text:
Have there been attempts to identify Chomsky's "language mutation" in humans?
I'm not versed in either biology or linguistics so please forgive any naiveties I may commit.
I've learned that Noam Chomsky thinks that language is a result of a single genetic mutation in humans. It would be a mutation allowing the human brain to conceive of natural numbers as I understand. Have there been any (even speculative) attempts by biologists to locate that mutation in the human genome and/or in time? Is it even feasible?

It seems a very simplistic view. After all, spoken language relies on vocalization, which plenty of species have. On the other hand, sign language can be used for communication. There are also other types of non-verbal signaling in humans and other species. So what exactly is language?

@Lubo As far as I know, most linguists agree that no animal apart from humans has been observed to use language. Animal communication lacks certain characteristics they require in a language. I understand that what Chomsky considers the constituent characteristic of language is what he calls recursion.

Please add a link to source your statement of Chomsky's theory. I very much doubt he claimed it was a single mutation. That is very unlikely.

@terdon http://en.wikipedia.org/wiki/Origin_of_language#Approaches That's all I've got. I understand that Chomsky's view is not shared by most scholars.

@ymar Chomsky's linguistic theories are rather mainstream, and have biological implications, as I discuss in my answer. The claim about a single mutation or gene is however a rather singular one, devoid of serious scientific support.

may be helpful https://www.pnas.org/content/104/19/8184

The anthropologist Svante Pääbo is more recently famous for trying to track down the 'language gene'.  There isn't a lot of reference to Chomsky in his work as I've noticed, but it is to me the same intriguing idea.
That being that the chimpanzee and the bonobo have 99+% identical to human genome sequences and we also have data from human variations as well from a few thousand individuals.  Using this data you could try to evaluate a small list of differences which might have led to the inborn trait human beings have to acquire language.
Pääbo's work focused on FOXP2, which leads to language disorders in humans when it is damaged in human beings.  On the other hand its also known that primates can learn to speak rather well if they are trained their entire lives by the right people.  They can even reflect on abstract ideas such as life after death.  This is a typical result when looking for a single gene that causes something- it rarely leads to a conclusive result as a phenotype like verbality, or even height or body mass is the result of the action and fine tuning of many genes acting in concert.
That is, if you introduced human FoxP2 into transgenic chimps its unlikely that they would be as verbal as human beings.  This current reference for instance talks about how important the slower development rate for human children is.  This is one of the most unusual thing about human beings - it takes 1/3 to 1/5 of the human lifetime before we are fully mature.  This phenotype is incredibly unlikely to be the result of FoxP2 alone, or any single gene.
There has been recent work published (2012) where the unique human FOXP2 gene was put into transgenic mice.  They seem to have different sort of personality tendencies and are said to vocalize differently - brain activity profiles are also different.  Kinda exciting, but not the Secret of NIMH yet....

Thanks a lot! As for "rather well", that strongly depends on the expectations. If you watch Koko on Youtube (and there are plenty of videos), you can indeed see many surprisingly human-like behaviors, but I was disappointed but her "language" personally. Her trainer was very clearly not objective. When Koko said the wrong thing, she'd say things like, "Why are you joking Koko?" and repeat that until Koko said what she was expected to say. Koko was largely unaware of syntax -- word order was random.

@ymar yes well - Koko and any other animal (including parrots) trained to cognate can't seem to get past 3-5 year old level.  Another question that never seems to resolve.

To my knowledge, Chomsky does not claim that there is a specific gene or mutation responsible for the human linguistic abilities - at least not in strictly biological sense. The claims of Chomsky and his followers, known as generative grammar, are more general: the study and the comparison of many human languages have shown that all the languages are structured according to the same principles (as opposed to the earlier Sapir-Whorf hypothesis that languages are products of purely random evolution). This similarity is the basis for the Chomsky's claim that this language structure is likely hard-coded in the human brain. This is further supported by mathematical complexity arguments, showing that the language rules are too complex, and the variety of the possible phrases that one can produce is too large to be learned within a reasonable time, without having a prior model of how the langauge is structured.
Thus, the linguistic ability, like many other traits, is likely a result of many mutations and action (and interaction) of many genes. Note that this involves not only the mental abilities, but also purely physical capacity to produce wide range of sounds that many animals do not possess.
Remark: Noam Chomsky is a renowned mathematical linguist, chose theories of generative/transformational grammar are pretty much the basis of the modern mainstream linguistics, and play an important role in the modern computer science. Thus, these are not to be dismissed, unlike his more controversial political views, which are anything but mainstream.

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


text:
How long can a unicellular organism live without nutrition? What happens after that? Does it depend on the domain?
Say I have three unicellular organisms: a eukariote, a bacterium and an archaeon. If I cut off nutrition from them at the same time, how long will it take for them to die? What will their death look like, and do they actually need to die? If so, why?

This is very dependent on the organism within each of the groups you mention. While for the most part, archea are the extremophiles and have the ability to withstand many extreme conditions, nutrient limitation survival greatly varies. I think you could easily find organisms in each group that could withstand nutrient limitation well.
A good example would be yeast, which is a single celled organism you may have actually worked with. If you take laboratory yeast, in their diploid state, and starve them, they will undergo meiosis, and in their spore form, live for a very very long time without nutrients, protected by their ascus (which is actual their dead mother cell).
Yeast can also completely desiccate and still live. When you pick up an active yeast packet for baking, those yeast have not only been starved, but have been completely sucked dry of their water. Yet when you add water back, they live (though a great number of them will die).
I think in general, most single celled organisms have a certain tolerance for low nutrient conditions. This does happen to them a lot. All it means is they slow their cell cycle down, stop dividing, and just undergo a caution period. There is all sorts of signaling in the cells that sense the nutrients, and slow growth based on their conditions.

Thank you. But why will they (some of them?) eventually die?

Why will they die? That's kind of difficult to answer. There are some hypotheses that unicellular organisms to a certain extent have multicellular characteristics. And this includes the ability to altruistically die for the benefit of the rest of the colony or species. By dying they would free up the limited resources, as well as allow their own proteins and cellular components to be taken up. Others believe it is just random, and some cells live a bit longer making them able to take advantage of what I said above, making the death in no way planned or organized.

I'm planning to ask about cell death later. But I would like to know what it is that actually kills those cells that don't commit suicide. Is it just random damage, or is there something else? And is there a criterion that allows to pronounce a cell dead as we can do with humans?

source: Stack Exchange

license: Creative Commons - Attribution Share-Alike - https://creativecommons.org/licenses/by-sa/3.0/

sort: votes


text:
What kind of fruit is this?

Just spotted this fruit while walking to school. It's the size of a small coin.The taste is almost sour and tangy and somewhat sweet (I only tried one of them and very little of it).  I admit, I've never seen it before. Does anyone know what this is?
Update: Location is two or three blocks north of UC Berkeley (Berkley, CA, USA).

It's probably Arbutus unedo, strawberry tree. Native to Mediterranean region and some part of western Ireland.
Edit: I've just spot that you found it in California, so it's probably one of north american Arbutus species, eg. Arbutus menziesii.

Awesome! Thanks so much. Now I'll eat the rest of them without fearing dying.

@darksky I've never eaten this kind of fruits so please don't blame me nor the SE community if they appear not edible.

Yes it is Arbutus Unedo. We have several in the garden. In Spain it is called a Madroño. The fruits are edible, but they don't taste that great. They are not very sweet and can have a mushy texture. Use them to make jams.

all_licenses: Creative Commons - Attribution Share-Alike - https://creativecommons.org/licenses/by-sa/3.0/


text:
How do trees use Adhesion and Cohesion to move water against gravity?
I have an AP Bio class where I have to name 3 properties of water and I chose adhesion and cohesion for one of them. I'm having trouble finding out how exactly trees use adhesion and cohesion to move water. There is a lot of different answers out there on the net. How do trees use adhesion and cohesion to move water against gravity?

In high school, we did an experiment that showed this.
Basically, if you take a glass of water, and let it sit out, perhaps in front of an open window, it will eventually lose water due to evaporation. It may take a few days/weeks to really see a large difference, but the level will go down. But, if you take a few flexible straws, put them in so the bendy part is submerged, the water level will drop much more quickly. (I'm not exactly sure if the bendy straw part is really that important here. Logically, I don't think it is, but I haven't done the experiment so I can't really say.)
The reason the straws cause evaporation to happen more quickly is because as wind blows across the top of the straws, it pulls some of the water with it. And because, as the last person said, of cohesion and adhesion, the column of water is pulled up with it and thus it evaporates faster.
Similarly, these fluid mechanics are why toilets and siphoning work. When you siphon, you create a low pressure area inside the tube, like you are sucking out of a straw. Because of this low pressure, liquid is pulled into the tube. If you fill the tube with liquid, and turn the tube down toward the ground so the liquid starts coming out the end, the force of the liquid coming out of the tube creates low pressure in the tube again, thus causing more liquid to be sucked up.
This is very similar to how trees work. In the stomata, or the pores in the leaves that allow the leaves to "breathe," wind helps to pull the water out of the pores. But because of the decrease in pressure cause by the liquid being sucked out of the pore, water gets pulled up the tubes in the tree (xylem).

The mechanism is called "capillary action". It requires a tube of a small diameter and happens because of the adhesion of water to the walls and the cohesion within the water (=surface tension).

Its important to add that the driving force for the actual water movement is the gradient in water potential in the system (atmosphere is dry, while the mesophyll of the leaf is wet). The plant expends no energy to move the water.

I don't buy this explanation. Trees don't have leaves in early spring and water comes up the tree with no problem. Also, if water was put under enough pressure to get sucked up a hundred feet, it would have so much heat that it would become steam. It's why buildings that are super high need pumps every so often to get it to go up.
I have a theory. In a tree you have different parts of the trunk. Heart wood, sap wood, cambium layer, and bark. I think because the heart wood and bark aren't taking up water, they aren't expanding like the sap wood is. The cambium layer is very slippery and let's the tension between the bark and sapwood to slip past each other. I think the expanding sapwood eventually gets squeezed and osmosis does the rest.

have any references to back up the claims you're making?

Trees don't have leaves in early spring and water comes up the tree with no problem you mean "no leaves = no gravity". buildings that are super high need pumps every so often to get it to go up so pumps don't use pressure to push water. Welcome to Biology.SE, but you seriously need references

Trees don’t use either adhesion or cohesion to move water against gravity.
It is impossible to “suck” above 10.3 m, which is equal to our atmospheric pressure.
Air Pressure is pushing up the xylem Micro-tubes - which have a lower pressure / vacuum at the top (created be evaporation from the leaf).
This “siphon effect” is powered by Air Pressure, pushing up a closed tube.

It has to do with heat transfer and Newton's Law of thermodynamics.  Matter that is heated will always travel to a cooler location.  The roots are like a sponge, soaking up water from the ground.  The water moving through the capillaries causes friction = heat,  These heated water molecules collide with carbon atoms and form CO2, which is expelled trough the leaves in summer, but is negligible in winter.

I somehow discovered that in some trees with thin bark, I could place my ear on the bark and hear the movement of the water in the tree.  It was not a continuous flow, but with hesitations like spurts or pauses.  I thought there might be a valve system to keep the water from coming back down.  But by saying it was pulled up by evaporation from the leaves, I can't explain the pauses.

Hello Martha. Welcome to [biology.se]. Your answer is not really addressing the asked question. Even if it did, your answer is based more on personal experience and not validated facts. You can [edit] your answer so that it provides relevant points that address the question or else it would be deleted.


text:
Isotype control antibodies in Flow Cytometry
In a Flow Cytrometry, one can add an Isotype Control Antibody to allow another antibody to bind more specific to the cells.
My question is, how can the Isotype Control Antibody add specificity to the other antibody?
My thought was, that the Isotype Control Antibody binds to all the antibody receptors, but with a "weak" binding. When the other antibody (e.g. CD73) tries to bind, it can make a stronger binding with the CD73 antibody receptor, kicking the Isotype Control Antibody off it.
However i'm entirely not sure this is correct... Could anyone explain how the Isotype Control Antibody helps the other antibody (eg.g CD 73) to bind more specific?

I don't believe that the Isotype Control Antibody makes the antibody bind more specifically but rather ensures that your signal is specific to your antibody.
The Isotype Control Antibodies tend to bind to the non-binding domain of the antibody, typically the constant (Fc) domain. By measuring the concentration of the control antibody, you can determine what percentage of your light signal comes from your primary antibody and not from non-specific binders to your light source.
This is very similar to having secondary antibodies in your assay.
Random link showing that I'm not making stuff up

This is correct. It adds credibility that your experimental primary antibody is actually binding what you think it binds.

While bobthejoe/leonardo's answers are correct, you also need to be aware of the quality and limitations of isotype controls. You need to pick your source very carefully, as extensive testing (at my former company) has shown that some isotypes stick non-specifically under certain conditions or with certain samples. For example, we found that one common isotype from a major manufacturer (I don't remember who, it might have been Jackson) stuck non-specifically to HeLa cells by immunofluorescence and flow cytometry (the chemistry in the two assays is very similar) when used with common IF and FC protocols. You should also run no-antibody and secondary-only controls to ensure that your samples are not auto-fluorescing and that the secondary antibody is not binding non-specifically to your sample. Finally, ensure that the control exactly matches the isotype of your primary - don't use a rabbit polyclonal isotype to control for a rabbit mono, don't mix IgG subtypes, etc. Good luck!


text:
What Defines a Food as Edible?
With many foods today containing chemicals, agents and preservatives etc... What biological criteria must a new food and its constituent components satisfy biologically, to be defined as edible?
For example do they look at the chronic/acute affects of chemicals in the body?
This question is just limited to chemicals, if a new fruit was discovered, how would it be decided if it was edible or not?

As far as I know, edibility (wow, I'm surprised that passes the spell checker!) is not a strictly defined term, biologically or otherwise. Humans have been around eating and drinking stuff long before the scientific method was around to study this question rigorously, and before there were regulatory agencies charged with approving new products as "safe." As one might imagine, knowledge of what is and is not edible was likely passed down by oral tradition and personal experience.
Honestly, I'm not even sure designating a food (or a substance) as edible or inedible really makes much sense. Let's consider wild fruit, as mentioned in your question. If ingesting 5 or more berries of hypothetical fruit X causes your body to have a nasty reaction, then we could probably agree that fruit X is toxic and inedible (even if eating only 1 or 2 berries might not elicit the same reaction). On the other hand, ingesting berries of hypothetical fruit Y causes no reaction unless consumed in much larger quantities (maybe 100 or more berries). Although fruit Y does cause a reaction when ingested in excessive amounts, it would be a stretch to call it inedible. This principle applies to many foods that we typically consider edible but can be unhealthy or even dangerous when taken in excess.
So where do we draw the line? How much of a substance do you have to ingest without an adverse reaction to deem it edible? I don't think there is an objective answer to this question. It is complicated further by the vast amounts of variation in the human population: food allergies, differences in tolerance to certain substances, etc.

+1: it has to be noted, though, that there is a very big difference between edibility and suitable for human consumption, where the second one is simply defined according to local regulation. A food that is suitable for human consumption for instance in Europe may not be suitable for human consumption in the US and vice versa (and many examples of this exist)

@nico Indeed. But whatever any arbitrary group (government, social organization, etc) decides to term as "suitable" does nothing to change the underlying biology, which was the original question (and should be considering the scope of this site). One would expect and hope that such policy decisions be based on the underlying biology...

surely I totally agree although, alas, these laws are seldom made by listening to scientist...

Much like Daniel Standage suggests, I think "edible" is more inferried than defined, sort of like looking at a black hole - its absence is defined by the activity around it. Human bodies are capable of metabolizing lots of compounds that become poisonous pass some threshold.
In medical terms there are LDmin and MLD and LD50: miminum Lethal Dose, Median Lethal Dose, Lethal Dose for 50% of the Population respectively.
There are also compounds that aren't lethal, but are definitely harmful. Trans-Fats are one, where the FDA hasn't determined any safe levels of Trans-Fats in foods; they're always dangerous and harm your system.
Then there are materials or chemicals that will simply pass through your system without being absorbed or interferring with anything. Cellulose (refined wood pulp) is a popular additive in pre-made diet foods because it adds mass and texture while being completely indigestable since humans do not produce cellulase. The same can be said for silicone dioxide (sand), which is also very unreactive and passes through your digestive system benignly.
So I'd say as long as whatever is eaten is below the LDmin and/or can benignly pass through your system without damage, it is 'edible.'

+1 And since LDmin and related values must be tested a verified for each substance individually, it is clear why a concrete definition for "edible" is elusive.

Definitely. :-)

This is more a legal question, so I'll quote from what is lex in the EU:
Regulation (EC) No 178/2002 of the European Parliament and of the Council of 28 January 2002 laying down the general principles and requirements of food law, establishing the European Food Safety Authority and laying down procedures in matters of food safety

Article 2
Definition of "food"
For the purposes of this Regulation, "food" (or "foodstuff") means any
  substance or product, whether processed, partially processed or
  unprocessed, intended to be, or reasonably expected to be ingested by
  humans.
"Food" includes drink, chewing gum and any substance, including water,
  intentionally incorporated into the food during its manufacture,
  preparation or treatment. It includes water after the point of
  compliance as defined in Article 6 of Directive 98/83/EC and without
  prejudice to the requirements of Directives 80/778/EEC and 98/83/EC.
"Food" shall not include:
(a) feed;
(b) live animals unless they are prepared for placing on the market
  for human consumption;
(c) plants prior to harvesting;
(d) medicinal products within the meaning of Council Directives
  65/65/EEC(21) and 92/73/EEC(22);
(e) cosmetics within the meaning of Council Directive 76/768/EEC(23);
(f) tobacco and tobacco products within the meaning of Council
  Directive 89/622/EEC(24);
(g) narcotic or psychotropic substances within the meaning of the
  United Nations Single Convention on Narcotic Drugs, 1961, and the
  United Nations Convention on Psychotropic Substances, 1971;
(h) residues and contaminants.

http://eur-lex.europa.eu/LexUriServ/LexUriServ.do?uri=CELEX:32002R0178:EN:NOT

So if we rely on the legal definition (well, that in Europe at least), then "reasonably expected to be ingested by humans" is about as much detail as we're going to get.

Indeed, but I tried to answer the intended question (as perceived by me, mind you) rather than the "edible definition" part. Anyway, the OP should probably look up "food safety" in the Wikipedia.


text:
Do antibiotics attenuate immune response on subsequent exposure to same bacteria?
A healthy immune response to a bacterial infection includes "memory" to permit the body to thwart subsequent exposure to same bacteria.  What are the dynamics of using antibiotics on initial exposure to the bacteria regarding a possible degradation of the quality of this "memory" and thus the body's possibly compromised ability to fight a repeat exposure to same bacteria ?
I am not speaking of vaccines ... focus here is on bacteria

A quick search on ISI Web of Knowledge yielded this paper:

R J North, P A Berche and M F Newborg (1981) Immunologic consequences of antibiotic-induced abridgement of bacterial infection: effect on generation and loss of protective T cells and level of immunologic memory. Journal of Immunology 127: 342-346

The authors investigated the effects of ampicillin treatement in mice infected with Listeria monocytogenes. They reported an abridgement of T cell-mediated antibacterial immunity and in particular an effect upon the development of memory:

Moreover, Ampicillin-induced abridgement of infection, either before or at the time of peak primary response, resulted in the expression of greatly reduced levels of immunologic memory at a later time. This indicates that memory cells are generated throughout the entire course of the primary anti-Listeria response, including the period of its decay.

Presumably any treatment that reduces the need for an immune response will have an effect upon the production of useful memory T cells.

It is also conceivable that the increased presence of the interior (cytosol) and cell wall parts of dead or dying bacteria will cause an enlarged adapted immunity response. I remember that EHEC patients were specifically not treated with antibiotics from fear of freeing more toxins from dead bacteria.

Edited for Clarity:
In order to invoke a memory response or create a memory response, there must be interaction with the Adaptive Immune System (usually CD40+ "Helper" T-Cells), and the interaction must come in the form of a protein since the MHC receptors only respond to proteins.
Antibiotics are usually smaller macromolecules that directly cause slower growth or kill the microbe. They will *not* create or illicit a memory response because they are not presented to the immune system to initiate the proper procedure, and may not be proteins and unable to be presented in the first place.
If you're asking about vaccines (which was my inference before the edit), then they stimulate what is basically the same memory creation mechanisms that normal infections do. Antibody counterparts recognized by B-Cells are paired with proteins from the disease you want to immunize against, called the Hapten and Carrier respectively. Then the protein is processed via the B-Cells, presented to T-Cells, and a memory response is made.
My apologies if the previous answer was more ambiguous.

I am sorry, but are you talking about antibiotics or rather vaccines?

Ah, good point. I think my answer had more to do with vaccines. I'll clarify it.

@MCM That makes a lot more sense, reversed my downvote.  I think the OP (and myself) was also interested in whether there is a reduced production of memory cells in an infection treated with antibiotics rather than one that was not (as opposed to a memory of the antibiotic itself).

For Antibiotics, I'm not aware of any change in the Adaptive response. Some vaccines don't have quite the same long-lasting memory response as having to fend off the infection naturally (though I've not been explained why), but can still last for years or decades. If someone else is more aware than I am, feel free to answer - I've only taken the basic courses thus far.

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


text:
What phenotypes can arise from gender-related aneuploidy?
Humans normally have 46 chromosomes (two copies - one from each parent - of each of the 24 chromosomes: [1:22] + [XX or XY]).
Aneuploidy is an abnormal number of chromosomes - Down's syndromes is an example of this, where individuals have an additional copy of chromosome 21.
I have read a little about gender-related aneuploidy, where individuals can have additional sex-specific chromosomes (for example XXY).
I was wondering what (roughly) the prevalence of the different combinations are, what the specific phenotypes are, and what (if any) medical complications can arise from these combinations, or indeed, what advantages could be conferred by the additional chromosome!

47,XXX
47,XXY
47,XYY

My question also stretches to whether the different combinations display a hermaphroditic phenotype?

Note that anyone with a Y chromosome is considered a genetic male. Also, aneuploidy is usually a result of nondisjunction (but can have other causes as well) and is usually not inherited.

47,XXX is called Triple X syndrome and occurs in approximately 1 in 1,000 female births. These individuals usually appear normal, but may have tall stature, a small head, and delayed development. According to this case report, the tall stature is possibly due to SHOX gene triplication, in some cases. The short stature homeobox gene (SHOX) gene is a gene on the X and Y chromosome and is associated with short stature if a copy of the gene is missing or mutated. The case report states, "The enhancing effect of SHOX gene triplication on growth was ascribed to the concomitant absence of gonadal steroids in cases of gonadal dysgenesis, allowing a prolonged period of growth."
47,XXY is called Klinefelter's syndrome. Here is an image/diagram of symptoms. These people may have gynecomastia (enlarged breasts), less muscle, less body hair, and hypogonadism (decreased testicular function, also resulting in smaller testicles and penis) due to lower testosterone production. These symptoms become more obvious after puberty, because individuals with Klinefelter's have less "masculinization" (for lack of a better word). Cognitive problems are usually present. It occurs in roughly 1 in 500 to 1 in 1,000 male births.
47,XYY is XYY syndrome and has an incidence of 1 in 1,000 male births. They appear normal but may be slightly taller than average. This study looked at the cognitive and motor phenotypes of boys with Klinefelter's and XYY syndromes. It found that both groups have generalized cognitive impairment, but XYY has more profound language impairment and Klinefelter's has more significant motor impairment. Their hypothesis is that "the more severe language-based cognitive phenotype in XYY versus KS is likely to be genetically determined on the basis of abnormal dosage of specific Y chromosome genes, but not abnormal levels of testosterone because XYY is not associated with testicular failure."

There's also 45, X0 (Turner syndrome), in which girls have a webbed neck,  broad chest, low-set ears, short stature, gonadal dysfunction, and often other conditions such as a bicuspid aortic valve, coarctation of the aorta, and vision problems. Image of symptoms. It occurs in 1 in 2,000 live births. Individuals usually have 1 X chromosome, but may also have 2 X chromosomes, with 1 of them being incomplete (source). The single copy of the SHOX gene (mentioned above) has been linked to the short stature in Turner syndrome.
Interestingly, people with 47,XYY and 47,XXX people often have normal fertility, but not in the other two cases. My uneducated guess is that the extra "normal" chromosome (for the person's sex) doesn't disrupt gonadal function.

Interesting that 47,XXX and 47,XYY both display a 'tall' phenotype, but otherwise appear normal. Any idea why this might be? You mention that 47,XXY individuals are defined as male due to the presence of the Y, but do they display feminine traits other than enlarged breasts? And what cognitive problems might occur? The more detail the better - had hoped for more than just wiki links :) Thanks

I added a little more detail. I'm not sure how 47, XXX individuals are taller, but I can see that the extra Y in 47, XYY individuals make them more masculine. Just a guess though. I'll see if I can find more info about how these disorders cause their cognitive and developmental effects.

@Luke Tried to answer some of your questions in the edits. I'm not sure about the cognitive problems though :( I hope someone else can add to it.


text:
Predicting and identifying microbes and enzymes DNA sequence with metabolic prediction
Presently I am working on metagenomics of coal biomethenation by bacterial consortium.
I have got the sequence result (Illumina). The sequence is huge and I can't predict anything from the sequence.
I have gone through different database like Metacyc, Biocyc etc.
Please help me that how can I draw an inference towards the metabolic enzyme that are involved in biomethenation of coal.

The first step after sequencing is finding probable genes. After that, genes and their proteins can be classified to belong to protein classes. This is the most what you can do with completely unknown genes. It's possible nowadays to predict the final structure using contact maps (if there is no homologous structure known) but this will still leave you unclear on ligands in many cases. So, the final step is to clarify the function with biochemical lab methods.
So, if you are stuck with a huge sequence, first try to find the genes in it.
http://en.wikipedia.org/wiki/Gene_prediction
For subsequent annotation/classification, I recommend InterPro and PROSITE.
http://www.ebi.ac.uk/Tools/pfa/iprscan/
http://prosite.expasy.org/scanprosite/

Well first off, we don't know how you sequenced the data. What did you actually sequence? Did you look at transcriptional activity using RNA-seq or did you do a full genome sequencing. Were there any paired-end reads? How did you create your library? Did you enrich the bacterial consortium for biomethanation activity?
Where do you reads map? The consortium complicates things but you will likely need to build a quality contig library before you do anything else. Without a doubt, much of your library will not map to anything interesting but you should still annotate the library by seeing where the reads map up. Identifying ORFs will be useful.
Likely, you will have a set of genes that will be involved with biomethanation. You should BLAST the bejesus out of your contig library for hits. Do they match any of your ORFs? Going the otherway, do your ORFs match any of the genes in EcoCyc or BioCyc. Do you need to use a larger database?


text:
Cheapest way to measure S. aureus and Rhinoviruses density at home
I would like to measure the surface density of Staphylococcus bacteria and Rhinoviruses (only those two, to be specific) within my home.  What's the cheapest way?
The textbook procedure is to:

rub a clean wet cotton swab on the surface in a controlled way
dip the swab into a clean agar (or some living media to detect viruses?) dish
incubate the dish
"look for genetic patterns from special enzyme reactions".

Is it possible to do the last step at home?  Or, is there some easier way if I only care about Staphylococcus bacteria or Rhinoviruses?

What sort of budget do you have in mind? A quick Google using the search terms "Staphylococcus home test kit" returns many kits, the top hit costs $64. There are bound to be other kits that can detect other pathogens.

Maybe $500 for 100 samples.  That $64 basically gets you a swab and envelope for one sample, so it sounds expensive (and doesn't include Rhinovirus).

Use care if you incubate at home - some bacteria in small quantity are low risk however, if you happen to incubate a contagin to colony size it could be dangerous indeed.  I saw this first hand with a fellow student who had recently recovered from a pneumonia bout - we had MASSIVE quantities of those and went straight to the lab steralization phase upon discovery.

For anyone getting ideas
S. aureus and Rhinovirus are risk class 2 infectious substances that should only be handled in a BSL or containment level 2 environment. Your only feasible step here is swab, seal, and send to a lab that can handle it.

There are some kits available to detect the presence of S. aureus on surfaces using agglutination factors like This one. These kits tends to be worth 70$+ though and they do not in any way quantify, only detect.
To have quantity results you would need to respect a protocol for swabbing a specific area and then have a lab do the testing for isolation and quantification of Staph.
Rhinoviruses on the other hand need more advanced techniques to detect and quantify, like PCR, and for this you need lab equipement which are costly.
There is always ways to send samples to labs for them to test but this is a costly solution.


text:
Evolutionarily speaking, why do humans have 46 chromosomes
In humans, each cell normally contains 23 pairs of chromosomes, for a total of 46. Monkeys, chimpanzees, and Apes have 24 pairs (twenty-four pairs), for a total of 48.
What caused humans to have 46?
EDIT:
@TomD is right, I was asking why we have one less chromosome pair than chimpanzees (for example) [23 pairs instead of 24].

I seriously doubt there was any selection on the number of chromosomes. It just happens that we have 23 pairs.

For info, all apes are known to have 48 (total), but monkeys vary (e.g. Rhesus monkeys have 42, but Capuchin monkeys have 54!). See the wiki list of chromosome counts here.

@nico Sure, but there was certainly (some) selection on conserving the number. Normally, large-scale mutations such as chromosome fusions are immediately fatal and even when they are not they potentially prevent procreation with individuals which don’t have that mutation. So at least superficially there should be quite strong selective pressure to preserve ploidy.

@Konrad Rudolph: but you are not selecting for the number of chromosomes, just for a configuration "that works".

@nico Sure. What I meant was: given that our close ancestors had a different number of chromosomes, when/why did it change? That’s an interesting question, and essentially what OP is asking.

@Konrad Rudolph: surely. It's just the question seemed to imply that a specific change in number had a particular significance, rather than being a side effect of something else that probably did have a particular significance. Semantics.

I think the OP is asking why we have one less chromosome pair than chimpanzees (for example) [23 pairs instead of 24].
The is an abundance of evidence, as alluded to above by shigeta, that human chromosome 2 is the result of a telomere-to-telomere fusion of two ancestral chromosomes (IJdo et al., 1991).  This event did not occur in our closest ancestors, hence we have one less chromosome pair.  In fact the sequence of human chromosome 2 contains the relic of an ancestral telomere-telomere fusion (IJdo et al., 1991).
The pdf of this key reference is freely available to all from PNAS
Reference
IJdo, J.W, Baldini, A, Ward, D.C, Reeders, S.T, Wells, R.A. (1991) Origin of human chromosome 2: an ancestral telomere-telomere fusion  Proc Natl Acad Sci U S A., 88 9051-9055.[pdf]
Actually it has now been shown that Neanderthals and Denisovans also exhibit the same chromosomal fusion as humans - http://m.motherjones.com/politics/2014/02/evolution-creationism-bonobos-neanderthals-denisovans-chromosome-two

This is a good Youtube video that discusses this, in the context of evidence for evolution. It's from a presentation given by Ken Miller about the Dover "intelligent design" trial. The whole presentation is here.

It seems to me this answers the 'how' question but not the 'why' question. I would guess the answer to 'why' is random chance but there could be a selective advantage? Is there any evidence either way?

@JackAidley It doesn't seem there is. Change in chromosome count cuts you off from sexual reproduction (unless you're self-fertilizing). It's an isolation from others of your (previous) species - in effect, if some population happens to undergo a change like this, they are guaranteed to form a new species. But that's not really a selection pressure - it's observaton bias; we see different chromosome counts in different species because they inevitably cause you to become a new species (dead or living). It's like a river forming between two populations of your species, a genetic rift.

@nico is right.  the number of chromosomes is the result of an evolutionary timeline, puncutated by sometimes spontaneous events which shape the DNA.
These events occur in the course of evolution:
1) Chromosomal rearrangements.  Large sections of the genome can flip around or become integrated in other chromosomes.  By homologous recombination, regions of the genome can clip themselves out or duplicate themselves as well.  If you look at the alignment of human to say chimp, there are many segments that move relative to each other.
2) chromosomal breaking or combination.  Two smaller chromosomes may combine to form a larger one, or a larger one may break into two smaller chromosomes.  An example of this is human chromosome 2, which is found as two smaller chromosomes in the great apes (see figure in wikipedia).  We infer that this is a combination event exclusive to humans by comparing the other apes on the evolutionary tree.  Birds and reptiles tend to have lots of chromosomal breakage, even to the point  where the number of microchromosomes (less than 20 million bases).  Mammals tend to be more conservative and not allow viable chromosomal breaks - chickens have 78 chromosomes to our 23..
3) idiomatic chromosomal behavior.  Sex determining chromosomes are examples of chromosomes where a pair becomes distinctly different in size and composition.
Another example is in trypanosome which has many tiny DNA segments which code for variant surface coat proteins.
4) @rwst points, what I clean forgot, that occasionally (like maybe just a few times) there have been whole genome duplications.  This can be identified by chromosomal alignments within a single genome and has not happened very often since we became eukaryotic metazoans.  Not sure how many times, but perhaps just once or twice in our lineage.  If anyone knows about animals/humans that would be great. As you can see the link shows whole genome duplications in plants, which don't seem care how many chromosomes there are.  Plants have polyploidy, you see, so such duplication events are much better tolerated.  On the other hand plants can't play video games.
P. Dehal, J. L. Boore: Two rounds of whole genome duplication in the ancestral vertebrate. In: PLoS biology. 3, 10, Oct 2005, e314, doi:10.1371/journal.pbio.0030314. PMID 16128622. PMC 1197285.
You can see that these events happen at particular moments and help shape the species and the composition of the chromosomes.  It is not a priori possible to predict the number or type of chromosomes just by looking at an animal, but only by looking at the related animals.
Fungi and Plants have even more variations in chromosomal composition than animals.

Also, I think it is important to note that a certain mutation in chromosome number may, indeed, be selected, because it is associated to some other advantageous phenotype. The change in chromosome number will then also be selected, but only as a "side effect".

segmental rearrangements that might reflect a change in the chromosomal structure can change the phenotypes and organismal behavior quite a bit.  its a significant factor in the evolution of bacteria.

@shigeta: you missed whole genome duplication (WGD) --- okay the OP didn't ask that

@rwst - no that's a good point.  It should be in here. added with an attribution

added a reference. I would expect more information with more pre-vertebrate genomes sequenced

thanks - I remember reading about a complete genome duplication event known from the mouse genome paper, but was not exactly sure where I read it.

Here is a paper you might want to take a look at:
Phylogenetic Origin of Human Chromosomes 7, 16, and 19 and their Homologs in Placental Mammals
From the abstract:

From their origin, these chromosomes underwent the following rearrangements to give rise to current human chromosomes: centromeric fission of the two submetacentrics in ancestors of all primates (∼80 million years ago); fusion of the HSA19p and HSA19q sequences, originating the current HSA19, in ancestors of all simians (∼55 million years ago); fusions of the HSA16p and HSA16q sequences, originating the current HSA16 and the two components of HSA7 before the separation of Cercopithecoids and Hominoids (∼35 million years ago); and finally, pericentric and paracentric inversions of the homologs to HSA7 after the divergence of orangutan and gorilla, respectively. Thus, compared with HSA16 and HSA19, HSA7 is a fairly recent chromosome shared by man and chimpanzee only.

the citation doesn't account for vertebrate (and earlier) whole genome duplication (WGD) events --- okay the OP didn't ask that

Evolutionarily speaking, why do humans have 46 chromosomes

This is a question of why human have 10 fingers. There is nothing magical about 10 fingers and nothing magical about having 46 chromosomes. In fact there are people who have 44 chromosomes. The are normal people. They have normal fertility. However if the children with people of 46 chr, the fertility of their children (ie people with 45 chr) is reduce. Normal fertility can only be maintained by marrying other people with 44chr... who probably are their cousins.
http://genetics.thetech.org/original_news/news124
So the reason we have 46 chromosome is because we are descended from a homonid species which had 46. No reason really. Not everything produced by evolution has a purpose.

This is being discussed in more detail at https://biology.stackexchange.com/questions/1051/can-two-humans-with-44-chromosomes-produce-viable-offspring


text:
Is vision a vestigial sense for deep ocean species?
Sunlight doesn't penetrate beyond a couple of hundred feet from the surface of the ocean. Species that exist at greater depth probably live in a state of perpetual night; yet from a quick google image search (i agree it isn't a very authoritative source) for deep ocean species I see that plenty of these have eyes.
So ...

Are the sight organs in deep oceans species merely a remnant from an earlier era?
If they are a remnant, has evolution/mutation modified these organs over time?
Regardless of whether the organs of sight are vestigial organs for deep ocean species, how do the eyeballs withstand the extreme pressure of water in the deeps?

I can't answer your third, but I can answer your first two. With one word, in fact:
Bioluminescence
http://brightnepenthe.blogspot.com/2010/08/palate-cleanser-90.html

That's the deep ocean at night for ya. Unlike underground environments and caves, it's not pitch black pretty much anywhere in the ocean. There are things to see everywhere, and they play an important role in predator/prey relationships and/or mating. The absence of natural light does make things harder to see, but that's why you see the enormous eyes on species which live far down. So, nope! The eyes on deep ocean critters are not vestigial. They're very functional (and, if anything, probably increased in sensitivity).
The basics are summed up here: http://www.lifesci.ucsb.edu/~biolum/functions.html

The answer provided by @MCM contains an important chunk of information (Bioluminescence!) but it does not answer the question entirely. First, let's correct a misunderstanding in the question.
Sunlight does penetrate beyond 200m in the ocean. The intensity is not enough for photosynthesis to occur (and thus no phytoplankton below 200m) but depths between 200-1000m can receive enough sunlight for vision.
The region between 200-1000m is called the mesopelagic. Because there is enough light for vision, many mesopelagic species have eyes to see. Because light is extremely dim (humans would not be able to see), mesopelagic species tend to have very large eyes to gather as much light as possible. Vision is very important to mesopelagic species.
Below 1000m, we reach the bathypelagic (and, continuing deeper, the abyssopelagic and hadopelagic). Here, light penetration is insufficient for vision. Below 1000m is pitch black. In the bathypelagic (and deeper), you tend to see a reduction of eye size and sometimes a complete loss of eyes. Bioluminescence is still present (although much more common in mesopelagic fishes) but much less important. The physiological cost of producing and maintaining eyes is energetically expensive, so most species that live below 1000m have very weak eyes, if they have them at all.
Because the eyes of bathypelagic (and deeper) species still serve their original function, I would say the eyes of deep-sea organisms are not vestigial, in the sense of having completely lost their original function or serving a new function.


text:
Making penicillin using animals - specifically, a goat
In the scifi novel Lucifer's Hammer, one of the characters (a biologist, if I remember correctly) finds himself in a post-apocalyptic world and tries to make penicillin to save his own life. To do this, he repeatedly states that he needs "a goat" - for some reason which is never explained.
I know that penicillin (in its various forms) is a byproduct of some types of fungi (see Wikipedia), but I can't make sense of the statement "I need a goat to make it". Assuming you don't have a chemical lab at your disposal (think "post-apocalyptic world"), does this requirement make any sense to any of you (apart from "I need to eat the goat to stay alive long enough to find a deserted biochemical lab" :-) )?
If not, how would you go about finding or making penicillin in such an environment?

Here is a link to a survivalist blog with a protocol for making penicillin. (I'm not recommending this by the way.)
Is it possible that the reference to the goat in Lucifer's Hammer is for the extraction of insulin (from the pancreas)? Have a look at the Wikipedia entry for Eva Saxl - in Shanghai during WWII her husband kept her alive with insulin extracted from water buffalo pancreas.

I'm kind of lost... what does insulin have to do with penicillin?

I gather from my research that the post-apocalyptic manufacture of insulin is a plot element in the novel - just thought the questioner might have mixed things up a little.

ahhh... OK, now it makes sense! :)

Absolutely. I read the novel years ago and I did indeed mix up insulin and penicillin. Thank you for this hint, I feel a little stupid now but at least I got two correct answers for one question. :-)

By the way, it would not necessarily need to be a goat, insulin has for many years been extracted from the pancreas of pigs.

True. (Now that I know what to search for, it was rather easy to dig out new sources ...) btw, wouldn't it make sense to change the question now? I tried yesterday but it seems my edit wasn't saved. PS: Thank you!

So - anyone who has read the novel - why is it a goat that is specified?


text:
Non-monotonic knock-out effects in prokaryotes
Typically, when performing gene-knockout, the experimenters select one gene to remove/replace-with-junk and then see if the prokaryote can still undergo fission. If it continues to reproduce then the gene is labeled as non-essential; if the organism cannot reproduce then the gene is labeled as essential; and some-times (if the organism can reproduce but only for a certain number of generations) the gene is labeled as quasi-essential.
Typically, if gene X is essential, and you knock-out both gene X and some other gene Y then the organism still dies; this is an example of monotonic behavior. However, this doesn't always have to be the case, it could be that gene X is essential only in the presence of gene Y (for instance if the two proteins produced are in a delicate feedback loop). Is there examples when knocking out gene X makes the organism nonviable, but knocking out gene X and Y maintains viability? In the most extreme case, is there an example where both gene X and Y are essential, but if both are knocked-out then the organism is still viable? I am primarily interested in simple prokaryotes (an answer for Mycoplasma genitalium or Escherichia coli would be best) but more complicated organisms are preferred over no answer.

Here is an example in which the knockout of a non-essential gene in yeast (Saccharomyces cerevisiae) suppresses the lethal effects of a different knockout.

Amy L. Kistler and Christine Guthrie (2001) Deletion of MUD2, the yeast homolog of U2AF65, can bypass the requirement for Sub2, an essential spliceosomal ATPase. Genes & Development 15:42-49

The SUB2 gene encodes a protein which is a component of the TREX complex required for nuclear mRNA export. Deletion of the SUB2 gene is lethal. The MUD2 gene encodes a non-essential protein involved in pre-mRNA splicing.
The authors show that -

"...the essential requirement for the SUB2 ATPase can be bypassed by deletion of the nonessential splicing factor MUD2..."

Detailed information about these (and all other) Saccharomyces cerevisiae genes is freely available at the Saccharomyces Genome Database


text:
What are the different, high-level programs along which a eukaryotic animal cell can follow?
What are the different, high-level, disjunct (mutually exclusive at one particular point in time) programs or pathways along which a eukaryotic animal cell can follow? Examples of programs would include growth, cell division, senescence and quiescence. Are there programs that differ between cell types?
Any I'm missing? If so, references much appreciated.

Are growth and division separable?: surely they are! Cells may change volume without change in number. Hyperthrophy vs hyperplasia

Ok. Any thing else I've missed?

I'd categorise differentiation as a subtype of division but apart from that seems pretty much complete to me. You may want to add migration to both.

I agree. Updated question accordingly.

Cells may also divide with no growth. This happens during early development.

I'm going to answer my own question with suggestions collected from the comments.
A multipotent stem cell:

Growth

Growth and clonal division
Growth, division and differentiation

Division and no growth

A differentiated cell:

Senescence (irreversible)
Programmed cell death

Apoptosis.
Autophagic cell death.
Necrotic cell death.

Quiescence (reversible)
Growth ==> Immortality (cancer cells)

Growth and division
Growth and no division (endocycles)1

Division and no growth

1:  Norman Zielke, Kerry J. Kim, Vuong Tran, Shusaku T. Shibutani, Maria-Jose Bravo, Sabarish Nagarajan, Monique van Straaten, Brigitte Woods, George von Dassow, Carmen Rottig, Christian F. Lehner, Savraj Grewal, Robert J. Duronio, and Bruce A. Edgar: Control of Drosophila endocycles by E2F and CRL4Cdt2

To see the width of your question, have a look at what the Gene Ontology considers a cellular process:
http://www.ebi.ac.uk/QuickGO/GTerm?id=GO:0009987#term=children
I don't think you can agree on what's high-level, so it's better to see them all, I think. Also, for completeness, there is a list with cell types which is admirably maintained:
http://en.wikipedia.org/wiki/List_of_distinct_cell_types_in_the_adult_human_body

I've revised my question to a search for disjunct, i.e. mutually exclusive (at one particular point in time) classes of program of roughly the same generality. I find GO is very poor on this: often there are terms that are siblings despite describing a much different granularity, e.g. cell cycle process and membrane docking are siblings.

It's just a collection of terms used in the literature, together with associated genes/proteins.


text:
Where can I find the tissue-specific protein expression levels for hTERT (telomerase subunit)?
I find a number of contradictory sources regarding the tissues in which hTERT - the protein - is expressed. Does anybody know some resource that authoritatively (as authoritative or widely-accepted as is possible) lists the various tissues and hTERT's protein expression levels?
Any similar resource for gene expression of hTERT?

I have found that biogps.org has all expression data I need:
https://biogps.org
https://biogps.org/#goto=genereport&id=7015

not heard of this before - just had a bit of a play and it does seem like a great tool!

Thanks but this is only gene expression. I'm talking of protein expression, which by no means correlates to gene expression. It's often assayed by immunohistochemistry with scaling up achieved with tissue microarrays


text:
What is a focal copy number variation?
Often, genetics studies, especially genome wide ones, talk about "focal copy number variations" in genes or regions of the chromosome. I know what a copy number variation is. What does "focal" mean, exactly?
Are there non-focal CNVs? What are they? Where did the term "focal" originate? Is there a specific paper that coined (and hopefully unambiguously defined) the term?
A search for "focal copy number variation" on Google Scholar should turn up plenty of papers about it. The GISTIC algorithm is a popular computational method for finding putative CNVs- so information about this algorithm may have some clues.
A documentation text for one GISTIC implementation on the Broad Institute's website states the following:

(8) Broad or Focal: Identifies whether the region reaches significance due
  primarily to broad events (called “broad”), focal events (called “focal”), or
  independently significant broad and focal events (called “both”).

You could probably even call an aneuploidy (variation in chromosome number) a CNV. So that’s pretty large-scale.

A copy number variation (CNV) is when the number of copies of a particular gene varies from one individual to the next.
From: the NIH Glossary

Focal CNVs are regions of repeated genetic information that only span a small proportion  (<25%) of the chromosome arm (although this does not seem to be a consistent rule), and can contain few genes. CNVs greater than this are termed either 'large-scale' or 'broad'.

Here are some relevant papers I came across (no doubt there are more);
This paper is about a program (VarScan2) the authors have made to robustly detect somatic mutations and CNVs;

To identify SCNAs [somatic copy number alterations], VarScan 2 compares Q20 (base quality >=20) read depths between tumor and normal samples for contiguous regions of coverage ... Therefore, we apply a circular binary segmentation (CBS) algorithm (Seshan and Olshen 2010) to delineate segments by copy number and identify significant change-points. A subsequent joining procedure merged adjacent segments of similar copy number and classified them as either large-scale (>25% of chromosome arm) or focal events.
From: Koboldt D, et al, 2012.

I continued searching, as I wondered whether this was a standard definition, or just one used by the authors.
This paper is reporting bacterial genes that drive focal chromosomal aberrations, but do not give a great definition (as it seem quite arbitrary to me);

Many of these [chromosomal] aberrations concern large chromosomal regions, which makes it difficult to identify actual driver genes. Increased resolution has led to the detection of focal chromosomal aberrations, defined as 3 Mb or smaller in size [5–8]. Inherent to their size, focal aberrations contain a small number of genes, facilitating driver gene identification
From: Brosens R, et al, 2010.

This extract is from one of the studies referenced by the previous paper (when they mention their definition of focal CNVs). This paper is about CNVs in different tumour cells;

Primary tumors contain varying proportions of nonneoplastic cells thereby obscuring focal amplifications, defined by the increased copy number of a small region of the genome, from simple gains of whole chromosome arms.
From: Leary RJ, et al, 2008.


text:
Looking for Kelly Chibale's paper on Malaria cure
From National Geographic, there has been a lot of hype on Kelly Chibale's work from University of Cape Town on the aminopyridine MMV390048. Unfortunately, this was from an announcement from an internal meeting so there is very little literature on the compound.
So I ask, does anyone have good literature on the compound?

A search for "Chibale [au] AND malaria" on Pubmed returns a few results. This may be related to what you are asking for: http://www.ncbi.nlm.nih.gov/pubmed/21966980

@TomD, I believe that you have identified MMV39008. Thanks to everyone for helping me with this search!

It turns out that TomD is the winner. That particular paper is an amino-pyridine class and exhibits single-dose efficacy. Amazingly, the other two papers mentioned by Satz and Alan Boyd are leads for other classes of compounds with Satz's paper focused on an amodiaquine derivative and Alan's paper focused on an alternative 2 amino-pyridine backbone also based off amodiaquine.
3,5-Diaryl-2-aminopyridines as a Novel Class of Orally Active Antimalarials Demonstrating Single Dose Cure in Mice and Clinical Candidate Potential

This may be the paper you are looking for:
Ongaroraa DSB, Gutb J, Rosenthalb PJ, Masimirembwac CM, Chibale K. 2012. Benzoheterocyclic amodiaquine analogues with potent antiplasmodial activity: Synthesis and pharmacological evaluation. Bioorganic & Medicinal Chemistry Letters, 22(15): 5046–5050, doi:10.1016/j.bmcl.2012.06.010.

I don't know anything about this topic, but I did find this recent paper:

Kamaljit Singh,Hardeep Kaur, Kelly Chibale, Jan Balzarini, Susan Little, Prasad V. Bharatam (2012) 2-Aminopyrimidine based 4-aminoquinoline anti-plasmodial agents. Synthesis, biological activity, structure–activity relationship and mode of action studies. European Journal of Medicinal Chemistry 52:82–97

The authors analyse a range of compounds for in vitro anti-plasmodial activity. The most active is named 5-isopropyloxycarbonyl-6-methyl-4-(2-nitrophenyl)-2-[(7-chloroquinolin-4-ylamino)butylamino] pyrimidine (referred to as 10r in the paper).
Although the code name MMV390048 does not appear in the paper the strategy that this group is following is discussed in detail. My guess would be that MMV390048 is a development of 10r.
This is the structure of 10r as depicted in Table 1 of the paper:


text:
Which part of a female mantises's DNA causes her to be a few times larger than a male mantis?
Which part of a female mantises's DNA causes her to be a few times larger than a male mantis?
Do other species have that part of DNA?

Please when you downvote explain why you do it, I see nothing specifically wrong with this question, sex differences in size are well known throughout the animal kingdom.

Are they really so much bigger? M. religiosa (75 vs. 60mm), T. sinensis (130 vs. 100mm), S. carolina (47-60 vs. 54mm) from english/german Wikipedia. As the numbers show this is a wrong statement, so I will downvote, too.

@rwst: 1) without reporting standard deviations those numbers are useless. Are they statistically different? 2) Sex differences in size/weight are a very well reported and have been studied for decades. I am no expert in insects but definitely for mammals it depends on the fact that the patterns of GH secretion are sexually dimorphic and result in different IGF-1 production by the liver.

@rwst: by the way, even if we don't care about SD (which is wrong) 75 vs 60 is a 25% increase which I would consider very relevant.

Insects and spiders have tremendous sexual dimorphism, with males often being much smaller than females.  They are pretty much just sperm carriers and sometimes do not eat.  Insects may have two or one sex chromosome, where males my have only one chromosome.   As is pointed out in the comments, not all mantis' species display this dimorphism.
Since such dimorphism is probably due to small changes in the genome due to environmental selection pressures and the genetic mechanisms of control are probably not simple.
Its difficult to say which genes are responsible for size per-se.  Recent studies of human height indicate that scores of genes may be involved in human size and insects have at least as many genes as humans do; it is pretty hard to look at a human genome sequence and say what height that person is without some other help.  I imagine for specific insect species this too would be difficult.

+1: however, as I was saying in the comments, in mammals the sexual dimorphism of the somatotroph axis is probably the main driver of sexual dimorphism in terms of size/weight.

@nico interesting... would love to see a reference - this is new to me :)

Any [neuro]endocrinology book should do. The literature about GH/IGF-1 is immense and obviously many substances are involved, such as steroid hormones (like testosterone). I guess the seminal paper to look at would be: http://www.ncbi.nlm.nih.gov/pubmed/2861084 Subsequent papers have investigated the story more in detail, see for instance studies like: http://www.ncbi.nlm.nih.gov/pubmed/7768925 and http://www.ncbi.nlm.nih.gov/pubmed/9207075 (and references within)

From the abstract of the Jannson paper: "The results suggest that high, infrequent GH pulses with low plasma GH levels in between (i.e. a masculine plasma GH pattern) promotes growth more effectively than an intermediate, rather constant level of plasma GH (i.e. a feminine plasma GH pattern). Since male sex steroids masculinize the secretory pattern of GH and have only minor growth-promoting effects in hypophysectomized animals it appears that the growth promoting effect of androgens is indirect and is due to an altered secretory pattern of GH."

nice reference!  I see that there is some possibility that insects have an IGF gene as well.  In any event, the same methods could uncover an insect's sexual growth pattern...


text:
Why are some viruses not communicable person-to-person?
Below are two quotes from the CDC about Hantavirus:

"Researchers believe that people may be able to get the virus if they
  touch something that has been contaminated with rodent urine,
  droppings, or saliva, and then touch their nose or mouth."

and:

"You cannot get the virus from touching or kissing a person who has HPS."

This is hard to believe.  So, since human saliva is not a problem, can you be contaminated
by human urine or human droppings?  The only way for me to interpret this logically is to
say that this virus lives at the end of the digestive tract (for both rodents and humans)
and people can be kissed because they have much better hygiene than rodents.  Is there a
better interpretation?
Also, is there a simple reason why Hantavirus leaves the mouth (moving to the end of the
digestive tract) of an infected animal, but influenza does not?

I think (after research) that we don't know enough. As to a possible explanation of the different behaviour in rodents vs influenza, rodents don't get ill from Hanta, so the immune system isn't involved.

Viruses can have many different conditions necessary for transmission.  Viruses which have membrane surface coats (like HIV ) need to be in water all the time to survive.  Cold and flu viruses are more resilient and can survive on a surface such as a doorknob with a halflife of 18 hours(!).  Fortunately we are also have a reasonable intrinsic resistance to cold and flu and I think most infections do not result in symptoms.
Viruses often only infect some parts of the body.  Venerial diseases are a classic example of this where only contact of genitalia might cause transmission. Its probable that Hantavirus is not excreted through the sweat glands or in saliva.  If it did it would certainly be a more devastating disease.   It may also only be serious when the virus is introduced into the lungs, which may make transmission difficult.
For Hantavirus human to human transmission looks possible as observed by these folks. Even so, transmission is still so rare that there is no accounting for it in public health policy.  (they might also have been mistaken!).   Its possible that the virus requires transmission from a mouse to be virulent in humans. Its possible that the human transmission mechanism is so improbable (ingestion of faeces of infected human for instance) that you just dont' see it happening with the few cases of Hantavirus infection we have on the books.

Thanks.  I understand much is not known, but in your expert opinion/guess, do you think the probability of catching Hantavirus from kissing an infected rodent is significantly higher than that from kissing an infected human?  If so, is it just because of the hygiene point in my question (i.e., the probability would be the same if the rodent's mouth only touched clean food after it got infected)?  I'm struggling with understanding why rodents are so different from humans; rwst's point about rodents not getting sick could be a factor here.

Probably somewhat higher, but the virus seems to come from the other end of the rodent.  It might not be a respiratory virus in mice at all.

This paper is referred to in the Wikipedia entry for hantavirus as an example of human-human transmission. It may discuss the reasons why transmission is not normally via this route.

Martinez VP et al. (2005) Person-to-person transmission of Andes virus. Emerg Infect Dis. 11:1848-53
Despite the fact that rodents are considered to be the infectious source of hantavirus for humans, another route of transmission was demonstrated. Andes virus (ANDV) has been responsible for most of the cases recorded in Argentina. Person-to-person transmission of ANDV Sout lineage was described during an outbreak of hantavirus pulmonary syndrome in southwest Argentina. In this study, we analyzed 4 clusters that occurred in 2 disease-endemic areas for different ANDV lineages. We found new evidence of interhuman transmission for ANDV Sout lineage and described the first event in which another lineage, ANDV Cent BsAs, was implicated in this mechanism of transmission. On the basis of epidemiologic and genetic data, we concluded that person-to-person spread of the virus likely took place during the prodromal phase or shortly after it ended, since close and prolonged contact occurred in the events analyzed here, and the incubation period was 15-24 days.

Wow, maybe you could've translated that to normal-human-understandable language :)

That paper doesn't help answer my two specific questions,and makes me worry that any Hantavirus might be person-to-person transmittable (maybe only in the prodromal phase).  I wonder what the CDC's confidence level needs to be to print something...


text:
Why do stranded marine mammals die so quickly?
Mammals have lungs, so do marine mammals. Nevertheless some marine mammals seem to die rather quickly when they strand on a beach.
As they have lungs and can breath while on land, why do they die so quickly? Not being in water only restricts them from food.
Do they maybe try to get back into the water so rudely that they get hurt by rocks and/or break bones? Pressure difference doesn't seem to be a problem as they can jump out of the water as well.
I was wondering after reading this article on stranded pilot whales that got spot but died rather quickly after.

I'd assume that old, sick, or otherwise weakened animals have a much higher chance of getting stranded at all, which adds to a quick demise.

In the case of whales, I always thought that it was something to do with the fact that they rely upon buoyancy to support their weight and this seems to support that view:

When whales, including small whales or dolphins become stranded on beaches
  they suffer from the pressure of their own weight on their organs,in the
  water they are weightless.  They also suffer from overheating as they have
  blubber that insulates them in the water and outside of the water causing
  them to overheat.  This is why we place wet towels and cold water on their
  fins and flukes when do they strand to help keep their body temperature
  down.  Unfortunately most stranded whales do not survive once they have
  beached themselves.

That's not exactly true, you are generalizing. For example seals are marine mammals (that's a rather large non-official group I think)  and they don't die so quickly.
Anyway, breathing is not the only thing necessary for survival. If you leave a human inside a 50°C room he can still breath but won't live for long.

I said "Nevertheless some marine mammals seem to die rather quickly when they strand on a beach.". So I was not generalizing on species. It's true that breathing is not the only thing necessary for survival, otherwise they wouldn't die, my question aimed to find out what was the other crucial thing for survival on such short time frames.

@StevenRoose That would depend between animal. I believe most of them require their skin to be moist or they get sunburns.


text:
Difference between genetic engineering and synthetic biology
I've recently seen the term synthetic biology being used to describe research involving genetic modification of organisms. What is the difference between synthetic biology and genetic engineering?
Is it just a new term for the same thing, or is it something different? Does one of the two terms encompass the other?

Hi @Green. Welcome to SE.Biology. If you'd like to get the benefits of a fully account (such as e-mail notifications and voting), register here.

@Luke: I actually have an account, but I was kind of embarrassed to ask such a soft question on it.

My understanding is that synthetic biology is genetic engineering 2.0. The difference is in the approach. Whereas genetic engineering projects are usually ad hoc, synthetic biology aims to apply proper engineering principles such as standardisation, modularisation, and reusability. Synthetic biologists create and use libraries of standard parts that are characterised, so they can be easily reused in projects. A part could be a gene, a terminator, a promoter, etc.
Synthetic biology also has greater ambitions. The focus is on creating whole systems/circuits of genetic regulation. This means there is a need for computational modelling and understanding of how biological systems work. In this aspect synthetic biology is a sister of systems biology a bit like synthetic chemistry (engineering) is a sister of chemistry (science).
You could of course argue that it's just a marketing ploy to invent a new name for something that is just the next step in genetic engineering, but the differences in approach are quite large and a new name signifies it.
With regards to synthesised vs. PCRed DNA: It doesn't really matter which you use in synthetic biology. However, cheap synthesis is one of the technologies that enable easier synthetic biology. The idea for the future is that you will be able to synthesise whole plasmids and chromosomes instead of having to "cut and paste" DNA. When that happens physical parts repositories will be obsolete, but they will remain crucial in silico. Cheap synthesis is nice, but doesn't make or brake synthetic biology.

I like this answer best - if you look at the partsregistry.org you can see there is a strong desire to put the components into an engineering framework that is more device like.

It seems to me that the difference is mainly semantic, although the aims of synthetic biology are undoubtedly more ambitious than those of genetic engineering in, say, the 80s and 90s.
The Wikipedia page on genetic engineering has this definition of the difference:

Synthetic biology is an emerging discipline that takes genetic engineering a step further by introducing artificially synthesized genetic material from raw materials into an organism.

I must say that for me this doesn't really stand up to close scrutiny. To give just just one example from my own experience - for a long time now yeast geneticists have used PCR to make DNA for targetted gene disruption. This seems to me to fit the definition in the quote: the primers were made chemically and the PCR product was made in vitro using dNTPs as raw materials. (Admittedly the template DNA would be normally produced in vivo.) But I don't think we ever thought that we were doing synthetic biology.
Perhaps the term synthetic biology was intended to herald a new approach that would be more fundable?
I look forward to reading the responses to this rather cynical answer :)

I don't think they mean synthetic as in 'made in the lab using PCR', as for all genetic engineering PCR will be essential at some point (at least, that is how I interpret it). The term synthetic probably is used to refer to specific sequences of nucleotides that are not naturally formed (i.e. they are de novo, synthetic sequences).

I see what you are getting at, but wouldn't most mutagenesis experiments fit this definition? Conversely, if I was to synthesis a gene for a protein but changing as many codons as possible without affecting the amino acid sequence - what would that be?

Interesting point. 'Silent' mutations (those that do not affect the protein sequence) could still affect regulation of transcription - for instance miRNA binding or alternative splicing (this is very situation dependent of course, but I'm just saying that 'silent' mutations don't necessarily have no effect). With mutagenesis I would say it's genetic engineering, as there is no 'synthetic' element to the DNA modification, other than it is done under experimental conditions... an analogous experiment using a manufactured/custom sequence of DNA inserted into the genome would be 'synthetic' IMO.

... however this is just my interpretation of things! I have not seen a concrete definition, so I may well be mistaken. Or indeed, there may not be a concrete definition, and this is quite subjective (like 'bioinformatics' vs 'computational biology'. People agree there is a distinction, but not on where the line is drawn).

PCR is not synthetic; although it involves biological synthesis, it has to start from a template. Synthesis as in synthetic biology involves artificial gene synthesis, i.e. starting just with a sequence on a computer and ending with biological sequence.

They seem to be practically the same, with the exception of the goals. Genetic Engineering is the direct modification of the genes of an organism which results in capabilities being added or taken away. Synthetic Biology aims to modify the behaviors of an organism or integrate the behaviors of multiple organisms into a singular whole.
As is explained in  Andrianantoandro E, Basu S, Karig DK, Weiss R. 2006. Synthetic biology: new engineering rules for an emerging discipline. Molecular systems biology 2: 2006.0028:

One useful analogy to conceptualize both the goal and methods of synthetic biology is the computer engineering hierarchy (Figure 1). Within the hierarchy, every constituent part is embedded in a more complex system that provides its context. Design of new behavior occurs with the top of the hierarchy in mind but is implemented bottom-up. At the bottom of the hierarchy are DNA, RNA, proteins, and metabolites (including lipids and carbohydrates, amino acids, and nucleotides), analogous to the physical layer of transistors, capacitors, and resistors in computer engineering. The next layer, the device layer, comprises biochemical reactions that regulate the flow of information and manipulate physical processes, equivalent to engineered logic gates that perform computations in a computer. At the module layer, the synthetic biologist uses a diverse library of biological devices to assemble complex pathways that function like integrated circuits. The connection of these modules to each other and their integration into host cells allows the synthetic biologist to extend or modify the behavior of cells in a programmatic fashion.

It's notable that in the paper's abstract the words engineer(ing) appear six times whereas synthetic appears just twice! The claim of the abstract is that synthetic biology is a new branch of engineering. The engineered constructs of synthetic biology will no doubt be achieved by use of DNA-based technologies. I stick by what I said in my answer: there is a difference of scope and ambition, but really there is nothing new; as the technologies have advanced and matured, so the possibilities have expanded.

In genetics engineering we use and manipulate natural genetic elements but in synthetic biology we make new gene elements and network.

In general:
genetic engineering = cutting and pasting existing DNA extracted from organisms
synthetic biology = chemically synthesizing DNA from scratch, which is used to create new genes and constructs from scratch. The synthetic sequences may not exist or may exist in nature.

I've been seeking the major achievements of synthetic biology. One that is frequently referred to is the production of the antimalarial drug precursor artemisinic acid in engineered yeast (Nature 440:940-3), a paper which has been cited hundreds of times. Upon reading this paper I find that everything that was done meets your definition of genetic engineering (and is what used to be called metabolic engineering). Please, can you point me to a research landmark that fits your criteria?

The parts registry, and BioBricks are key examples of synthetic biology. And Randy's is the correct answer, except that there's no reason to exclude sequences found in nature, as long as they are ab-initio synthesised. The clue is in the name... synthetic biology involves synthesised, not cloned, biological sequences. Synthetic biology is still a subset of genetic engineering.

I am not a big fan of definitions and terminology in molecular biology, because biology is not physics, and things that we might describe and define change, as does our understanding of them. However, as this question has surfaced again after a number of years, it might be worthwhile giving a more recent example of synthetic biology, rather than just defining it. That way the reader can get an idea of what it is about.
I would say that:

Synthetic biology is a particular type of genetic engineering.

Definitions
A reasonable definition of genetic engineering is given by Encyclopedia Britannica:

The artificial manipulation, modification, and recombination of DNA or
  other nucleic acid molecules in order to modify an organism or
  population of organisms.

So this could include making a single base change to inactivate a gene or introducing and expressing the gene for human insulin in, say, yeast.
The definitions of synthetic biology are more contorted, e.g. that from the Royal Society

Synthetic biology is an emerging area of research that can broadly be
  described as the design and construction of novel artificial
  biological pathways, organisms or devices, or the redesign of existing
  natural biological systems.

Example
So why is the expression of insulin in yeast not considered synthetic biology? Basically because it lacks the complexity of a completely novel system. Consider the following description of an arsenic biosensor designed to test for arsenic in drinking water:

“Chris French at Edinburgh University led a team that turned the E.
  coli bacterium into an arsenic sensor by rewiring two genes. One gene
  senses arsenic and activates genes to pump it out of the cell; the
  other allows the bacteria to digest the sugar lactose, producing
  lactic acid. The rewiring involves putting the gene for digesting
  lactose under the control of the arsenic sensor. When arsenic is
  detected, the lactose-digesting gene switches on. The lactic acid it
  produces makes the water more acidic, which can be detected using a
  cheap pH indicator: if the reading is blue, the water is safe; yellow
  means it is dangerous.”

So they have engineered a completely new system with two different genes, which have been modified and their regulation co-ordinated (“rewired” in the article) in an original manner. And there is a tendency to embody some of the complexity into modules that can be reused by others allowing even more complex and sophisticated systems to be constructed.
You could say that the difference from insulin expression in yeast is only a matter of degree, but here the devil is really in the detail.


text:
Literature about putative epigenetic state changes in mammal sequences after cloning steps in Escherichia coli
I would like you to point me out some literature about putative epigenetic state changes in mouse/mammal sequences after cloning steps in Escherichia coli.
This are the last search details I used in NCBI PubMed:

"epigenomics"[MeSH Terms] AND "cloning, molecular"[MeSH Terms] OR
  "molecular cloning"[All Fields] AND "sequence"[All Fields] AND
  ("escherichia coli"[All Fields] OR "e. coli"[All Fields])

Where do these epigenetic changes happen? while cloning a mammal DNA in E.coli?

I am interested in finding any record of epigenetic changes while cloning mammal DNA via E. coli (so, the initial DNA would have its epigenetic state, the purified plasmidic DNA after the molecular cloning would have another, possibly different, epigenetic state). By the way, any paper suggesting conservation in the epigenetic state through the cloning steps is also welcome, as it would provide evidence of the lack of changes.

I think you can narrow it down to DNA-methylation since bacteria don't have histones.

This is mostly true, but in principle I would like to include any possible bookmarking event.

E.coli strains that have dam or dcm methylases can methylate plasmid at adenines or cytosines respectively. See here — It is a NEB web page but has links to the cited references.
DH5α has both the methylases- dam+ dcm+ , BL21 is dam+ dcm− and ET12567 is dam− dcm−


text:
Rosetta ab initio prediction and protein-protein interaction fitness help
I have designed several proteins which I predict have interactions with another protein using the sequence based Conjoint Triad Method. I would like to know which ones structurally are predicted to dock and have interactions. I have Rosetta installed and have looked at the examples a little. Rosetta doesn't have much "how to" documentation on protein design and fitness selection. Could someone please walk me through the process line by line of taking a fasta with a series of proteins through rosetta's ab initio pdb generation and then how to and where to look for a fitness of each proteins interaction/docking? Also I read in "Design of Protein-Protein Interaction Specificity Using Computational Methods and Experimental Library Screening" page 91 that it was possible to generate specific protein combinations that map to a structure using Rosetta. How do you do that?
thank you :)
Rosetta commons links to additional software add ins but omits the crucial Sparks-X. I found Sparks-X from at this webpage. And I found that the code for make_fragments.pl needs to have many changes made for it to run properly. Several files are listed in make_fragments.pl. Two files without links pdb_seqres.txt and entries.idx are found at RSCB, below.
The NCBI nr database requires about 100 gigs of free space to properly load and process. Anything less than that results in errors.
make_fragments.pl requires a single gene in a fasta file. multiple genes in the fasta file cause it it crash.
Psipred nolonger has a dat4 so this line needs in make_fragments needs to have the dat4 removed.
"$PSIPRED sstmp.mtx $PSIPRED_DATA/weights.dat $PSIPRED_DATA/weights.dat2 $PSIPRED_DATA/weights.dat3 $PSIPRED_DATA/weights.dat4 > psipred_ss",

My make_fragments does not always finish it sometimes gives an error
ERROR: Error reading in FragmentPicker::read_spine_x(): does not match size of query!

This error was caused by a ^M in the fasta file removed with vi.
I'm attempting to bypass the fragment picker with csrosetta toolkit from .csrosetta.org/
libstdc++6 32bit version must be used for talos+
I used a Ubuntu 32 bit machine to copy the /usr/lib/libstdc++.so.6 and uploaded it here.
http://www.mediafire.com/?j0133qqwiilsuz1
cs-rosetta does not create fragments for unknown reason. I have emailed the creator and I have emailed rosetta commons support as well. For now I recomend the on-line server roberta.
There are examples of how to use prepacking and docking in rosetta_tests.
PPI can be designed by docking a protein to another protein then running sequence tolerance. Though the resfile doesn't seem to be able to limit the changes to certain nt at this point.
Sequence tolerance has an extra rotamer bug and fills up memory and the page file for certain proteins if the "ex" series flags are use. It also sometimes ignores the resfile so double check the initial scripts results before begining a multi-generational study.
Ab initio relax has a bug which prevents it from running twice in the same directory. Remove default.out to rerun the structure prediction.
Docking can be forced to one location by using a constraints file but the radomize and spin options must be turned off for it to work properly.
-constraints:cst_weight integer
-constraints:cst_file cstfile
http://www.rosettacommons.org/manuals/archive/rosetta3.4_user_guide/de/d50/constraint_file.html
http://www.rcsb.org/pdb/static.do?p=general_information/about_pdb/summaries.html

as this question is more concerned with how to use Rosetta instead of the biological implications, please ask it at http://biostars.org/ . There you're also more likely to get help.

@MichaelKuhn Theres nothing wrong with being a methodist. :) All good biology papers have a methods section and most journals require it. Protein-engineering is by definition a process...a group of methods. Rosetta is considered the best method as far as I know at the moment. "This is a free, community driven Q&A for biology researchers, academics, and students."

See the FAQ: "Questions on interdisciplinary subjects like bioinformatics are also welcome, as long as they focus on the biological part of the subject."

@MichaelKuhn this falls under "questions about techniques in a biological or biochemical laboratory". Dr. Keating's labs results are being reproduced.

still its been quite a few days and nobody has given an answer... maybe not a bad idea to cross post

@shigeta yeah i'm cross posting but biostars is very slow and not many people are interested in rosetta i figured if i answered my own question it might help the next person as rosetta support is slow at best

@caseyr547 this is probably some rare expertise you are looking for indeed. looking forward to the answer tho


text:
From which ancestor species did humans inherit orgasm?
From what ancestors did humans inherit orgasm?
Do fish experience orgasm?
Are the male and female orgasm the homologues that can be traced to the time when there was no difference in sex between individuals (as in fish) or developed independently?

You're going to have to clarify. What do you mean by 'orgasm'? Do you include the pleasure, or just the act of ejaculation?

-1 using the term "Invented" makes this question nonsensical.

Perhaps maybe you should ask instead when did we begin to sense pleasure.

The meaning is completely distorted. I was asking about human ancestors, namely, fish, not "asexual species".

@nico I consider you vandalized the question. My main question was wehether female and male orgasms are homologues but you removed that part.

@Anixx: I did leave a comment exactly for that reason. Your last sentence does not really make much sense in English. By the way you wrote: to the time when there was no difference in sex between individuals. I don't read that as fish (and I did leave the fish part in my edit).

@nico fish exhibit androginous behavior with the same individual follows through male and female stages.

@Anixx: then you should rephrase it, because your sentence does not mean that. Fish DO have a sex, they do reproduce sexually and there are differences between male fish and female fish.

Let's assume that pleasure from sexual intercourse might be indicative of some sort of orgasm. Then this would suggest that any evidence of autoerotic behaviour would point to the existence of orgasm, or certanly physical pleasure.
I found this quotation on the Wikipedia page for Animal sexual behavior, amongst a lot of information about mammals :

Many birds masturbate by mounting and copulating with tufts of grass, leaves or mounds of earth...

apparently from Bruce Bagemihl: Biological Exuberance: Animal Homosexuality and Natural Diversity. St. Martin's Press, 1999. ISBN 0-312-19239-8
If this is taken to imply that the last common ancestor of birds and mammals experienced this pleasure then we have got fairly deep into evolutionary history, although not as far as fish.


text:
What are good practices with reusing desalting columns
At least according to a few sources Prozyme and Protocols-Online, it is possible to reuse desalting columns and since I'm cheap I would like to also.
Key things seem to be washing with several column volumes of your buffer of choice. Also certain columns like crosslinked desalting columns are not amenable to regeneration. I'm curious about other factors.
I'm mainly using Bio-Rad micro-spins

Regardless of what protocol you use, and what the advertised efficacy of that protocol might be, in any situation like this I think the important thing to consider is: what would happen if the material taken from a re-used column was contaminated by a previous application? Can you live with the consequences of such contamination?
If you are preparing DNA for further use (PCR and/or cloning and/or transformation) then you run the risk of propagating a contaminant through subsequent steps and getting into a real mess. I worked in a lab once where one postgrad ended up spending several weeks working with a cloned fragment that was actually derived from someone else's work in the same lab (although not due to re-use of a column as far as I remember).
If you are preparing protein samples then the risks are possibly reduced, but if the protein sample is going to be subjected to sensitive methods (blotting, MS) then again, could get messy.