assertion that they do not exist, but a recent review on the relationship between plant and animal viromes does not include any examples, and our general understanding of the mechanisms by which viruses infect organisms and cells suggest that this is unlikely. There are, however, examples of plant viruses replicating in the insect vectors that transmit them.
Evidence
In 2011 Dolja and Koonin of the NIH published a review in Current Opinion in Virology 1 322-331 entitled Common origins and host-dependent diversity of plant and animal viromes. In this they considered:

“…three distinct scenarios for the origin of related viruses of plants
  and animals: i) evolution from a common ancestral virus predating the
  divergence of plants and animals; ii) horizontal transfer of viruses,
  for example, through insect vectors; iii) parallel origin from related
  genetic elements.”

The very fact that there was a need to argue for a relationship indicates the assumed distinction between animal and plant viruses, and indeed they write:

“…plants are not known to support reproduction of dsDNA viruses and
  retroviruses.”

The only reference in the whole article to an actual biological relationship between animal and plant viruses is the following:

“Strikingly, viruses of the order Mononegavirales and the family
  Bunyaviridae… can also reproduce in their arthropod vectors.”

The paper referenced in support of this statement is by Hogenhout et al. and was published in the Annual Review of Phytophathology (2008) 46 327–359, and is entitled Insect Vector Interactions with Persistently Transmitted Viruses. From this it emerges that there is a class of plant viruses called persistent propogative viruses which replicate in the circulation of their insect vectors, in contrast to most types of circulative viruses. The insects involved include the leafhopper (illustrated below in Fig 1 from that review) and the thrip.

Schematic representation of persistent virus transmission by a leafhopper. Viruses that are transmitted in a circulative persistent manner do not replicate in the insect and usually enter the salivary glands from the hemolymph. In plants, replication of circulative viruses is frequently restricted to the phloem tissues. In contrast, most propagative viruses replicate in several plant tissues and in different organs of the insect vectors ( yellow arrows) and may enter the salivary glands either from the hemolymph or from other connecting tissues, e.g., the nervous system or trachea.
It is not clear to me whether the virus is in any way detremental to the insect vector — certainly it is not the primary target of the virus, and replication can be regarded as allowing it to survive longer before the insect transmits it to the plant.
Today insects, tomorrow people?
The very fact that persistent propogative insect viruses can replicate in their animal vectors raises the question whether the insects could somehow transmit them to human beings. In an answer to a different question on whether insect pathogens can infect humans I have argued that the absence of examples in situations where people come into close contact with insects and the  difference in anatomy and molecular structure of cell membranes makes this unlikely. In the present case we are not even talking about an insect pathogen, but a plant pathogen.

This is a great biological question! I'm glad we encourage such questions from curious people who want to learn more about modern biology.
Much as other animals can be vectors for diseases that infect humans, plants can be vectors for pathogenic infectious agents.
You may occasionally read news stories of disease-causing strains of Escherichia coli which contaminate vegetables and force product recalls. There is currently a CDC advisory to not eat clover sprouts, as an example, because of contamination with E. coli O103, a strain which can cause a variety of health problems (including kidney damage, in severe cases).
This kind of contamination is becoming more common, largely as a consequence of how we produce food:

Fresh fruits and vegetables once were thought to be relatively free of disease-producing pathogens. In recent years, however, outbreaks of foodborne illness linked to fruits and vegetables have become more common. These outbreaks come from produce grown both in the United States and in other countries. Outbreaks have been linked to Escherichia coli O157:H7 and Salmonella on apples, lettuce, cantaloupe and sprouts; Listeria monocytogenes on cabbage and cantaloupe; Shigella on parsley and lettuce; and Cyclospora on imported raspberries.
Changes in microorganisms have undoubtedly contributed to this increase, as have changes in growing, harvesting, distribution, processing and consumption practices. Listeria monocytogenes, Clostridium botulinum and Bacillus cereus are naturally present in some soils. Their presence on fresh produce is not uncommon. Salmonella, E. coli O157:H7, Campylobacter jejuni, Vibrio cholerae, parasites and viruses can contaminate produce through raw or improperly composted manure, irrigation water containing untreated sewage or manure, and contaminated wash water. Contact with mammals, reptiles, fowl, insects and unpasteurized animal products are other sources of contamination.

Wash your fruits and veggies!


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How to isolate host cell RNA (tRNA,mRNA,rRNA) from viral RNA?
A retrovirus with RNA genome infected a host cell. You would like to isolate the host cell’s RNA (rRNA, tRNA, and mRNA) from the virus RNA. What properties can you rely on to determine the three types of host cell RNA- for example, in terms of their size, complexity, GC content, or abundance in the cell? The undetermined RNA can be identified as the virus RNA.

This is a homework question, right?

@Chris I am a Bioengineering student preparing a presentation for the next lecture, so it kinda is a homework.

So what's your idea of solcing this problem?

Here in Germany we are at the beginning of the 2. semester and up until now what i can think of is using radioactive Uracil, but that would only 'seperate' the DNA from all RNA. Another idea would be using Polymerase-Chain-Reaction.

Does this question assume an unknown virus? So you're separating the RNA so that you can sequence and identify the virus?

@user137 no just a arbitrary retrovirus. But the question was how to seperate the Virus RNA from the hosts cell RNA? so you dont need to specify what kind of virus it is .

@Sam Well if you know the virus and know its gene sequence, you might be able to use RT-PCR to get DNA copies of its RNA. I can't think of a way to take total RNA from a cell and physically separate host RNA from viral RNA.

Thermo Fisher has a protocol for the separation of host mammalian RNA from prokaryotic RNA, optimized for E. coli vs human, mouse or rat sequences. Capture oligonucleotides bind portions of the mammalian RNA and hybridize. These hybridized oligo/RNA are then removed from solution via "oligonucleotide-derivatized magnetic beads," after which the remaining RNA assumed to be from whatever prokaryote can be precipitated out w/ ethanol. If you know enough about your virus and your host, I don't see why a similar assay can't be created. Otherwise, Thermo Fisher has additional links to RNA isolation protocol.. most of the viral assays, however, utilize serum, plasma, etc. because host DNA/RNA will elute along with the viral RNA if they're present, as in samples containing cells.

Retrovirus is not prokaryotic; so that kit may not work. But the the principle is, as you mentioned, the same: adsorb oligos that will bind specifically to viral RNA on beads and remove the viral RNA. Modified oligos such as LNA can be used for a stronger binding and longer life.

Right, i was thinking more of a modified assay based on the same principles.


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Why does my anti-ubiquitin antibody visualization not work on my PAGE gel?
I am using 2D gel electrophoresis to visualize polyubiquitinated proteins. However, while I can see actin and heat shock protein using when appropriate antibodies, I cannot visualize them using anti-ubiquitin antibody. Could it be degradation problem?
I run isoelectric focusing at 200 V overnight (at least 18 hours) and 700 V the last 30 minutes. I am worried that I am applying more volts than needed, because the standard protocol is 200 V for 20 minutes, 450 V for 15 minutes, 750 V for 15 minutes, 2000 V for 30 minutes, but due to problems with the power unit I cannot do this.
I am sure I have polyubiquitination because I use a drug that triggers polyubiquitinated protein accumulation inside the cells.
I would like to add also that cells are collected by scraping in cold PBS and then they are placed in ice and the pellet is also collected at 4 degrees to prevent protein degradation.

Do you have protease inhibitors in your lysis buffer? If so, which ones? Also, does your anti-ubiquitin antibody work when doing a straight SDS-PAGE Western blot?

MattDMo, My anti-ubiquitin antibody works doing Western blot.

MattDMo, My anti-ubiquitin antibody works doing Western blot, but I don't use lysis buffer, after collect my cells by scraping using PBS I centrifuge the eppendorf and I freeze the dry pellet (withouth PBS) in liquid nitrogen, then I resuspend the pellet directly in rehydration buffer (urea, CHAPS, ampholytes, bromophenol blue, DTT) and I add Urea and vortex until I see a litle urea precipitates at the bottom, then I centrifugate it at 10.000 rpm 5 min and I use directly the supernadant to rehydrate my strips.

Do you have a positive control you could use next to your samples?

That is what I am looking for, I am trying to show that is possible to distingue polyubiquitination from negative control, but I have never done this before, so I don`t have anything to compare as a positive control, if so, that would mean that finally the procedure works and the spots appears.

@Biomedi when addressing a comment to someone, please put an @ symbol before their username so they can be notified.

There are stable ubiquitinated proteins in mammalian cell lysates even if active proteosomes exist in cells.
First, you might want to make sure that the antibody is applicable to WB.
Then, you would ask if your WB system using the antibody works. You could optimize the condition using just 1D SDS-PAGE followed by WB.
For the condition for isoelectric focusing, when focusing is completed, you get very high electric resistance, so you might want to monitor current after you change the voltage to 700 V. Current decreases gradually, and get stable at some level. But I do not know you can see stabilization by 700 V.
You also might want to check if major proteins such as actin form spots nicely at the expected pI. That could tell if forcusing is completed roughly.

Yes, the antibody is applicable to WB because I have used it before. I use a kind of homemade circuit connecting my system to electrodes that are connected to a water recipient, so the current I think is ok. The proteosome is alterated by the drug I use, so the proteins are accumulated  in the cells. So if I put more time that the procol say, it could be that a problem because polyubiquitinated protein could be more sensitive to be destroyed or some reason?

Urea is strong denaturing effects, so you would not have protease activities in the rehydration buffer. I am not sure about proteasome activities during freeze-dry process. Maybe ok, but no guarantee. Can you directly add the rehydration buffer to cell pellets? Or you can add acetone or 10%TCA to precipitate proteins so that proteases are immediately denatured and inactivated, and proteins you are interested in can be protected from degradation.


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Are there any auto-immune diseases caused by T cells not detaching from antigen presenting cells (APCs)?
By not detaching I'm referring to after they have formed an immunological synapse, if they don't ever detach.


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Conjugated deoxyribonucleotides
I'm currently learning about using PCR techniques to make fluorescently labelled DNA probes, and the textbook mentions "conjugated deoxyribonucleotides"
Can someone explain what these are? Nothing too in-depth and detailed. Just a decent description/explanation so I can get somewhat of an understanding.

To "conjugate" means to join or couple something together. Deoxyribonucleotides are the "letters" of DNA - A, T, C, and G. In biology/biochemistry, when you conjugate something you chemically modify it by adding something to it. Given the context of your question, the conjugated deoxyribonucleotides are fluorescently-labeled — a fluorescent dye has been covalently attached to it.


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What kind of larvae are these?
My uncle was helping us spray the garage for ants, and he stumbled across a huge batch of some type of larvae. According to him...

"It looked like a long, narrow clump of mud. When I broke it open, all of these larvae fell out. Whatever bugs were inside scattered pretty quickly!"

Geography: We're in Los Angeles, CA (southwestern USA)
Season: It's late summer here (early September)

Exhibit A: The pile of larvae...

Exhibit B: A similar husk of "mud" found in our garage. When it was shattered, nothing fell out...

My uncle thinks it's termites... I'm certainly hoping it isn't.

Not a bug guy, but it does look like termites.

Sorry, but its termite larvae.

I think that it is termites larvae. For more info check this :  Termites follow the typical life cycle of insects that have a gradual life cycle: they begin as eggs, and then enter nymphal to adult stages. In termite development, newly hatched termites are sometimes referred to as “larvae,” which is not to be confused with the larvae of complete metamorphosis insects like flies.
Termite larvae typically hatch within a few weeks. They are approximately the same size as the eggs from which they hatched and are immediately tended to by worker termites. They often comprise a large part of a termite colony.
Similar to other insect young, termite larvae go through a series of molts, during which they shed their skins. From the larval stage, termite larvae may evolve into other members of the colony’s castes.
If you suspect you have termite activity in or near your home, contact a pest control professional. Termite damage can go undetected and result in significant financial loss from their damage. A termite inspector can inspect a home for signs of activity and conditions that are attractive to termites. They also can offer services to treat and protect the home from potential future damage.

Bummer... certainly not what I wanted to hear, but seems to be the consensus. Thanks!

UPDATE: Inspector came today and said "yep, you've got subterranean termites"... so it's officially official.


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Why do we add salt when precipitating DNA?
All the DNA extraction protocols I have seen involve adding salts to the extraction buffer. What is the purpose of the salts? What happens if they aren't included?

The role of the salt is to neutralize the charge of the DNA's sugar phosphate backbone.  This makes the DNA less hydrophilic (less soluble in water).
Ethanol has a lower dielectric constant than water so it's used to promote ionic bonds between the Na+ (from the salt) and the PO3- (from the DNA backbone) causing the DNA to precipitate.

since precipitation is one of the methods to purify biomolecules, which separate them from the other components in the solution.


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Can fat cells get into muscle cells?
I heard a prof. saying that when people are getting older that there aren't only fat cells getting between and around muscle cells, so that humans gets weaker and weaker, but also that fat cells can get into muscle cells.
Is this true, and how is this done?

Fat in muscle cells or fat cells in muscle cells? The latter seems unlikely.

She talked about cells

I might double-check with your professor about what exactly she said. Fat accumulating in muscle cells is something that happens, but fat cells entering muscle cells seems pretty far-fetched.

I got her answer, and indeed she meant droplets of fat. So by this my question is answered


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how to make plasma cells adhere to the bottom of a microplate?
I am isolating single plasma cells by FACS sorting into 384-well plates, with the intent to assay the supernatant and clone H/L chains from positive wells. The efficiency of the PCR is however low, because the medium must be removed, yet many plasma cells get sucked up during medium removal. Is there any way to make plasma cells adhere to the bottom, and therefore withstand sucking? I am thinking of poly-L-lysine, gelatine, or similar things - but I do not know whether these would be effective, or even tolerated by the plasma cells.

Have you tried spinning the plate down (say, 400xg for 5 minutes) just before removing the sup, then using a robot to slowly aspirate 1/2 or 2/3 of the well?

We use a PE Janus to suck the medium, and may be moving to a Biotek robot. The problem is that >95% of the medium must be sucked off, or else the PCR won't work. Spinning will not help since microscopy shows that the cells are already at the bottom of the plate. I still wonder whether some kind of gluing may help.

Oh, I didn't realize the PCR wouldn't work with excess liquid. How long are you culturing the cells before assaying for Ig (I assume) in the sup and deciding to PCR? If it's a relatively short amount of time (maybe 24-36 hours or less?), I can't see great harm in trying poly-D-lysine or gelatin or something. Have you tried Corning's Cell-Bind plates? I've had mixed results with them increasing adherence of suspension cells. Unfortunately, I haven't every tried adhering plasma cells, as I've always had microfluidics devices available should I need to do single-cell cloning.


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Current understanding of abiogenesis
I am trying to understand the current work on abiogenesis in biology, e.g. primordial soup, the Miller-Urey experiment, etc.
How has our understanding of abiogenesis been revised since the Miller-Urey 'primordial soup' hypothesis?

Start with the references in the Wikipedia page, do some targeted googling, and work from there.

@MattDMo I realize I can do this. However, this is an academic discussion forum. I would like to hear from academic biologists for the state of the field.
That's distinctly different than just googling. I can read biology textbooks too, but the point of this question is to hear from academic biologists.

This is not a discussion forum, it's a question and answer site. Not everything goes. Matt's comment is very appropriate; not possible when I was studying molecular biology (I read Oparin's The Origin of Life.) But for the history and an intro to where we are now, the references given in Wikipedia are a fine start. You can always ask more specific questions then. Please see the site tour and the help sections for more information about the site, particularly what kinds of questions are on topic here. Thanks!

@anongoodnurse I think "who is currently at the forefront of the field" is a fairly specific question. Also, I don't think it's helpful for learning to close down/vote down such questions because they are borderline discussion questions---this is a bit too pedantic. Stack Exchange was set up for learning, and that's exactly what I'm trying to achieve.

While your question might be specific, based on the fact that academics are humans its answer will be primarily opinion-based and thus out of scope for this site anyway. Person X might think, they are on the top of the field and their area of expertise is one of the major research topics, but their favourite academic competitor Y might disagree and instead bring herself and her topic in the discussion. And now it is a discussion. Unless there is a publication (from a field like sociology?) which studied the "academics of abiogenesis" there is no scientific answer to your question.

@skymningen Ok, how would you prefer I rephrase this question: "How has our understanding of abiogenesis been revised since the Miller-Urey 'primordial soup' hypothesis?" That is also strictly speaking not an objective scientific question, but it has educational merit. That is the point of Stack Exchange. Not all questions should be homework-esque questions.
Also, where else would you suggest I post this question in order to reach academic biologists, if not here?

@ShanZhengYang The question you pose in your comment is answerable in a way where one can cite the most important (published in high impact factor journals and/or highly accessed/cited) publications. Then maybe you sort them in a timeline and there you have a development. It might not picture everybody's opinion on it, but it will picture how this scientifically developed and the answer can have a objective approach.

@skymningen OK, that sounds reasonable. I've edited above. You are welcome to edit as well. Thank you :)

My "answer" to this question may interest you: http://biology.stackexchange.com/questions/19316/first-rna-polymerase-mrna/19737#19737

Our understanding of how life began on earth has indeed advanced substantially since Haldane, Oparin, Miller, and Urey. To learn about the latest ideas, I can't think of a better place to start than this excellent video series with Nobel Laureate Jack Szostack, who is currently doing some of the leading work on the subject.


text:
If you only ate fruits, vegetables or smoothies would you be able to skip drinking water?
If you only ate fruits, vegetables or smoothies would you be able to skip drinking water?
I do not see some animals (like squirrels) drinking water daily (doesn't mean they don't have a water source) so I am wondering if that's they case are they getting water from what they eat and can we as humans can go without water.
1st Researched Question:
https://www.livestrong.com/article/555187-can-you-drink-smoothies-in-place-of-fruits-vegetables/
Excerpt:

Fresh fruits and vegetables are considered low-calorie, energy-dense
foods. That means the food contains few calories in a high volume of
food. They tend to be high in water – dried fruits such as raisins are
an exception – high in fiber, high in volume and low in fat. The high
volume and fiber help you to feel full. A smoothie, in contrast, may
or may not be high in water, depending on how much fluid it contains.
Most importantly, a smoothie may have little fiber or the fiber it
does contain may have been chopped into tiny fragments by the
manufacturing process.

Summary:
Fruits and veggies contain water but smoothies do not. No answer if can be a replacement for drinking water.
2nd Researched Question:
Can you live just on smoothies and juicing?
https://www.quora.com/Can-you-live-just-on-smoothies-and-juicing
Summary:
Some say people can survive eating fruits and vegetables but do not specifically if humans can survive without water.
3rd Researched Question:
What would happen if I drank only a smoothie everyday for a month?
https://www.quora.com/What-would-happen-if-I-drank-only-a-smoothie-everyday-for-a-month
Quote:

Without diving all the way into Maslow’s Hierarchy of human needs, we
can pretty easily prioritize the elements of our diet according to
urgency and importance. The order will be something like:

Water
Energy
Proteins and lipids
Vitamins and minerals

Nobody will argue with the first one. A single smoothie would be harshly restrict fluid intake. Ideally a mid-sized person should have 2.5 liters of water each day. Estimates vary on the minimum required to maintain
life, but some sources estimate it to be just over 1 liter per day. If
it were a very large smoothie made with large amounts of either juice
or water, you might be ok here.

FYI This is not information for me but information in general. Some animals in nature seem to get by without drinking water but eating fruit. Would it be safe for a human do the same? We found out a human survived by drinking sea water (although it caused other issues). Also, I'm not advocating for it but I'm wondering if it causes issues.

What research have you done on your own to answer this question? The Biology.SE community has agreed that questions that show little or no prior research effort are off-topic on this site unless you have shown your attempt at an answer. Please [edit] your question and tell us where you've looked for answers, what you do know about the topic, and where exactly you still have questions. Our goal is not to simply be an answer site, but rather a site that promotes self-learning with some expert help along the way.

@MattDMo I did not find any specific answers online regarding this question. I have added my notes for what I did find.

That looks a lot better. I'm voting to reopen.

Is there anyway to reopen this? It is not personal medical quesitons. It's general. It's an in general question.

Thanks everyone for voting this down! I didn't want to learn anything new anyway! Only 8 downvotes?

Note: this question is being discussed on Meta.

A good number of vegetables and fruits have >90% water contents; this includes cucumber, watermelon, etc. Even oranges, broccoli etc. have >80%. So it would not be hard to have enough water intake if the veggie/fruit/smoothie diet is not restricted to particular fruits or veggies.
Slightly less detailed, but more reliable source agrees:


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Regarding the apoptosis mechanisms in cells and cancer
If all the cells in a cancerous tumour had their apoptosis mechanisms 'turned back on' or reactivated or repaired by some 'yet to be discovered' process would this cause the tumour to 'self destruct' or be destroyed? Are there known processes that can repair or reactivate the apoptosis mechanisms in a cell?

Theoretically yes (but since nobody did that, we don't know). Yes there are therapies which aim to reactivate apoptosis. "Inhibiting the anti-apoptotic Bcl-2 and Bcl-XL proteins may allow cells to restore their ability to undergo apoptosis" Btw. there are many more programmed cell death mechanisms, not just apoptosis (e.g. necroptosis).

The processes of apoptosis is not so simple, there is a lot of genes and proteins that participate in it. In cancer cells some of them mutate and not working properly.
Lack of apoptosis is the main problem in cancer. If cell not working properly, it dies. But not in cancer.
So theoretically, yes. If we will fix the apoptosis, the cell probably will die.
It's gene engineering direction. You need to target the cancer cell, and to change problem genes. It's really difficult processes. And every type of cancer has different mutations ...
Read this for example http://www.jeccr.com/content/30/1/87
(Journal of Experimental & Clinical Cancer Research )

Welcome to biology SE - it would be great if you could add some references to your answer(s)

Is there a process or set of biochemical events that can repair or re-initialize the apoptosis mechanisms in any cells whether they're normal, pre-cancerous or cancerous. If there is some such process one wouldn't have to specifically target cancer cells.

No such processes as far as I know, and to "target cancer cells" is the main problem in curing cancer. If we could "target" them, to kill them is pretty easy task.

Read this for example http://www.jeccr.com/content/30/1/87 (Journal of Experimental & Clinical Cancer Research )


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Optimum gibson assembly overlap length
Does anyone know the optimum length of overlap your primers should have to your vector for gibson assembly. Most manufacturers say to do at least 20 bp on both side but don't give a maximum. Sometimes I add 30-35 bp on both I don't know if that hinders efficiency.

Increasing overlap should not hinder. However, you'll waste money in synthesizing more oligoes.

There has to be some diminishing return.


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Is there any natural blue rose?
I had recently read an article that the possibility of having natural blue rose is extremely rare because of the absence of delphinidin in most roses. Are all blue roses just a product of cross-breeding?

Wikipedia article on blue roses has a pretty comprehensive explanation.

There are no roses (that is, flowers of genus Rosa species) that naturally express a "true" blue color. Through cross-breeding, there are lilac-mauve rose horticultural varieties ("Blue Nile","Blue Moon","Lady X", etc.), and through genetic engineering (actually inserting delphinidin-producing genes) there are mauve-lavender varieties ("Applause"). The insertion of delphinidin-producing genes did not yield blue colour roses as hoped is due to the acidity of the rose petals, which itself changed the delphinidin blue to mauve-lavender instead. The next breakthrough will be to switch off the acidity of the rose petals to create a true blue rose.
More info
Wikipedia article Blue Rose gives good coverage.
Here's a nice scientific bibliography of rose pigments with some good information on blues.


text:
Difference between pipette and pipettor
I've been translating a text listing some analytical laboratory equipment, and found that some fellow translators translate the Russian word "автоматическая пипетка" (avtomaticheskaya pipetka, which literally means "automatic pipette") as "pipettor".
I consulted the producer's website and found that the proper word for my particular model (thankfully the model code was mentioned) was indeed 'pipette'.
However, in case I come across a Russian 'pipetka' that really means "pipettor", how to distinguish between the two? Maybe the terms are largely synonymous?
Bear with me, I'm not a specialist in this sphere. I googled and found a discussion on Reddit that shed little light for me.

I think, that pipettes are handeled manually and pipettors are electrical like pipetboy and some steppers

In my mind, pipette and pipettor are generally* synonymous in the life sciences. Pipetman, which is actually a trademark, is also commonly used to refer to these instruments.

Gilson UK
That being said, there are some other things that you need to differentiate between. A pipette tip is the (usually plastic) thingy that goes on the end of the pipette, shown in the image above as clear white plastic on the left end. There are also serological pipettes

Argos Tech
and volumetric pipettes

Pro Lab Supply
together also referred to as transfer pipettes. These can be made of plastic or glass, and are used in conjunction with an electrical or mechanical pipettor, or a bulb (not your mouth!). Just to be confusing, sometimes lab personnel will refer to serological pipettes as just pipettes, even though they refer to the things pictured above in image 1 as pipettes as well.
Some people, such as SeRe above, distinguish between pipettes (the first image above) and pipettors, such as those used with serological pipettes:

Drummond
These are also known as Pipet-Aids or by other brand names.

However, in case I come across a Russian 'pipetka' that really means "pipettor", how to distinguish between the two? Maybe the terms are largely synonymous?

So yes, the two terms can be synonymous, so just be consistent, whichever you choose. I would stick with pipette unless it's clear from the text that the authors are transferring larger volumes than 1 ml, in which case they're probably using a pipettor in conjunction with a transfer pipette. If it's unclear, sticking with pipette should be good enough. If your readers are familiar with lab techniques, they'll understand what's going on.

You didn't include volumetric pipettes (similar to the serological (Mohr) pipettes, but only has the one volume mark, and may have a bulb to contain the fluid). https://en.wikipedia.org/wiki/Volumetric_pipette#:~:text=A%20volumetric%20pipette%2C%20bulb%20pipette,a%20fixed%20volume%20of%20liquid.

@LDC3 you are correct. Please see my edit above.

I look at the difference as being whether you are referring to the actual vessel that holds the fluid (the pipette no matter what its size) versus the pipettor, a device that allows for suction of air to draw liquid into the vessel (the pipette).
Pipet tips come into play when referring to very small volumes to be drawn into the vessel, but the device is still a pipettor or a micropipettor. Before real lab safety came along the human mouth was often the suction device, or the pipettor! We have tried to clarify this also for student lab manuals.


text:
In what circumstances does a mammalian egg copy its DNA?
In the 2nd episode of the new Cosmos series, the host Neil deGrasse Tyson shows how the white-furred bear could have evolved (reasonable scientific speculation, of course).
If you haven't seen that episode, here's the link. Great show, by the way.
So, it shows the bears eggs, and then goes on to show how there can happen an error in the DNA copying, that leads to the brown pigment production malfunction. Here's an excerpt from the subtitles text:
- great bears roamed the frozen wastes of Ireland.
- This might look like an ordinary bear,
- but something extraordinary is happening inside her.
- Something that will give rise to a new species.
- In order to see it, we'll need to descend down to a much smaller scale, to     the cellular level, so that we can explore the bear's reproductive system.
..
- Those are some of her eggs.
- To see what's going on in one of them,
- we'll have to get even smaller.
- We'll have to shrink down to the molecular level.
..
- When a living cell divides in two,
- each one takes away with it a complete copy of the DNA.
- A specialized protein proofreads to make sure
- that only the right letters are accepted
- so that the DNA is accurately copied.
- But nobody's perfect.
- Occasionally, a proofreading error slips through,
- making a small, random change in the genetic instructions.
- A mutation has occurred in the bear's egg cell.
- A random event as tiny as this one can have consequences on a far grander scale.
- That mutation altered the gene that controls fur color.
- It will affect the production of dark pigment in the fur
- of the bear's offspring.

From my (not professional but kind of passionate amateur) knowledge of biology, I I was under impression that all of the mammalian eggs are present at birth. But the story depicted in the show involves the (erroneous) DNA copying. I see dissonance there, and I'd like to solve it.

The episode isn't available outside the US, so can you provide some more details? When does the DNA copying happen? When the eggs are produced?

I edited the port to include the text. Perhaps this is the point where I fail to grasp what's happening: "A mutation has occurred in the bear's egg cell" - at which point a mutation could in fact happen in an egg cell? To my understanding, only a fertilized egg cell divides.

The writers of the show may have been somewhat imprecise either by accident or intentionally to avoid excessive details.
There are several different stages of egg cells, with distinct names for each and for the process that leads from one to the next. The whole process of egg cell creation is called [Oogenesis].1 To quote Wikipedia:

Oogenesis starts with the process of developing oogonia, which occurs
  via the transformation of primordial follicles into primary oocytes, a
  process called oocytogenesis.[4] Oocytogenesis is complete either
  before or shortly after birth.

To our current knowledge all primary Oocytes are present at birth. The next stage in the maturing process is called ootidogenesis, which produces an ootid.

The succeeding phase of ootidogenesis occurs when the primary oocyte
  develops into an ootid. This is achieved by the process of meiosis. In
  fact, a primary oocyte is, by its biological definition, a cell whose
  primary function is to divide by the process of meiosis.[8]
However, although this process begins at prenatal age, it stops at
  prophase I. In late fetal life, all oocytes, still primary oocytes,
  have halted at this stage of development, called the dictyate. After
  menarche, these cells then continue to develop, although only a few do
  so every menstrual cycle.
Meiosis I of ootidogenesis begins during embryonic development, but
  halts in the diplotene stage of prophase I until puberty. The mouse
  oocyte in the dictyate (prolonged diplotene) stage actively repairs
  DNA damage, whereas DNA repair is not detectable in the pre-dictyate
  (leptotene, zygotene and pachytene) stages of meiosis

DNA replication is completed before Meiosis occurs. So oocytes do not replicate DNA after birth, but they do repair DNA to fix mutations that may occour after birth but before conception. If DNA repair fails, then mutations may persist. So the show would appear to be wrong about egg cells copying DNA in an adult bear, but right in that mutations might occur during its lifetime affecting its offspring.

Wow, that's elaborate, thank you. On what authority I could decide that I can mark your answer as "correct"? I am not competent to decide :)  Why would the show writers choose this particular stage for addressing the mutation introduction? Is that the prevailing hypothesis of how the persistent, evolution-driving mutations occur?


text:
List of np-hard problems in biology/bioinformatics
I'm not sure if this is the right place for this but...
I am looking for a list of computationally "hard" problems such that if a problem from this list could be solved effectively, it would be (significantly, or otherwise) beneficial in some form or another to the biology community.
Some examples I have found (or atleast were tagged as "np-hard" problems):
Multiple sequence alignment problem
Protein threading / design problem
Map / sequence assembly problem

The list does not have to be extensive, but hopefully more than a few.
Thank you!
(Also, I couldn't think of any more tags to add so feel free to help out there as well.)
Note:
Same question at biostars: https://www.biostars.org/p/98112/

Try asking this on http://www.biostars.org, the people there probably have thought more often about the question if a problem is np-hard.

Why has this question been downvoted? btw, this post might interest you @Colton

Just a curiosity: an NP-complete problem (Hamiltonian path) solved with molecular computing http://www.ncbi.nlm.nih.gov/m/pubmed/7973651/

Hope the below answer is somewhat helpful.

@MattiaRovetta Here is a related paper

I think this is a great question but it may have been misunderstood to mean literally NP-hard problems in bioinformatics, whereas it is really seemingly asking about hard computational problems that would be of great use in biology or bioinformatics. Perhaps it should be reasked here.

Constructing a phylogenetic tree for N taxa.

I'm no expert in computational biology but I am very much interested and do some big data analysis using R for my own projects so I will try to provide some information.
This (http://www.ncbi.nlm.nih.gov/books/NBK25461/) is an excellent book talking about all the grand challenges in computational biology and the emerging fields so I definitely recommend looking through at least the list on the page, if you don't want to read the entire book. To me all this points to the fact that we are in the big data era, where we have masses of data but making sense of them all and putting them into prospective and analysing them in a way to show us new insights into problems is difficult.
You might also be interested in BOINC, which runs a few computationally challenging projects through crowd sourcing/grid computing (http://boinc.berkeley.edu/projects.php). In more theoretical aspects, here is a list of unsolved problems (http://en.wikipedia.org/wiki/List_of_unsolved_problems_in_mathematics), solving of which will excel our understanding of many modelling problems, which percolate in biological problems as well although I'm not at all an expert in biological systems modelling.
Hope this helps!

De-novo assembly
To construct a genome from short reads, it's necessary to construct a graph of those reads. We do it by breaking the reads into k-mers and assemble them into a graph.

In this example, we have a k-mer of 3. We can reconstruct the genome by visiting each node once as in the diagram. This is known as Hamiltonian path.
Unfortunately, constructing such path is NP-hard. It's not possible to derive an efficient algorithm for solving it. Instead, in bioinformatics we construct a Eulerian cycle where an edge represents an overlap in two k-mers.

This is more of a long comment than an answer, but I thought it might still interest you. We usually care about NP-hardness because it means that we can't do something or solve some problem. But that isn't the only intractable complexity class that should be important to biologists.
If we re-frame NP problems as optimization problems (instead of the strict definition as decision problems) then what NP-hardness usually says is that we can't (in general and in reasonable time) find the global optimum. However, in a lot of evolutionary settings we wouldn't even care about a global optimum, we'd be happy with a local one.
The difficulty of finding local optima is captured by the complexity class known as Polynomial Local Search (PLS). And here we also have surprising complexity barriers. For example, Kauffman's NK-model of static fitness landscapes (also, see this blog post and SE question for overview) is not only NP-hard [Weinberger, E. (1996), "NP-completeness of Kauffman's N-k model, a Tuneably Rugged Fitness Landscape", Santa Fe Institute Working Paper, 96-02-003] but also PLS-hard (Kaznatcheev, 2017; see here for an overview or here for the final paper). This means that not only can arbitrary evolutionary dynamics not find global optima, but in general they can't even always find local optima on these finite (but exponentially large) landscapes. Suggesting that local optimality might not be a reasonable assumption even on static landscapes.


text:
Why don’t bone marrow donations harm the donor in the long term?
I have googled about this, and the most I can really find is that donating bone marrow/blood stem cells is not harmful in the long run, but I want to know why and how much is really known about this.
My question “stems” from my maybe cartoonish notion that you have all the stem cells you’ll ever have at the beginning of your life and that their depletion relates strongly to aging.
In my googling, I have read studies that lifespans of older mice can be extended with bone marrow stem cell transplants from younger mice. Based on my cartoon, I guessed that perhaps older mice have some depletion of and/or damage to their own hematopoietic stem cells that reduces overall formed element production, and this is the state that a transplant helps to fix. With this frame of mind, I have a hard time imagining that even a young donor of blood stem cells is not harmed in the long run. Hasn’t their pool of stem cells effectively been aged somewhat by the donation? Or is damage to the population of cells over time by environmental factors much more significant, more the “bottleneck” in cell health than the gradual deterioration caused by repeated division? Is it that donation effectively only forces something on the order of one extra division per cell? I also wonder whether that “bottleneck” could vary depending on the typical longevity of the animal under study.
Regarding my question about what is known—I suppose I’m asking what kinds of principles or studied effects are likely being referenced in laypersons’ articles declaring that donors do not experience long term harm.
I’m sure that I am probably saying some nonsense things because biology is not my field. Any corrections and disentangled conflations would be appreciated!

Hematopoietic stem cells (HSCs) can regenerate themselves, with no loss of "stem-ness". When bone marrow (which contains high numbers of these cells) is harvested for a transplant, the remaining HSCs divide and eventually repopulate the area that the marrow was harvested from, leaving it no different than before. There is absolutely no identifiable difference between the "old" and "new" HSCs - they both have the same lifetime, the same markers, the same functionality, etc. There is no long-term damage to the donor.


text:
How can a recessive allele propagate until they manifest?
Suppose a specific gene has two possible alleles. In a given population all members have only the dominant one. By a mutation on member receives the first recessive allele of that population. Is it possible that one day the descendants of this population have this allele manifested? I think it's very unlikely that this allele survive until another similar mutation occurs and they get manifested in the phenotype.

The short answer is: Because of genetic drift. If a mutation does not influence the fitness in heterozygote individuals, then its frequency varies only through genetic drift while it reaches some high enough frequency. If by chance, the frequency of this new allele achieve a high enough level so that the homozygous for this allele given by $x^2$ where $x$ is the frequency of the new allele is high enough to have considerable effect, then the selection coefficient $s$ between the recess if homozygote and the two other genotypes matters.
Hope that helps you. Don't hesitate to ask further more accurate question if you need more details. Or let us know if this does not answer your question.


text:
What is the point of being selection-free?
I'm reading "Highly efficient endogenous human gene correction using designed zinc finger nucleases" by Urnov et al. They propose a way to use zinc finger proteins for gene therapy. They repeatedly claim their method is "selection free" and it seems they are claiming that as an advantage to their method.
Why would selection free be an advantage? Wouldn't you have to select for the transformed cells anyway to be relevant in a clinical setting?

Urnov et al. are trying to effect gene therapy - where a mutation causing a genetic form of severe combined immunideficiency (SCID) (also known as the bubble boy syndrome). Affected SCID patients can have little to no immunity to infection what so ever.  SCID in this case is caused by a single site mutation in the IL2R-gamma gene.
Their method is to use a DNA binding protein (containing zinc finger domains that bind the DNA) which attracts a DNA repair enzyme.
The result is that 18% of the cells have the SCID gene repaired.  This would have been a trivial result if they had applied selection, which generally refers to any method which eliminates cells which were not affected (in this case having their DNA repaired) by a transformation like their treatment.  They claim that 18% of all the cells were repaired (I assume this is in a cell culture).  This implies that if their treatment were applied to living tissue, 18% of the cells would be repaired in situ, which should be enough to restore immune function.
While its possible to apply a selection method to gene therapy, it would be far better if you did not.  Cancer chemotherapy for instance is a selection based treatment for instance, relying on toxins which kill fast dividing or growing cells preferentially, leaving the slower growing tissues relatively viable.   Still its quite toxic and disruptive to the patient.

-1. "This implies that if their treatment were applied to living tissue, 18% of the cells would be repaired in situ." Not at all. If only it were true that findings in a dish could draw such a straight line to results in the body!

i used the word 'implies' for this reason. I think this is a Nature article because they have suggested this very thing.  They are trying to demonstrate potential for in vivo gene therapy without selection as far as I can see.

I agree that they are trying to demonstrate a method that will be applicable for in vivo gene therapy. The results are suggestive of some rate of efficacy for in vivo repair. However, an 18% fraction of repaired cells in a dish does not point to, or even imply, an 18% fraction of repaired cells in a body.

I'm sure most would agree with that. Gene therapy has been an extremely difficult idea to realize in practice.  So much so that what is a preliminary result like this is published in a top tier journal.  This is promising, but far from a resolved problem.  It would be a strong contender for a Nobel Prize in Medicine if it did turn out to be a real treatment for SCID.

Thanks shigeta - this makes it very clear. I understand yamad's point, but I also get that this points to a possibility that some non-trivial amount of cells could in theory get transformed if this treatment were developed in situ.
So this does mean, right, that this treatment could only be applied to cases where cells are deficient in some manner or have some loss of function. If the cell were to gain some active malfunction - repairing a small proportion of the cells may not actually have a great impact. Would you agree?

The idea is to make an in situ edit in the DNA - it could be a repair of function or, less likely, a disruption of function that corrects a disease.  in many cases of repair of function a proportion of 20% of the cells probably would be a cure in many cases.  This condition was perhaps chosed because the repair in question would be helpful; in this case it would confer immune activity and most cells are not active all the time in any case.  The better the yield the more diseases would be ameliorated, but there are many where 1 in 5 would be a major lifestyle change for patients.


text:
Can an adult without genetic lactase persistence still develop a tolerance for dairy foods?
While investigating the rise of adult lactose tolerance, I came across the news that China has been encouraging its citizens to drink more milk, even though most of the Asian population lacks the SNP (single-nucleotide polymorphism) which conveys lactase persistence.
Is it still possible for an adult without lactase persistence to build-up a tolerance for lactose over time? If so, what's the mechanism?

@shigeta SNP is a single nucleotide polymorphism (i.e., an allele that differs from another by just one base pair). Many important genetic polymorphisms are SNPs, but not all. I don't know if persistent lactose tolerance is caused by a SNP, or even by a single gene.

It seems that yes, it is possible to increase the tolerance for lactose over time, and it has to do with the adaptation of microbiota.
A simplistic explanation comes in the following article:
 Hertzler SR, Savaiano DA. 1996. Colonic adaptation to daily lactose feeding in lactose maldigesters reduces lactose intolerance. The American journal of clinical nutrition 64: 232–6.
In which the authors claim the following:

"Colonic adaptation appears to reduce the symptomatic response to lactose via several mechanisms. (...)
(...) increased β-galactosidase activity after regular lactose ingestion indicates that colonic bacteria are able to ferment lactose more rapidly. (...)
(...) This metabolic shift is thought to result from the proliferation of lactose-fermenting, non-hydrogen producing organisms such as Bifidobacteria."

This article makes reference to another one which supposedly explains the microbiota adaptation:
Hill Mi. Bacterial adaptation to lactase deficiency. In: Delmont J, ed. 1983. Milk intolerances and rejection. New York: Karger: 22–6.
But unfortunately I could not find the full text. I hope you are luckier than me.

The second 'article' is actually a chapter in a book, which is why you couldn't find the full text :)

Here are my thoughts on the topic.
Dairy good is not only milk, but also the following milk products: sour milk products (like yougurt, kefir, katik, buttermilk, etc.), cheese, etc. These products can contain less lactose than in the milk solids (due to fermentation during processing). It is also common for some of these products to contain living lactase-active bacteria, that can digest lactose.
Regular intake of these products can lead to certain changes in our small intestine microflora, so that the lacking lactase activity is substituted by the bacteria and thereby the tolerance grows. Maybe this is the intend of the Chinese government? Maybe they encourage the intake of sour milk products and not solid milk?
It is known, for example, that children with congenital/primary enzymatic deficiency develop the tolerance at the age of 6-10 years so that no special diet is needed anymore. This is true at least for such common enzymatic deficiencies like phenylketonuria and coeliacia.
In Russia, where I got my medical degree, it is common to use bacteria in the treatment of many types of primary intolerance combining this treatment with dietary support.


text:
Shouldn't evolution have taken care of baldness already?
It is my understanding that the hair on the head is there to protect us from sunburn.  I've never seen a bald animal, so isn't evolution in charge of addressing these type of things?
How is it that evolution gave us a thumb, but hasn't found a way to keep the hair on our heads?

Your question doesn't provide very compelling evidence for reduced fitness due to baldness.

Because we use hats?

There are tons of bald animals. Fish immediately come to mind. Then there are naked mole rats and lots of other critters. Also, your last sentence can be used to ask the equivalent question “why didn’t evolution give chimps thumbs?” – This is simply not how evolution works.

fish never grow hair, they don't get bald within their lifespan  I don't see any correlation between a fish and my question.

@Rafael.IT The correlation is that fish have (some of) the same supposed disadvantages due to their hairlessness, so according to the argument they should have evolved hair by now. But if you don’t like this example, take the other ones, where animals have lost their ancestors’ hair. Actually, nico’s comment above is excellent (and not at all a joke!): we evolved the ability to manufacture hats. This is an adaptation to combat the disadvantages of baldness.

research claiming bald men get less cancer: http://news.bbc.co.uk/2/hi/health/8569826.stm

the article actually talks about the level of testosterone, baldness is  consequence of high testosterone but the baldness itself holds no correlation with  cancer

If testosterone causes both baldness and cancer then that is a push towards baldness and cancer correlation. The article states baldness to cancer correlation.

using that premise you can link pretty much anything you want, for instance if high testosterone causes that men have more sex than usual would that mean that sex causes cancer?

No, absolutely not. but it would push sex towards being correlated with cancer.

@isJustMe it would also mean there was a selective advantage to being vulnerable to that form of cancer,  no trait exists in a vacuum.

Can you demonstrate any reason baldness should be selected against?

As is typical for questions about fitness, this question has more than one valid answer.
The essential question @AndrewSalmon is answering is the right one:
"If evolution eliminates disadvantages, why can xyz trait still be seen the population?"
Here is a more complete list,
1) The trait is not eliminated by evolution since it is manifested after reproduction.  The classic example of this sort of trait is senescence.  Why do we grow old and die?  Clearly it doesn't stop us from having offspring.  I generally don't find this sort of answer informative. Its not a bad argument for the traits of bipolar and schitzophrenic tendencies which can manifest as a chronic mental condition, often in the 30s after many people have children.
These traits are fairly common (1 in 6) in the population.
It is usually arguable that these traits are of some sort of advantage from some perspective (including my examples).  In this case @Andrew argues this.  I'm not sure I agree, but you can read his post for the argument.
2) Pleiotropy. The idea that the negative trait evidences more than one trait.  In this case one might say that baldness is tied with another trait that is beneficial.  Some say that the cause of male pattern baldness, which is an excess of testosterone, would be tied in with other masculine signals, which can often outweigh disadvantages of being bald and trying to find a mate.  A trait like baldness could also for instance be tied to a desirable trait in women, causing it to persist in men as a result of the advantage of say, less hairy women.  I probably wouldn't take this stand either, though its conceivable.
3) "Neutral variant" The third explanation that I will put out is that baldness simply isn't a trait with enough disadvantage (if any) that it should be removed from the gene pool.  While there is evidence that baldness is a disadvantage come friday night, to say that a trait is disadvantageous we have to see, in the long run - over the lifetime - really is a disadvantage.  I think I would agree with those who say that while some women do not find bald men attractive, its not enough to stop them from having kids, which is all evolution cares about.
And if you happen to be balding probably what you should care about, guys!
If evolution should eliminate male baldness, then why not eliminate sterility, homeliness, impotence, poverty, obesity, being dull, living with your parents and adolescent awkwardness?  These are probably even more important obstacles to finding a mate? All of these traits are beneficial traits that are maladapted to modern life or genetic accidents.  Evolution can't get rid of them at all I think.
For an even more complete discussion of the general subject, see Dawkin's "The Extended Phenotype".  Baldness is not discussed however.

It needs to be pointed out homelessness, poverty, and living with your parents do not have genetic components so they make bad examples, evolution cannot do anything about them.

The closest research I can find with a little poking is this paper.  The results are somewhat inconclusive, because AGA (the technical term for male pattern baldness) has many separate genetic components.  Nonetheless, there appears to be evidence that AGA is under positive selective pressure in Europeans and possibly Asians.  That is, there appears to be a fitness advantage to baldness in some circumstances.  However, there are other possibilities, for example, it may be that an adjacent gene is being selected for and this gene is coming along for the ride.
Note that AGA is less frequent in Africans than Europeans, which suggests that indeed there may be selective pressure against baldness in sunnier climates for the reason you suggest.  Note that in cold climates, on the other hand, there can be selection for increased UV exposure to avoid Vitamin D deficiency (the evolution of lighter skin).

+1 The fact about africans having less tendecy to baldness is interesting

The linked paper says "Epidemiological data for African populations is sparse, but it has been reported that males without AGA are four times more frequent in Africa than in Europe" citing a paper from 1970.

Care to explain the downvote? Did I get something wrong?

I voted up man, must be someone else

Yeah, sorry, I didn't think it was you.

Or it is simply under less negative selection in populations living in places with lower UV incidence.


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Where does vasoconstriction occur in limbs?
When cold or in shock a person's blood vessels constrict in order to preserve heat or to move blood flow to protect vital organs.  I am interested in the mechanism by which this is achieved.  Does this occur along the entire length of the limb or are there 'pinch points' (for example is it possible to simply have a point of vasoconstriction just below the shoulder which would reduce blood flow to the entire arm)?  Am I correct in thinking that the response is neurological rather than endocrinological ?

Reduced blood flow to a region of the body occurs through 2 principal mechanisms.
1) The smooth muscle fibers in the tunica media layer of the arteries contract and reduce the diameter of the artery, limiting blood flow due to increased resistance (this is the mechanism in @agrimaldi's answer).
2) Circularly oriented smooth muscle fibers at the junction of a metarteriole (the distal end of an arteriole) and a capillary bed form a precapillary sphincter, which serves as a valve and prevents blood flow into a the capillary bed.
So to answer your question, it is both.  The narrowing of the arteries would occur rather continuously across the limb but there are "pinch points" where metarterioles joint the capillary beds.
The endocrine and nervous systems are pretty integrated so in most cases it would be the result of the actions of both systems.

So it would be possible to, for example, have one hand receiving less blood flow than the other?

I would think so, yes.  You could likely test this by placing one hand in cold water and the other in hot water.  The blood vessels in the hand in cold water should constrict and the ones in the hot water should dilate. (I think)

Vasoconstriction is a phenomenon that can be caused by many factors, from mechanical events (such as stretching) to hormones (epinephrin, neurepinephrin, angiotensin ...). But no matter what is the cause, the end-result is an increase in intracellular calcium concentration in smooth muscle cells (which compose the arteries and veins). So it seems that constriction does not happen in specific points but rather all along the limb. Furthermore angiotensin receptors are found in high concentration in smooth muscle cells [1], suggesting that every such cell has the ability to change it's morphology in order to induce vasoconstriction.
As for your second point, I think the response is as much endocrinological as neurological, since it involves both peripheral and central regulations. (Well, as a side note, endocrine systems rarely have no interaction with central ones).
Angiotensin receptors : distribution,
signalling and function


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Do we get 1/4 of our genes from each grandparent?
I know that we get half of our genes from each parent, but does it necessarily mean we get 1/4 of our genes from each grandparent? Or is it possible that we might get say 30% from one grandparent, 20% from other, 15% from another, 35% from another?

possible duplicate of How many genes do we share with our mother?

If you know that you get half of your genes from each of your parents, would that make your parent's parents any different? -1

I have answered a similar question before: "How many genes do we share with our mother?".
It is not that you "get half your genes" from each parent, and thus a quarter from each grandparent, it is that you inherit the versions of the genes (we all have the 'same' genes).
The method that determines which traits are inherited from each parent by the offspring is known as homologous recombination, and this process is (essentially) random, and thus you end with ~50% of your traits (the alleles of the genes) from each parent, and ~25% from each grandparent, so you are right in this respect.
This is, however, a generalization; due to the chance nature of the recombination it is entirely plausible that you may inherit more traits from one grandparent in comparison to another, but this is unique to each individual (with the exception of course of genetically identical twins).

This comes down to the ever confusing use of gene to mean allele and loci. Just as in the "How many genes.." Q you answered before, the term gene is often used for both leading to the confused idea that we share 99% of our genes with chimpanzees yet we only share 25% with our grandparents.. Alleles are all the different variants (or versions as you called them) present at each loci (non-recombining region of DNA). We share 25% of our ALLELES with our grandparents (assuming no mutation and recombination) and 99% of LOCI with chimpanzees. Perhaps this can be added to both of your answers.

And we should wipe the word gene from the English language and just use Allele and Loci!

I agree with the person above. But it might be more correct to say we get 1/4 of our total DNA from each of our grandparents, because though the genes are really important to code for specific proteins, there are tons of non-coding DNA in between them. In fact, 98% of our genome is non-coding! Although we are discovering awesome novel functions for this DNA slowly but surely. But it is important to think of it as 1/4 of your DNA and not genes because it is in this non-coding DNA where a lot of mutations can occur, and these mutations are what we inherit and make things like DNA fingerprinting for forensic analysis possible, like in CSI.
I just wanted to add three more thoughts:
Though it is true that 1/4 of your DNA would come from each grandparent, that is only true for your autosomal genes, not your necessarily for your sex chromosomes. The X chromosome does recombine regularly in the mother, but in the father the X and the Y do not recombine. (Actually I think part of the Y can recombine, but for the most part, the sex-determining part of the Y and its associated genes stay completely intact). This means that if you are a male, your father, and his father, and his father all share the same Y chromosome.
Additionally for the women, because the woman makes the egg, and thus all the early embryonic organelles and RNA's, the woman donates the mitochondrial DNA, which has its own sets of genes that are really important and have been linked to many diseases. So every child of a woman, shares their mother's mitochondrial DNA, as she shares her mother's and her mother's mother, etc.
If ~1/4 of our DNA comes each grandparent, then 1/8 of your DNA comes from each great-grandparent. So then 1/16 of our DNA comes from each great-great grandparent, which are your grandparent's grandparents. And thus it continues exponentially upward. The result is that there comes a point where your ancestors have contributed so little to your actual DNA, that it becomes almost negligible. So if you are an American, who most likely has ancestors from all over the world, even if you have 1 great-great-great-great grandparent who was a French immigrant while the rest of your ancestors were all British, the French DNA is only 1/64 of your total DNA. So even if you are a complete mix, there comes a point where so many different people have contributed to you being you, that you can establish a cut-off and just say, 3/4 of my ancestors were born in America, I'm American!

Good point about the mitochondrial contribution from the maternal lineage.

Humans do not get an even 1/4 of DNA from each grandparent.
The main reason is that meiosis is not a precise 50/50 split. Parent cells undergo meiosis to recombine the grandparent chromosomes and produce a set of chromosomes to pass on to a child. This process is not a precise 50/50 split and produced chromosomes will have more of one grandparent DNA than the other.
The second reason is that different chromosomes have different DNA base pair lengths. So, while every human gets exactly 23 nuclear chromosomes from each parent, some of those chromosomes have more DNA base pairs than others, and children receive a different quantity of DNA base pair content from each parent.

Please put up references to prevent your post being flagged. Thank you.

Although you share 50% of your chromosomes with each parent, it is not necessarily the case that each of your four grandparents contributed 25% of your chromosomes. Ignoring the effects of recombination, the chromosomes in each gamete (think egg or sperm cell) are randomly either from one grandparent or the other. It is possible, for example, for the 23 chromosomes in a sperm cell to be (more or less) the exact same 23 chromosomes this male inherited from his father. There are 2^23, or about 8.3 million, different combinations of chromosomes possible for the gamete of a diploid organism with 23 chromosomes. It's possible that the gamete gets an even split close to 50:50, but it's also possible that the gamete got 100:0 making the offspring effectively not related to one of their grandparents. Unlikely, but it's not actually impossible.

The question asks for genes, not chromosomes.

Genes are located in chromosomes.

Although some of the previous answers also acknowledge it, this answer comes the closest to pointing out the surprising fact that we don't inherit equally from each Grandparent, and that it's possible that in the limit, we could inherit nothing from a grandparent.

There is a phenomenon known as genomic imprinting where the allele of the gene would only get expressed if it is passed on from the father (e.g. IGF2). This means that although the same genes get passed on from both your father and mother, only the copy from your father will get expressed. Thus, although you get 50% of your DNA from your parent (and probablistically speaking 25% from your grandparent), the same gene can be deferentially expressed depending who you get them from).


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Fossils of intermediate stages?
If Humans are evolve from Monkeys, there must be stages in the evolution process, when it was 1% human and 99% monkey, 2% human and 98% monkey  and so on. This is because evolution was a very slow process that occurred in a span of thousands of years. So we expect there must be fossils of this intermediate stages under earth. These intermediate-stage fossils must be many times in no. as compared to 100% human or 100% monkey.
But why do we do not discover these intermediate fossils?

Humans did not evolve from monkeys, we are apes (along with chimps, gorillas, and others).  We apes evolved from earlier primates, as did the monkeys and prosimians (like lemurs).

you have to remember that we are also getting further from our ape cousins all the time, even if we do not change into a new species.  Just the passage of time accumulates mutational differences between us and other species we are related to like the apes.

in addition to the comments above and the answer provided, note that we created the labels "monkey" and "human" based on the characters of these organisms.  There is no absolute "human" or "monkey" to partition into fractions.

We do, all the time. Here's a nice graphic from Dr. Douglas Theobald. (Images copyright 2000 Smithsonian Institution.):

That's 14 Hominid species, ranging from about 4 M.Y. ago to a modern human skull ("N").
Here's a nice genealogy as well (although these change frequently as more evidence is gathered):


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When can a virus modify DNA in every cell of a living organism?
I've recently heard about experiments with brain tissue, where a virus is introduced in a rats brain, causing a "glow when electric charge is present" protein to be created. This protein then helps to study the brain using optical techniques to detect this glow. As far as I understand, not all cells in the brain were affected by this virus.
It seems like this kind of "virus operation" on DNA is pretty powerful, so my question is : at which point in an organism's life can a virus operation be done in such a way as to affect the entire organism for the rest of its life?
In other words, will a virus is introduced into a young embryo(or sperm), affect all cells and stay with an organism until death? Can it be introduced later and still have "complete effect"?

Note that in the type of experiments you are referring to (for instance look for "in vivo optogenetics") you generally do NOT want to infect all of the neurons in the brain, but rather a very specific subpopulation. This is achieved by using various strategies, which essentially depend on the presence of specific DNA sequences in the virus or in the target neurons. Also, if you do this in adult animals, the virus will only infect cells around the site at which it has been injected.

The answer depends on two factors:

The type of vector (virus) you are using
How well your vector can be integrated.

The bottom-line is that there is no guarantee the vector will work even if you start from the embyro.
As far as I know, the problem of using vectors in general is that the vector you are using might not be integrated into the genome of the host. (Not necessarily get into the DNA, but just keep replicating during each S phase.) Therefore doing it earlier gives you a better chance to actually get them in the organism.
For example, there is a linear vector used in C. elegans that was injected into the oocyte even before fertilization. The cell later treats the vectors as broken DNAs and linages them so they could be pull to one side of the cell during mitosis. However, the huge chunk of vector DNA is mosaic. (i.e. only some of the cells in that worm have the vectors.) Other vectors like engineered HIV have better chance to integrate themselves.


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Gender of BEAS-2B cell culture
I recognize some interesting patterns when analysing DNA methylation of BEAS-2B cells. Does anybody know, if the cell culture is female or male? I already asked the customer support of Sigma Aldrich without success.
Information on the official website just mention "non-cancerous individuals" as source organisms.
http://www.sigmaaldrich.com/catalog/product/sigma/95102433?lang=de&region=DE

The cell line is most likely genetically male. On the English (US) site, the Description box has several sections, of which one is DNA Profile. In there, it lists amelogenin as X, Y. This gene is located on both the X and Y chromosomes (AMELX and AMELY, respectively), which have distinct PCR-detectable sequence differences. It is often used in helping to determine the gender of unknown samples in the realm of forensics - it is not 100% accurate, so other genetic tests (such as for SRY) are also performed.

My DNA methylation data don't show a clear male oder female status. There is definitly an observable "male" effect, but a clear classification is not possible with my dataset. The results indicate a mixture. Anyway, I will remove gonosomal probes from further analyses. Thanks for your answer!


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cell specialisation and their location
When we create new cells, how come they are of the 'right' type at the 'right' place?
For example, when I make a new cell on my lips, it's obviously not the same as a new one in my kidneys.
Is the differentiation done by using a different part of the DNA each cell has?
How does the mechanism of growing specific types of cells at a specific place work?

Yes differentiation is primarily about using only a portion of the genome as you pointed out. However, differentiated cells possess a kind of "memory" which enables the daughter cells to continue the usage of the same set of genes. This "memory" is enabled by epigenetic mechanisms which leave inheritable "marks" on the DNA such as methylation (I won't explain further as this would take an entire book).
About the place: each part of the body can produce cells locally (except for some tissues). For example the epithelial cells in your lips will arise from your lips. What signals the division of cells in response to a signal such as lets say injury is again a broad question. One simple mechanism is this (not an independent mode but just one aspect of a complex process): cells generally divide but stop dividing if there is no free space i.e. the cell is surrounded by other cells. This is called lateral inhibition of growth.
I would suggest that you pick up some good cell biology and molecular genetics books to understand these processes.
Cell Biology:

Molecular Biology of the Cell - Bruce Alberts et al.
Molecular Cell Biology - Lodish and Baltimore

Molecular Genetics:

Molecular Biology of the Gene - James Watson et al.
Genes - Benjamin Lewin

so, if I understand, the 'specialization' gets replicated as well, so a 'lip' cell will only make another 'lip' cell; is that correct?


text:
What's the difference between Kd and IC50?
What's the difference between the equilibrium binding constant ($K_d$) and Inhibitory Concentration 50 $IC_{50}$? They both seem to mark halfway points. Is the only difference that $K_d$ refers to any binding, whereas $IC_{50}$ refers exclusively to inhibition?

For a reversible inhibitor, the relationship between Ki and IC(50) will critically depend on the mechanism of inhibition, and IMO IC(50) values are at best misleading (and at worst meaningless).  Consider a (reversible) competitive inh: the IC50 value determined at a substrate conc equal to Km will be very different to that determined at, say, a substrate conc equal to 10-times Km.  There is a great paper by A. Naqui who explains this very well. For a reversible inh, IC50 only equals Ki if the mechanism of inhibition is non-competitive.

I have expanded on this topic ( a bit too much perhaps) in the section "Reversible Inhibition & IC50. A Brief Comment" of this old answer.  For a much too detailed treatment of reversible inhibition, see this answer

First, let's review the definitions of $K_d$ and $IC_{50}$.
$K_d$
$K_d$ refers to the dissociation rate at equilibrium and is calculated by $\frac{K_{on}}{K_{off}}$. This is the rate at which the peptide is bound to the target protein ($K_{on}$) divided by the rate at which the peptide unbinds or comes off the target protein ($K_{off}$). So when you look at binding curves, it's the 50% bound/unbound point on the curve (the inflection point).

$IC_{50}$
$IC_{50}$ indeed refers specifically to the inhibition of binding or inhibition of a function at which 50% of the peptide is bound and 50% is not bound (or 50% of the function is active and 50% is inactive).
Comparison
In some cases $K_{d}$ and $IC_{50}$ may be very similar values even identical, but in other cases $K_{d}$ and $IC_{50}$ values actually differ.
Pragmatically, $K_{d}$ values generally are considered more "constant" and vary less with changes in concentration of the target protein and peptide. They are more independent from the assay set up and type. In contrast, an $IC_{50}$ value can range depending on the assay set up (not considered constant values). For example, the $IC_{50}$ values in Fluorescence Polarization depend heavily on what "probe" molecule was used and the concentrations of the target protein and peptide.

(+1) [I am not the downvoter]

If Kd has dimensions of concentration (Molarity, say), shouldn't Kd be defined as k-off/k-on? (Kd will be the ratio of a first-order rate constant (k-off) divided by a second-order rate constant (k-on), giving overall dimensions of concentration. For example:  time^(-1)/( conc^(-1) time^(-1)), giving 1/conc^(-1), which is just conc


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How were the synaptic areas identified in the somatic sensation pathways?
I'm studying the somatic sensation pathways in neuro-anatomy and I was wondering what was the experimental procedure for identifying the number and location of the synapses in these pathways? Additionally, how were they known to not branch anywhere? Did they use dyes or green fluorescent protein? These are the only visualization techniques I know.

Check out the work of Denny-Brown in humans.  I suspect this work that you describe was done much earlier, but you may be able to follow some of the references backwards from him.


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Is this claim about equine anatomy true?
While bumping through obscure corners of the Internet, I encountered the following image posted somewhere.

The horse anus is a marvel of evolutionary biology.
Like most mammals, rhythmic contractions of the bowels move the feces up to the end of the gut to be expelled.
What sets the horse anus apart is the bafflingly complex autonomic contractive motion of 4 muscular rings which function like sphinctoral guillotine. As the feces is squeezed out, the rings expand and the
  outermost ring is retracted into an interior skinfold resembling the human foreskin, leaving an interstital tissue fold to open air.
The two inner rings then contract, and push apart, severing the horse feces cleanly, allowing to drop free as the outer ring folds back through the interstital flap, creating a intrinsic wiping motion with the fourth ring as it contracts back into the horses rectum.
This advanced biological mechanism is so effective that many industrial companies have copied Nature's design for self-cleaning viscus liquid dispensers housed within complex machinery.

Quite interesting, but anyone who saw one, recognizes an imageboard post - probably the infamous 4chan, where each page bears the warning: "The stories and information posted here are artistic works of fiction and falsehood. Only a fool would take anything posted here as fact." Accordingly, I'm skeptical. So, a verification please?

Can you please quote them by posting their text as text and not as image. It is hard to read from this image. Also, images are not searcheable and poses trouble to visually impaired people. Also, if the text makes a number of claims, then which one exactly are you willing to question in this post?