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What are the positive and negative effects of insulin on cognitive function?
A UCLA study seems to imply that insulin interferes with cognitive function.

The DHA-deprived rats also developed signs of resistance to insulin, a
  hormone that controls blood sugar and regulates synaptic function in
  the brain. A closer look at the rats' brain tissue suggested that
  insulin had lost much of its power to influence the brain cells.
"Because insulin can penetrate the blood–brain barrier, the hormone
  may signal neurons to trigger reactions that disrupt learning and
  cause memory loss," Gomez-Pinilla said.
He suspects that fructose is the culprit behind the DHA-deficient
  rats' brain dysfunction. Eating too much fructose could block
  insulin's ability to regulate how cells use and store sugar for the
  energy required for processing thoughts and emotions.
"Insulin is important in the body for controlling blood sugar, but it
  may play a different role in the brain, where insulin appears to
  disturb memory and learning," he said. "Our study shows that a
  high-fructose diet harms the brain as well as the body. This is
  something new."

At the same time, increased levels of IGF-1 seems to be implicated in higher level of intelligence. IGF-1 is not the same thing as insulin, but it does seem to have many similar effects.

And the question is?

Don't take it personally, but this is a ridiculous question. You have in hand a study that "seems to imply" it has an effect, but you ask anonymous users of an internet website to tell you whether the authors are right or not - something which only further experiments can clarify. The only answer to such a question is "Do your own study, and then draw your own conclusions".

Diabetes
I've not read about any conclusive evidence for a link between insulin and differential cognitive function, but I have read studies that link type-2 diabetes and impaired cognition (1). I will point out now that this is cross-sectional, so the study only reports associations (i.e. diabetes may not necessarily cause the cognitive impairment).
The study I have mentioned does not conclude that this is caused by raised insulin, but rather the effects on the vascular system (specifically microvascular). They also find a significant interaction between diabetes and smoking status, in the context of cognitive impairment. Again, this seems likely to be the vascular system, rather than insulin levels.
A recent review paper also refers to the links between diabetes and executive function (2), but again makes no reference to insulin as the cause, but rather microvascular changes, hypertension, and other associated traits (again, the causes are not known, these are speculative based on the evidence).
Diabetes may not be the best model for studying this though, as it can be characterized by either high insulin (tolerance), or low insulin (impairment) - therefore the association may not be found this way.
Insulin
In a separate review (this may be the best one for you if you only read one of the papers I've referenced) the author posits that whilst insulin may have a neuroprotective role, it also increases amyloid-Beta metabolism and tau phosphorylation, possibly contributing to Alzheimer's-like pathologies (3). Studies have found that insulin directly improves cognitive performance (4) after infusion of insulin, but the long term effects are less certain - it is unlikely to improve overall health having constantly raised insulin serum levels!
However the link between IGF-1 and improved cognition is less disputed, so you may well be right in thinking that the 'overall' effect of insulin on cognition may be protective, but this may just be a marker of good health overall, which is certainly protective!


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If D1 receptors stimulate adenylate cyclase (through GPCRs) and D2 receptors inhibit it, then why do mutations in both have similar effects?
D1 and D2 both refer to specific types of dopamine receptors.
I'm sure it has something to do with the fact that the D1 receptors are in regions different from D2 receptors.
I know that adenylate cyclase usually triggers a signal transduction cascade that leads to increased cAMP+calmodulin, resulting in increased gene expression of proteins that help promote long-term potentiation of postsynaptic neurons (presumably lowering the absolute value of the voltage threshold that's needed to trigger another action potential, which increases neuron excitability).
But an increase in dopamine is going to cause more neuron excitability in postsynaptic neurons in some regions (those that have D1 receptors), and less in others (those that have D2 receptors). What then explains the fact that increased expression at all dopamine receptors can help modulate attention span?
I know that D3 and D4 are also involved, but they have to be either excitatory, inhibitory, or neutral.

Could you please split your questions into several ones? You currently ask 3 questions within the text and the question in the title seems to be the 4th question unrelated to the previous ones.

okay I've deleted the separate questions for now.

There are two problems with your hypothesis: 1) you cannot assume that the same receptor will be involved in the same process all over the brain and 2) you cannot assume that something as complex as attention span be the result of the action of only one receptor.

Okay - that's true. I think that would serve as the basis for a follow-up question about where D1 receptors are expressed relative to D2 receptors - I've asked it http://biology.stackexchange.com/questions/752/which-brain-regions-are-d1-dopamine-receptors-expressed-and-which-brain-regions.
That's also true, but changes to one receptor most certainly do affect attention span.

@InquilineKea: they probably do, but the result may be indirect and dependent on other factors. I do not know enough about that to give you a proper answer though

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How do circulating androgens contribute to higher rates of hirsuteness in some women?
I was reading up on ethnic groups in which the women are naturally more hirsute (such as South Asian women) in the context of evolving standards of beauty. I came across this statement on a forum:

Hirsutism is much more common in South Asian women (particularly North Indians such as Punjabi Sikhs) asymptomatically because they tend to have higher levels of circulating androgens than your typical [North or Western European ethnic group]. This is also true of Eastern European women to an extent.

Per Wikipedia, I learned:

Circulating levels of androgens can influence human behavior because some neurons are sensitive to steroid hormones. Androgen levels have been implicated in the regulation of human aggression and libido. Indeed, androgens are capable of altering the structure of the brain in several species, including mice, rats, and primates, producing sex differences.

So: do circulating androgens trigger higher testosterone production in some women? Is this what yields higher instances of "hirsutism" among certain populations? How are some women more prone to this than others? (That is, per the forum post, why are South Asian women more likely to have this than Western European women?)

I'm something of an armchair biologist, so please edit this to use better/more standard terminology as needed. I don't mind at all!

Testosterone IS an androgen, so I'm not really sure what you are asking.

@AlanBoyd Ah! See, that's the piece that I'm missing. I guess then, I'm asking: why do some women have more testosterone than others? And does this directly relate to how "hirsute" she is?

This review may be of interest:
Sharma D, Shanker V, Tegta G, Gupta M, Verma GK. Clinico-investigative profile of patients of hirsutism in a tertiary level institution. Int J Trichol [serial online] 2012 [cited 2013 Feb 9];4:69-74. Available from: http://www.ijtrichology.com/text.asp?2012/4/2/69/96904
As for the genetic causes of hirsutism, researchers thought the number of CAG repeats in the androgen receptor gene might play a role, but there was no evidence to that effect, as of 2000.  I couldn't find any newer papers, but here you go: http://jcem.endojournals.org/content/85/4/1735.
This paper was cited by the previous review, but Sharma et al didn't read more than the title, because they cited Calvo et al as evidence for the role of CAG repeats in hirsutism.
tl;dr: read Sharma et al, and look up the references.

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Why do mammalian red blood cells lack a nucleus?
How did the red blood cell in humans get to lose its nucleus (and other organelles)? Does the bone marrow just not put the nucleus in, or is it stripped out at some stage in the construction of the cell?

Red blood cells are initially produced in the bone marrow with a nucleus. They then undergo a process known as enucleation in which their nucleus is removed. Enucleation occurs roughly when the cell has reached maturity. According to one research (Ji, et al., 2008), the way this occurs in mice is that a ring of actin filaments surrounds the cell, and then contracts. This cuts off a segment of the cell containing the nucleus, which is then swallowed by a macrophage. Enucleation in humans most likely follows a very similar mechanism.
The absence of a nucleus is an adaptation of the red blood cell for its role. It allows the red blood cell to contain more hemoglobin and, therefore, carry more oxygen molecules. It also allows the cell to have its distinctive bi-concave shape which aids diffusion. This shape would not be possible if the cell had a nucleus in the way. Because of the advantages it gives, it is easy to see why evolution would cause this to occur. However, since little is known about the genes the control enucleation, it is still not a fully understood process.

Are there references for the second paragraph?

I can't find any references to journal articles, but the facts mentioned are often stated in text books or lecture notes. For example: http://faculty.ucc.edu/biology-atsma/misc/blood.htm

It's too bad they don't have citations. It would be nice to get away from just so stories and have a real evolutionary answer.

I don't have access to the full text, but this article proposes resistance to oxidative stress as a reason for enucleation: Red blood cell extrudes nucleus and mitochondria against oxidative stress

So how do birds manage, with a lumpy nucleus in the red blood cell?

I'm guessing there is no real reference. Its hard to prove that the nucleus is a problem for rbcs - the control experiment - comparing to rbcs with nuclei - is technically difficult.   It makes sense to say it so, its passed on.

Shown to be in mice & rats (and sick humans), the cell-cell interaction between a macrophage (this is a big engulfing cell required for immunity) and young red blood cells (RBC), is known as the erythroblastic island (commonly known as EBI). If you googled it, there is a scientific review in 2008 that describes this structure.
At the embryonic stage (in humans), we still retain our RBC nuclei. But as we developed into fetus and adult, we no longer have RBC nuclei. This is thought to be related to the EBI present (in the fetal liver and adult bone marrow respectively). Currently, there is a lack of information of the EBI in other mammals. The only proven ones are mice, rats and sick humans. It is widely assumed (not proven) that mammals have EBIs. Besides mammals, some other animals (e.g. birds) have enucleated RBC, and some don't. It is unclear why is it so. Our lab thinks that it might be related to the formation of the EBI.
In addition to engulfing the RBC nuclei, it is believed that the macrophage acts as a "nurse" cell as proposed in the 50s. In other words, possibly providing iron, and possibly providing some proteins required for young RBC to mature. In early 2013, for the first time, it was showed that these macrophages are important in animal models (published by 2 research groups in nature medicine journal).
As for enucleation (the removal of erythroid nuclei), the exact mechanisms are unknown. But cytoskeleton proteins are important players in enucleation. However, there isn't enough information, as these proteins are essential for other important cellular activities as well. For example, bringing in nutrients, development and cellular migration. Most animal models that lack these proteins are unavailable for studies, and these animals usually die at the embryonic stage.
The research mentioned by EdoDodo is a proposed model on how enucleation takes place, and is a widely accepted model. Currently, our lab are working on another model that could partially explain how enucleation is being triggered.
Advantages of enucleation
In addition to better oxygen diffusion across the membranes, some older scientific papers mentioned that it lightened the cardiac workload. Each extruded RBC nuclei is approximately 40 picograms. A normal healthy adult individual would produce about 2 million RBC per second. That would be 0.08 milligrams of weight per second are required to be removed. However, I couldn't trace the scientific evidence for this claim, but this have been cited by some scientific papers.
The other advantage would be to reduce risk of hemolysis when transversing through the microvasculature. In other words, mature RBC can move along tiny blood capillaries by changing their biconcave shape (to bell-shaped I think), so that they will not rupture (and die).
Also, not all RBCs have similar shapes and sizes. You might want to google it for more information. I think camels have slightly different RBC morphology.

I checked for the publications you mentioned here. I did not find any publication for macrophages and EBI in Nature Medicine, but I found two reviews from 2008 about EBIs: The Erythroblastic Island and Erythroblastic islands: niches for erythropoiesis. In case somebody wants to read them: they are freely available. It would be nice if you could add the other two papers, too. Thank you!

The only function of the red blood cell is to transport oxygen, and nothing else. Its concave shape is to increase its surface area, so more oxygen can be transported per cell. The absence of a nucleus means it can be significantly more concave than an other cell of analogous size, meaning it can carry more oxygen.
Other answers are more detailed, but this is the main reason that there is an absence of a nucleus.

The relationship between carrying more oxygen per cell and surface area does not follow logically to me. Enucleation will lead to increased surface area per unit volume, which will relatively increase the area for transport across the membrane. But aside from increasing Hb content or concentration, that won't lead to more oxygen carrying capacity.


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How do you calculate or predict the charge of a protein at pH 7?
How do you calculate or predict the charge of a protein at pH 7 given a fasta sequence?
Any papers or online servers to do this is well appreciated.

Check this answer http://biology.stackexchange.com/questions/2459/are-bovine-serum-albumin-avidin-ficoll-70-and-dextran-70-positively-charged-or/2511#2511

ExPASy to the rescue! Although I didn't comb through all the tools, this nifty website provides quite the myriad of bioinformatics resources which most certainly contains the tool to calculate what you want.
Bear in mind though, most tools will tell you the isoelectric point of your protein. However, bearing in mind the relationship between pI and pH (i.e. if pI < pH, then protein is - charged, and vice versa), you can easily figure out the charge of a protein at pH 7.
http://expasy.org/tools/
*Update
Here's the exact tool to calculate isoelectric points: http://web.expasy.org/compute_pi/

Thanks for the info. Saw that though, so how would you calculate the charge - any hint on that?

Here's a tool that will give you charge: http://www.scripps.edu/~cdputnam/protcalc.html

Thanks! But wish it could in batch...

To calculate the charge at different pH:
At pH 3 K, R, H are + and D,E have no charge so add up all of the K,R,H in the sequence and that is your net charge at pH 3
At pH 6 K, R, H are + but now D,E are (-) so subtract one total from the other to figure if your net charge is + or -.
At pH 8 K and R are +, H has no charge and D,E are (-).
At pH 10 R is +, K, H have no charge and D,E are (-).
That can give you a general idea.  You can estimate the charge at pHs in between.


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Lateral, axional and temporal resolutions for imaging in vivo
What are the spatial (lateral and axional), and temporal resolutions that one is expected to get with the following optical imaging techniques?

Optical Bioluminiscence Imaging (BLI)
Optical Fluorescence Imaging (FLI)
Multiphoton Microscopy (e.g. 2-photon microscopy)

Are they any better than the  others in providing higher resolutions?

The lateral and axial resolution depends on the numerical aperture of your objective (lateral = lambda/2NA; axial = 2lambda/NA^2). You can improvee the axial resolution with FLI by using a confocal approach or with 2-photon microscopy (2PM). In 2PM you need absorption of two infrared photons to get emission. The probability of 2 infrared absorption depends quadratically on the excitation intensity. Therefore, fluorescence is restricted where the illumination beam is focused which give a better sectioning. An advantage of 2PM is the higher penetration depth and reduce phototoxicity. Indeed you can use 2 infrared photons to excite fluorophore which required visible excitation.
Temporal resolution depends on the area you want to measure and the integration time.
Resolution is limited by the diffraction. In the best case with the 3 imaging techniques you mentioned you can get ~200-300 nm in lateral resolution and 500 - 800 nm in axial resolution
Higher resolution can be achieved by using super resolution techniques. They are separated in two groups. The first one exploid the photo-physical properties of the fluorophore to excite and de-excite it. This allows to resolve sub-diffraction areas. This is the case STED (Stimulated emission depletion) microscopy or SSIM (saturated structured illimination microscopy). The second group use the fluctuation of the fluorophore emission to localize it better. It includes techniques such as STORM (STochastic Optical Reconstruction Microscopy, PALM (Photo-Activated Localization Microscopy) and SOFI (super-resolution optical ﬂuctuation imaging).


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What are the effect of microtubule or microfilament inhibition on yeast expression profile?
I was wondering whether anyone has looked at what are the expression changes in yeast when the microtubule or the microfilament polymerization is inhibited? Have there been whole-genome studies?

Browsing around GEO, I see 13 experiments focusing on microtubule disruption in yeast.
This CHIP-CHP experiment actually uses nocodazole.
This is a microarray experiment with benomyl treatment.
The rest focus on specific mutants that try to perturb the microtubules in specific ways.
What's more if you broaden the search there is an extensive body of work including human cell lines work as well...

Thanks for the answer. Could you summarize what was discovered? Which genes were downregulated/upregulated/unchanged? Thanks.

GEO doesn't store results.  I'd have to go and redo the analyses myself....


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How many genes do we share with our mother?
Somewhere I have read we share more than 99% of our genes with every other other person and 98% of our genes with chimpanzees. What does this mean? Don't we share 50% of our genes with our mother and 50% with our father?
I've found an another article stating that.

There is a distinct difference between the 'genes' that we share, and the genome (the DNA) that the genes are made of.
All humans (excluding genetic disorders) have the same genes, but the same gene in different individuals may have a slightly different DNA sequence, and this may be manifested in the different traits you can observe between people (eye colour, height, etc) or be ’silent’ (have no observable effect).
So you therefore have 100% of the genes that your mother has.
However, as stated in another answer, you inherit the different 'alleles', or versions, of the genes from your parents, and end up with ~50% of the alleles from each parents (but all the genes).
With regard to species differences; many of the genes we inherit have evolved over millions (in fact billions) of years, and thus many of our genes are present in most other organisms (but in very different forms - the DNA). Chimpanzees are our closest relatives in evolutionary terms, and thus their genes are very similar to ours in the genome (~98% the same). But this only applies to the coding regions! Less than 2% of your genome actually codes for genes - the rest is mostly regulatory (not junk, as it used to be called), and this is where the true inter-species variation lies. So whilst we have ~98% homology in the protein-coding regions, this is MUCH less if you count the whole genome.

Nice answer, +1. Actually, recent analysis of 1000 Genomes data shows that each person has some 25-40 homozygous LOF (loss of function) variants not found in either parent. Thus, one could lower the 100% figure to ~99.9% shared.

How many kinds of genes are there in humans? If we all have same kind of genes, so is it just the combination of these genes that affect our personality?

+1 but you should probably change the word "code" for something else. The great majority of the species on Earth use the same genetic code (I do understand you did not mean it like that but...)

@user103431 I think there are around 23,000 accepted protein-coding genes in humans. We each have a copy of every gene. But at the DNA level the genes can vary ever so slightly, and this is where the different alleles come from (slight variations in the same trait). With regard to your personality, that is another kettle of fish: your genes can certainly affect your predisposition to certain mentalities, but it should be fairly clear that it is your life experiences that mostly affect how you develop, and thus what kind of person you become.
And 'code' is a bit layman, but it is 'correct'

Also, the DNA formerly known as junk is called heterochromatin. This was long thought to be inactive but I believe that is has now been shown to contain protein coding genes, not just regulatory elements (I spoke to Gary Karpen in the summer and think this is where I heard it). It is quite an unknown entity because it is so damned hard to sequence thanks to lots of repeating units!

In addition to the other answers, let me show you a logical error in your reasoning:

Don't we share 50% of our genes with our mother and 50% with our father?

You get 50% of our genes from each respective parent (disregarding mutations for now). But if you shared only 50% with each parent, this would imply that your parents don’t share a single gene:

But your parents do share genes – or rather, alleles1 – which is why the you also share more than 50% of the alleles with each of your parent.

1)  They share all genes.

Very good point! I had not thought it before. I had too the same misunderstanding.

In every cell of your body, you have two physical copies of every gene (ignoring gametes, / copy number variations), one from your mother, one from your father. (Humans are diploid.) That's why it's correct to say that you got 50% from either parent (ignoring the 13 mitochondrial genes that are inherited from the mother only).
The second approach is to look at genes as abstract entities. In the abstract sense, you share 100% of your genes with fellow humans, and more distant species will have a number of different genes. (This difference can be quantified in many different ways.)

I like the physical vs abstract take on this.

glad the mitochondria got mentioned :)

Let's not forget in these explanations about the special case of X and Y genes. If you are a boy, you share 100% of your father's Y chromosome (with a few mutations/transcriptions errors and slight recombinations in between) and a 50% mix of a X chromosome from him and a X chromosome from your mother.

@ogerard: Boys get one complete Y chromosome from the father, and one complete X chromosome from the mother. (The sperm was carrying a Y, and not an X.) Girls get one X from each of their parents. (So no 50/50 mix in the X for boys.)

@Michael Kuhn: Sorry, I was really not correct in the end part of my comment. What I should have written is that the X from their mother is a recombination of the two Xs of their mother. There is a small recombinable part in the Y chromosome but it does not contain the key genes for sex determination.

Say x is the percentage of an allele in your mom (or cousin, or brother). Say c is the filial similarity (brother=.5, son=.5, cousins=.125, etc.) of the allele. Say y is the general probability of having that allele in that population (assuming mom is the same species with you). Say f(x,y) is the expected value of the number of allele that you have.
Then f(x,y)= c * x+ (1-c) *y
In other word. There is no contradiction in the idea that we are 98% similar with monkeys and yet only 50% similar with our own mom.
Here, the world similar is used in totally different sense.
f(x,y) is 99% for most allele. Now let gy(x)=f(x,y) then
gy'(x) is c.
In other word, for every allele your mom have, it'll improve the expected value of you having the same allele by half. For each allele your cousin has, it'll improve the expected value of you having the same allele by 1/8th. That is for the same y. For most y, similarity is 100% nevertheless.
Say Ann, Beth, and Cindy has AA, Aa, and aa alleles.
Then Ann's sons have 25% higher expected value of having A alleles than Beth, and Beth have 25% higher expected value of having A alleles than Cindy. I say nothing of actual probability distribution.
Ann's cousins have .0625% higher expected value of A occurrence than Beth's cousins and .125% expected value of A occurrence than Cindy's cousins
Disclaimer: We do not take into account that people mate with those who are genetically similar but not too similar (i.e. no inbreeding).
Another way to see this is to look at y. For rare genes y is small. Hence.
50-50 is for genes that are rare and family specific. If your mother is color blind (100% carrier), the expected value of the number of color blind carrier is improved by 50%. It doesn't mean you'll be color blind. We'll have to go to the technicality of dominant vs recessive. But that's the idea.
For genes that are NOT rare, say genes that make you have 2 feet and 2 hand, you still share all your mom's genes. That's because everybody have that. Your mom have that, and your dad have that, and so is everyone else, including chimps.
Is this what most directly answer your question?
Again the issue is rarity. For rare genes P(You have it|mom have it) is 50%.
For common genes,
P(You have it|mom have it) = P(You have it and mom have it)/P(mom have it). //By bayesian rule
That is 1/1, which is true.
It's just obvious, probability = 1, that everybody has it.
Source: selfish gene by Richard Dawkins
I am a mathematician. Now prove me wrong.

C'mon. I got the math right here. Is it wrong?

Can someone tell me if I am wrong? I could be the only correct answer here.

Just a note that red/green colour-blindness is X-linked so it's much less common to find an affected female than male.

no body like math here

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Shortest strings not present in the human genome
What length are the shortest strings of DNA not present in any known person's genome, and what are they?
And is there a database online by which I could find this out?

Just for my personal curiosity... why? Anyway, the fact that not everyone's genome has been sequenced may pose a problem

I was about to write a description of how to find this out yourself but after closer reflection, this sounds hard. Essentially you’d have to build a dynamic programming solution but the solution will still have an exponential runtime with a huge exponent in the length of the result string (which we don’t know).

I would love to see an actual algorithm for this. The answers so far are tempting but remain quite theorethical

@KonradRudolph can you turn that into an answer and expand on it? Sounds interesting but I'd love to know why it would be that hard and what that solution would look like.

@Richard Actually, Ilmari’s algorithm would work in linear time. My approach was approaching the problem the other way round because I assumed generality, whereas Ilmari (correctly) assumes that we can give an upper bound on the length of the non-present infix, which allows the usage of look-up tables. My approach would have iterated over the whole search space of all possible k-tupes for k=2… (which is exponential) and check whether each of those exists a pre-built index of the genome.

I think you can count their possible length with statistics. I think finding them is impossible, because you cannot check the DNA of every living person... There are highly variable regions in the DNA, so in theory every combination van happen there... I think the shortest region - if there is such a thing - will be related to some functional stuff about DNA regulation (not my favorite topic), and it will be lethal if present. E.g. it will break chromosomes, or do some other fancy stuff...

Sequences that don't appear in a genome are called "nullomers".
That article claims that there are no 10bp sequences that don't appear in the human genome, and 80 11bp sequences that don't, citing this paper.

This is just about the protein coding region, but good point, there are diseases caused by specific DNA sequences. E.g. fragile X syndrome.

The human genome contains less than 416 base pairs, so, even after including a factor of 2 for the two strands and another to allow for some genetic variation, there must certainly exist some 17-base string not found in either strand of the genome.
Now, 417 bits is two gigabytes, which fits easily within the memory of a typical desktop computer these days, so a simple and efficient algorithm for finding such a string would be to set up an array of 417 bits, initialize them all to zero, and then simply iterate over the entire genome (including all known variations), taking each 17-base subsequence (and its complement), mapping them to base-4 integers and setting the bits in the array at the positions given by those integers to one.
Once you're done, any remaining zero bits will correspond to strings not found in the genome.  More to the point, the longest consecutive block of zero bits will give you the shortest base string not present in the genome.

simply iterate over the entire genome (including all known variations):  simply is not really the word I would have used but still...

@Ilmari: What you find with your method is those 17-sequences not in one human genome. But the question was about any known person's genome.

@rwst: The method I described can just as easily process multiple genomes, or fragments of genomes, and find those k-mers which are not present in any of them. I'm sure there are other complications one would need to deal with to apply it to actual genome data, but this should not be a major one.

@nico There are special data structures for this which do make it as simple as iterating over a single string (except that for each position you don’t have a single 17-mer starting there, but a list of 17-mers).

this is a good answer - there are certainly some 17mers that do not show up in the human genome. its certainly not possible to say that a given 17mer doesn't show up in any human genome, at least until we have sequenced every cell in every human being's bodies (non germline mutations happen too often).  That sounds hard.

This is why DNA PCR primers are about 20 bases long, helps ensure uniquiness. Also puts the melting point at a more reasonable temperature.

This actually wouldn't be too difficult to find. A common algorithm in genome assembly first takes stretches of DNA and finds all the substrings of length k that are present. (These are known as k-mers and the algorithm then builds the assembly based on how k-mers overlap.) So, given a genome(s) it's not that difficult to find all the k-mers of a certain length.
As Ilmari's answer points out, there are definitely 17-base k-mers that don't exist in a string of DNA the size of the human genome. Given the amount of repetitive content present in actual genomes, the actual shortest string will almost certainly be less than 17 base pairs.

Even if you give such a string you will never be 100% sure that you covered all human genomes, as asked.


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Use of amino-acid sequences versus use of nucleotide sequences in phylogenetic analysis
Reading a  paper about gene evolution, I see that they do phylogenetic analysis for bacteria using protein sequences. They take the method from another paper.
I can suspect that amino-acid sequences are more stable than nucleotide sequences, to the presence of synonymous substitutions.... but, is this stability required between closely related species? doesn't it make the analysis less powerful? does it make it more reliable? In other words, what's the advantage of using amino-acid sequences versus using nucleotide sequences for phylogenetic analysis?

This is a good answer to a similar question. http://www.quora.com/What-are-the-advantages-disadvantages-of-using-Protein-Alignment-vs-DNA-Alignment/answer/Alex-Siegel

In general, many sequence alignment programs can use multiple substitution models, distinguishing between nucleotides, amino acids, and codons. A protein sequence has functional information that is not directly visible in the nucleotide sequence.
The papers you link deal with horizontal gene transfer, where a gene is passed to more distant  organism. Different species have different codon usage biases, i.e. the translation efficiency is different for different codons. On one hand, this means that HGT is more likely to occur between species of similar codon usage. On the other hand, "codon usage of horizontally transferred genes approaches the host usage over time." Thus, on the nucleotide level, the phylogenetic signal will get lost due to the evolutionary pressure on translation efficiency, while on the protein level, there will be more conservation.

Due to the fact that several codons can code a same amino-acid, the amino-acid sequence is usually more conserved than the nucleotide sequence.
For small scale studies, the higher variability of nucleotide data brings useful characters to establish relationships between closely related organisms that might not be differentiated at the amino-acid level.
With long evolutionary distance, the nucleotide signal tends to become erased by multiple substitutions at a same site. A more annoying feature is that genomes tend to have a preferred nucleotide composition. A site undergoing substitutions will have an increased probability to display of the preferred nucleotide, particularly if the substitution has no effect at the amino-acid level (synonymous substitution). This mainly affects third codon positions, because, as you can see in the genetic code, this is where most codon families vary. It may happen that distant species share a same composition preference. The sites free to vary will then tend to display the same nucleotide in both species as the number of substitution increases. This can induce phylogeny reconstruction errors, especially if the models of nucleotide evolution are not sophisticated enough.
The larger the evolutionary scale, the higher the chance that such misleading features will appear in the nucleotide data. This makes amino-acid more suited to large scale studies. But ultimately, one could hope that using better models will enable to use the signal present in the nucleotide data to its fullest without being too much mislead. Using amino-acid data amounts to discarding some of the information present.
It should be noted that some methods use codon evolution models instead of nucleotide or amino-acid models: all the signal is kept, but it is possible to incorporate the knowledge that some codons are more likely to transform into one another, due to synonymy.


text:
Can humans survive without consuming life?
Some people say that it's awful that humans eat animals.  They feel that it's barbaric, because you're killing life and then on top of that, you're eating it, and that you should eat vegetation instead.
But isn't vegetation life too?  Personally, I see no difference between animals and veg as all life has cells, dna etc
So my question is, is it possible for humans to live healthy long lives without eating any type of life, i.e no animals, no plants, no cells (dead or alive) etc? If it is possible, how would it be done?

you might be able to survive on animal products such as milk (protein source) or an egg (although whether egg is life or not is up for debates) but I would imagine it would be pretty touch so I would say no if you can't use any plant/veg although you might be able to use rice (source of carbohydrates) from rice grains but then whether a grain is living or not is debatable (grains are quiescent) so the question is quite opinion based!

@Bez, In my view, milk, eggs, rice are all life or part of life. So there is no clear cut nutrition a human can consume which has no link to something living?  Basically, humans must consume life to live... ?

based on your definition of life, yes!

You mean on a strictly vegan based diet? No, that is not possible as we are not able to synthesize many important factors as Vitamin B12. There is no vegetable source for it.

What about eating things that have died without you directly or indirectly having killed them? E.g. a fruit on its own is not alive and if you remove the seeds and plant them you are in no way killing anything.

It would require the ability to synthesize all the sugars, fats, amino acids, vitamins, etc necessary for life totally from chemical sources. It would be very expensive and burn a lot of energy. You might be able to engineer bacteria or yeast to make them, but then you'd still be eating living things.

@oshirowanen just remembered this (http://www.bbc.co.uk/news/science-environment-16972761) but I do not know if that falls in your definition of life and killing the living.

"any type of life" asks for the most inclusive reasonable definition of life, and that would include any type of cell or cellular material as alive.

It's possible since 1972:  https://en.wikipedia.org/wiki/Vitamin_B12_total_synthesis

Clarification, please? Consuming "life" seems too ambiguous as many answers/comments point out. Various seeds, and many other similar plant parts, are intended (by evolutionary tendencies) by the plant to be eaten and somewhat spread by animals. Some number of plant species would become extinct if parts of them were not eaten/spread by animals. By not eating them, is that contributing to the extinction of a species? (Probably wouldn't happen due to other animals, but it might have philosophical implications for the question.)

Also, food synthesis technology is progressing rapidly: Breakthrough reveals how vitamin B12 is made is from a full year ago.

The vague definition of life and intangible solutions presented makes the question and any solution offered highly speculative and philosophical in nature, deviating from any practical solutions or biology.

Hi all - I've removed a lot of the comments on this question that were not requesting clarification etc. - please remember to use Chat for extended discussions

@oshirowanen In the question you have "without eating any type of life, i.e no animals, no plants, no cells (dead or alive)..." Dead cells and life are in the conflict here and may cause confusion.

@MichaelT are eggs intended to be eaten?

A related question I asked on Hinduism - Why can we eat 'living' plants but not 'living' animals?

The answer to your question is yes it is certainly possible.
At one time it was thought that there was something special about "organic" chemicals which meant that they could not be artificially synthesised out of fundamental elements. In 1828 Frederick Wöhler synthesised urea (CO(NH2)2) which is often taken as the first demonstration that the organic v inorganic distinction was not a sound one (for more on this see the Wikipedia article on Wöhler synthesis.
As far as we know all essential human nutrients can be synthesised from inorganic ingredients, even complex molecules such as Vitamin B12.
Other contributors have pointed out that organic pathways for synthesising our food have evolved over long periods to be very efficient - at least in the conditions prevailing on Earth. You haven't ruled out copying biochemical pathways using chemicals that are entirely of inorganic origin. Anyone trying to do this seriously could create glucose (for example) by artificially creating enzymes (perhaps via artificial DNA) to do the job. The thing is that we already have self-replicating and repairing machines to do that already (plants).
There might be circumstances when we needed to use artificial synthesis. I can think of two science-fiction stories that deal with this question, the first of which goes into some detail:

The Moon is Hell by John W. Campbell, in which astronauts are stranded on the moon and forced to make food from what they find there.
Technical Error by Arthur C. Clarke, in which a man is accidentally rotated through the fourth dimension. His employers contemplate the difficulty caused by the "handedness" of many biological molecules meaning they would have to artificially synthesise many of his foods.

It may be that a future expedition to Mars (say) might have to think about these things.
A little searching fails to come up with standard inorganic syntheses of glucose and similar substances. The reason for this is almost certainly because it is so easy to use organic inputs. Glucose is easily made by the hydrolysis of starch. Starch is very common and cheap. Even l-glucose is usually made out of organically derived precursors (or sometimes even using d-glucose).
UPDATE: sources etc
One problematic question is: where do you get your input for making nutrients? As others have pointed out, exactly where to draw the line is difficult.
This problem starts in defining what is alive in the first place. Do you count viruses (which can go down to a few thousand base pairs of RNA) or satellite viruses (STobRV has only 359 base pairs) or prions? In a sense these are "just" very large molecules. But then really simple bacteria are not many orders of magnitude more complex. As an aside most systems of ethics that do not permit eating meat do not make an alive/non-alive distinction, choosing some other aspect such as sentience, though Jainism comes close to doing so.
The second problem is, if we reject living things as sources of food, how far removed from those living things are we allowed to get? You say no cells in any state including "dead". That would exclude (say) fruit even though most fruits are expressly created by plants in order to be eaten (and in some cases must be eaten) - something that vegans, jains, fruitarians and others would be happy with eating. If we could use dead material things would be much easier.
But would you also include hydrocarbons (coal, oil, gas) which were once living organisms? If you do, then you are in difficulty because terrestrial carbon is recycled through the biosphere. All CO2 was (to a close approximation) once a part of a living thing. If you take that position then of course you are going to have to go off-planet to find your source chemicals and your problem becomes very much harder.
I was assuming that you were restricting yourself to consuming cells that retain some of their cell structure but had not completely degraded. If that is where you draw the line then there are ample sources of raw materials on earth.
Genetic modification is much more science fiction though not entirely impossible. Some nutrients could be made by humans without much difficulty. Our inability to manufacture vitamin C is down to one missing enzyme (L-gulono-gamma-lactone oxidase) which is present in most vertebrates (I think of mammals only guinea pigs, humans and some bats are unable to synthesise it). You could certainly imagine some very careful genetic modification changing humans so they no longer need to consume vitamin C.
But photosynthesis would be much harder. Chloroplasts (which do the job in most plants) are really a very primitive form of life living in plant cells which may independently reproduce  (and for that reason might be excluded by you - they aren't "cells" but they have membranes). They could easily end up in conflict with our mitochondria (since intracellular conflict between organelles is possible) and you would need to do enormous amounts of work to make human cells co-operate with them properly.
More in keeping with your theme would be adding photosynthetic systems directly to human cells along with a suite of enzymes to manufacture all the things we cannot. That is of course in principle scientifically possible (since plants do it) but much harder than it looks. Living systems are very complicated and small changes can have unexpected consequences. Even very minor genetic modifications are problematic. The human autotroph is likely to be some way off.

+1 for the Asimov story! It is possible to survive on poisons only if one can rotate oneself through a fourth spatial dimension. I must also mention "Technical Error" (aka "The Reversed Man") by Clarke.

A "yes" would indicate that it would be possible right now. Do we have readily available technology for it available now? I guess not. Wouldn't that make a "No, but theoretically possible in the future"?

I had a go at finding pricing for artificial synthesis of things like glucose but got nowhere (for reasons that are obvious). We know how to do it (i.e. we have the technology). Doing it might be insanely expensive, but humans are well known for doing insanely expensive things :-).

Just to understand better: say we have set up a laboratory to inorganically synthesise every necessary nutrient. What would we use as raw materials? Where would we get carbon and the other elements? Would we able to obtain them without violating the OP's provisos?

All organic components can be found in air and it is certainly possible to make them useful (plants do it too). Inorganic nutrients would need to be drawn from the ground but no live organism would need to be used or killed for that.

FWIW, the summary of Left to Right is quite inaccurate. Here's the full text: http://www.scribd.com/doc/209177509/Asimov-Isaac-Gold-02-Left-to-Right

@TimS. Well spotted. My mistake, I had in mind Technical Error and a hurried search found me the wrong story. The reference to chirality in amino acids made me think Asimov for obvious reasons.

Did you mean to say, "most fruits are expressly created in order to be eaten ... by the plant", or did you actually mean "most fruits are created by the plant expressly in order to be eaten"? +1 for considering the variety of angles.

Ooops, yes, "by the plant" got a way from its antecedent.

Interestingly the GM to restore Vitamin C production has already been tried: http://www.sciencedirect.com/science/article/pii/S0888754303002714

If you count coal or CO2 as "life", why not water? In that case you're boned as it was all once in a dinosaur: https://what-if.xkcd.com/74/  Granted, most wasn't molecularly incorporated and liberated (via dehydration/hydration reactions).

@NickT - that's exactly my point. How difficult this is depends very critically on exactly where the line is drawn. If you are allowed to use dead leaves/wood etc then it is much easier. If you aren't, it is unclear why CO2 and as you say H20 is OK.

It would be helpful to consider photosynthetic efficiency, en.wikipedia.org/wiki/Photosynthetic_efficiency since plants can be thought of as biological solar panels. If we wanted to replace all food with abiotic sources, we'd have to burn a lot of energy to do it. Thankfully, artificial solar panels are already more efficient than plants at energy capture, it would still require methods to use that electricity to fix carbon and nitrogen and produce nutrients. But it's at least possible to estimate the energy cost.

An excellent answer, but I don't think it satisfies the parameters, given from http://what-if.xkcd.com/74/ that "This means that while the chances are that most of the water in your soda has never been in another soda, almost all of it has been drunk by at least one dinosaur" so that even the inorganic compounds (say, water) you're using for synthesis have at one point been part been part of a living organism. It's possible, but not guaranteed. We could collect hydrogen and oxygen from Jupiter to make water avoiding this issue, assuming Jupiter is lifeless and formed from lifeless origins.

@DonBranson: I think we can distinguish between chemicals that were once part of a living organism and chemicals that were actually produced in a living organism. If you take my blood to make heme, that's very different from making it using an iron splinter that had previously been stuck in my hand.

@ruakh Your point is that the chemical would exist regardless of whether it was one part of creature? That's a good point.

Living organisms can be divided into hetrotrophs and autotrophs. Autotrophs like plants and algae are able to produce complex organic compounds from relatively simple inorganic components. They are satisfied with sunlight, water and other abiotic stuff and do not need to consume "life".
We -- along with all other animals -- are not autotrophs, but heterotrophs. This means that we cannot produce organic compounds by ourselves but need to 'reuse' the ones that are produced by autotrophic organisms. That's why no human will ever be able to live without consuming other life.

Ever? Are you sure about that?

As user137 pointed out, you would need to synthesize ALL nutrients from anorganic sources. No one will ever do this because plants have had hundreds of millions years time to become really really good in that. Why would you want to compete with them? In so far: Yep...never ever.

@N0ir OP defines milk as life if you look at the comment threads so it becomes difficult to offer any solutions apart from synthesis or food.

@antonone key word probably being possible for a "human"...possible for something a human evolves into? I don't see why not. But it'd be different enough that it probably wouldn't be classified as a human any longer.

organic != life. vultures? bacteria that decay matter? organisms consuming milk, eggs, fruit, pollen?

The question was whether it was possible, not whether we would. Also "never" is a long time.

This answer is wrong. As explained by @FrancisDavey, it is certainly possible for us to synthesise every single nutrient we need from inorganic substances, at the expense of energy which we can gain non-organically too for example through solar or nuclear sources. That is, by all ways of understanding it, "without eating any type of life".

Following this logic, you would have to answer almost every question with "yes, it's possible". Can we travel between solar systems at warp speed? No, but some people imagine it to be possible at some point far, far in the future. But based on our current knowledge that's fiction and does not mean anything. My answer is based our current knowledge, too. At the moment and in all foreseeable future it will not be possible to live without consuming 'life' (as defined by oshirowanen). I doubt it ever will...

At the very least current technology would allow you to build bacteria to synthesise all nutrients you need, in which case you would then not need to consume any live organisms but only chemical products they're not using themselves. It is true that you could consider everything within physical boundaries as possible, but what this question asks is either within or not far off available technology. Of course you are correct that the chance of it happening anytime soon is zilch due to lack of demand, but that's not what's being asked.

It has neither been asked if there is some way imaginable. Apart from the fact that in the OP's sense there is no difference between bacteria- or plant-synthesized substances, I interpreted the question in a more practical way than you. It seemed to me that the OP wanted to know if there is some way how he/she can live without harming or exploiting any living creature.

There is no known technology that would allow interstellar travel at warp speed (indeed there's no scientifically known process that would allow it - the Alcubierre "drive" doesn't allow it in the conventionally understood way) whereas all vitamins, amino acids etc have known inorganic syntheses (and obviously so with artificial enzymes) so it isn't the same thing.

I'm sorry to hear. Perhaps this site suits you better: http://scifi.stackexchange.com/

re. your second comment, have you BEEN to a grocery store. what is a vitamin pill in the first place. have you seen how animals are raised on a factory farm. as far as competing with nature, mankind's stance has always been "bring it on."

Even on a purely synthetic diet, your body would still use living cells as an energy source. Our bodies contain more bacterial cells than human, mostly contained in our gut. These microbes process any nutrients we ingest and when they die, we absorb their cellular components as nutrition.
The lining of the gut is the most rapidly dividing population of cells in the body. Unlike skin cells, when these die, our intestines recycle much of this as nutrition. Throughout the rest of our bodies, when a cell dies, its components are recycled: red and white blood cells, mucosal membranes, invading microbes, etc.
When you kiss, engage in intercourse, there's also an exchange of living cells which die in the process.
Abstaining from organic food, human contact will not stop the fundamental processes of autophagy, apoptosis, digestion, cell turnover of both our own and microbial cells.

The most beautiful answer.

Human solid body waste is as much as 50% dead bacteria from the gut.

Your question is phrased somewhat ambiguously as to whether you're asking about the theoretical possibility, the feasibility, or the practical ability in everyday life.
1) Theoretically, yes. It is chemically possible to produce all substances that humans need to survive without the use of living organisms in the process. In the end, biological systems use chemical processes, so at the very least it would be possible to isolate the biological (enzymatic) machinery and use it without the live organism around it. The latter is within current biotechnological capabilities.
2) Feasibly, no. Going through the hassle of making all those substances in that way would probably be less efficient than simply using the biological (live) systems that already exist and are very efficient at it - in particular, plants.
3) Practically, no. Using only currently commercially available products (i.e. things you could buy right now), you will probably not be able to source a full human diet without relying on some live organism at some point in its production exactly because of number (2) above.

So now we agree.

I don't think we ever disagreed XD I felt like number 1) in my answer was what the question asked and so that would be the correct answer - but it's true that the question is sort of ambiguous and hence I decided to post this general answer.

mattkaeo's answer provides an interesting additional consideration for (1), though. I don't know whether it's clear what happens when you stop "eating" your symbiotic gut flora. One might suppose that if all the necessary nutrients get into the bloodstream somehow then you're good to go, but there's probably more to deal with than just synthesizing the nutrients, since various systems in and around the digestive tract will be perturbed and need sorting. People fed entirely IV tend to be fairly unhealthy, admittedly they're usually unhealthy to start with, that's why they're fed by IV.

As long as the necessary nutrients are consumed orally and go through digestion, your gut flora and your own health should be fine. You could synthesise and consume indigestible carbohydrates (i.e. fibre) to support that additionally. His answer is an interesting thought though and does answer the question "Can humans survive without consuming life?" in a different angle.

@SteveJessop there have been experiments on animals, rising them in a bacteria-free environment and thus without gut flora. http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1500832/ for example. The current verdict seems to be that this is possible, but unhealthy; if we ever would raise humans in sterile environment (interplanetary colonisation by growing people from fertilized cells and local resources?) then we should 'infect' them with the common gut bacteria.

Depends on how you define "life"? Is unfertilized chicken eggs alive?
What about cow milk? Well there are bacteria in it. What if you get rid of that bacteria? Then some people would not be able to utilize lactose...
Also as Bez mentioned rice grains are quiescent, meaning they are in a dormant state and not really "alive" but again depends on how you define "life". Even top biologist have trouble defining "life" and there exist many competing definitions of "life". All of them have their advantages and disadvantages, but there is no universal definition of life on which all biologists would agree.
If you consider everything above as "life" then it is not really possible for humans to survive without consuming other life.
If only we could sustain chloroplasts in our epidermis layer we would be able to synthesize sugars for ourselves. But then we would become little green men...
So it is much better to respect your meat. Whenever you eat meat just be conscious that something had to die to produce that meat. Be grateful for that lost life and realize that part of it will live in you.

Ask you asked, my definition of life is something has cells/dna in any form (dead, dormant, or alive).

Viruses have DNA/RNA in them yet they are not living, they are more like containers. So not everything that has DNA is actually life. You can have a bunch of DNA in a tube, you wouldn't consider it life would you?

Question: Is it possible for humans to live healthy long lives without eating any type of life, i.e no animals, no plants?
First, according to a definition of a living organism(biology-online), milk is not live, because it does not have an ability to reproduce itself, among other...
My claim: If you consider milk and honey non-live (no DNA), then, yes, humans can survive for some time by consuming only these, and water. An example are infants, who can live exclusively on human breast milk and water for more than 1 year.
This is human milk composition (Nutritiondata), from which you can see it contains all essential nutrients (Nutrientsreview) (essential amino acids, fatty acids, vitamins and probably all essential minerals - not all essential minerals are listed in Nutritiondata milk composition, though).
But to actually prove that humans can or cannot "live healthy long lives" by consuming only milk and honey, one would need to do a human trial...and I'm not aware of any.

I think if you live off the by-product of a creature that consumes life, it would be cheating to claim that you don't.

You do not need to kill or harm a living being to use its milk. I believe, from what is obvious to me, this is how things are meant to be, at least for infants.

And how will the cow produce its milk? It has to graze, therefore killing thousands of organisms.

No.
It is possible but extraordinarily impractical to nourish yourself without killing animals, plants or even bacteria, as many have explained in detail.
However, your immune system constantly kills pathogens that infect your body. What's worse, the macrophages literally catch and eat these bacteria alive, so you are very much "consuming" them.
You could live in a bubble, but even then there are bacteria in your gut. In your gut, they are not attacked by your immune system, but they can sometimes get through the gut lining into the body, where they are attacked. They could also escape from you anus into the environment, and then end up elsewhere in your body.
Even if you had a magic force field keeping the gut flora inside the space of your intestinal lumen, they could still mutate and become immunogenic, then get consumed by your macrophages. Anyhow, collectively, your gut flora has more cells than your body, so is it really fair to say "you" did not consume any life when this symbiotic bacterial mass living inside you (more like you are the parasite living outside it) consumes some of its own cells?
But let's say you get rid of your gut flora, too. It's a hell of a life, and you wouldn't wish it on your enemy, but it solves that problem. Now only human cells are present inside your bubble. What happens when eventually your cells mutate and you get cancer? There are natural killer cells that will try to consume the cancer. So you have still consumed life.
Let's say you made yourself immune to cancer. That's impossible, but let's say you made your DNA polymerase so high fidelity that it takes millions of years for even a single mutation to occur (this is also almost impossible). Your body still has to kill cells through apoptosis as part of maintaining its own function. Again, to conserve resources, these cells are literally swallowed. It's debatable whether an apoptotic cell is alive, but it is made to die by influence of other cells, so this is very analogous to killing a chicken and eating it. In principle.
The answer is no, but your question becomes meaningless if you define "life" scientifically. It is only possible to live without consuming life if "life" means only plantae, metazoa and fungi. But that is not what it means, because at least some Eastern religions do consider eating microbes to be "consuming life".

Lame, boring answer
The Universe has a finite reserve of (dis)entropy. When that runs out, no more life can exist, because all life must increase entropy. Even on Earth, by simply being alive you are taking up space that could be used by other organisms. To be alive you require some form of energy; even if this energy is solar, you would still be using up energy that could have been used by a plant.
By simply existing, you are irreversibly destroying vital resources necessary for other life. Thanks to you, at least some life somewhere will be left without resources and starve. Therefore you cannot exist without harming life.

Well, technically if you are eating something from a plant or animal without killing that plant or animal, then technically you would not be "consuming life" as nothing as been killed. Fruits, for example, can be removed from the tree without harming it and in fact are meant to be removed as that is how the tree reproduces. Ditto with berries, melons, squash, cucumbers, peppers, beans, seeds, nuts, etc.
As for animal products I think only milk and honey would qualify as technically an egg is a future animal.
So yes, I would say that it is completely possible to live a healthy life without once killing another living thing.

As far as I understand, fruits are alive, they have cells and dna just like animals and humans.  A single cell is a simple form of life.  So if you're eating fruit, technically, you're consuming life.  Therefore, no different from eating an animal.  If you think about it on a larger scale, you could say that animals are the fruit of the earth...

There is no way you could go through life without EVER consuming something with cells. Even while you are sleeping several hundred ants, insects, spiders, etc WILL crawl into your mouth and be swallowed over your lifetime. Why the problem with consuming cells, anyway? Fruits and the like will fall off and decompose anyway and they are not sentient, so why the moral dilemma?

Ah, I see. Then I suppose it's theoretically possible to survive without INTENTIONALLY consuming living cells, but great scientific effort would have to go into making the synthetic products available

@oshirowanen if you count even single cells as alive, then that includes bacteria and other single-celled organisms that aren't even plants. Such a diet isn't currently feasible, for some key nutrients the only vegan options are obtained by killing bacteria.

It may be feasible to live without consuming anything that was alive, but it would be incredible difficult.
For example, all humans need to consume glucose to survive. Glucose is the only food source used by cells in the brain. Plants are the easiest source of food source for glucose. If we can't get glucose from plants, then we would need to synthesize it without the aid of enzymes or any sort of organism. A quick google search does not yield any hits for how this synthesis could be performed. Probably because it is so easy to get a plant to make the sugars for us.
Now think about all the amino acids, vitamins, fats, and minerals that we would also need to synthesize or extract without any organism intervention.
You have gone from the good intention of not harming another organism to the creation of a whole chemical industry dedicated to the production of nutrients for people.
Think about this as well. When you poop, a lot of the poop is actually dead bacteria that was living in your gut.

Can you please improve your answer and add some references? If you want to know about glucose synthsis in the human body, look up gluconeogenesis.

It would be great if you could add references to your answer specially regarding the last line!

@Chris Gluconeogenesis is how your body generates glucose as a last resort. It is a lot easier just to eat glucose. It requires the use of enzymes. I suppose you could synthesize the enzymes in vitro.

@alex But what about glycogen? Doesn't the breakdown and synthesis of glycogen not require enzymes? And doesn't glycoysis, the TCA cycle and the Respiratory Redox Chain make extensive use of enzymes in turning glucose into "energy"? IMO Chris makes a very good point (to which we may add that no net synthesis of glucose can occur from fatty acids).

"When you poop, a lot of the poop is actually dead bacteria that was living in your gut." Some of them are still alive... imagine their horror... Now all vegetarians are gonna stop pooping

@N0ir As John Lennon put it "Imagine there's no heaven..."

Sounds surprisingly, but neither glucose or any other carbohydrate is essential for human life. Humans can produce all carbohydrates, including glucose, they need. Also, human brain, when no glucose is available (prolonged fasting), can use ketones as a fuel.

It is entirely possible to live without consuming life using only current technology.  In fact, there is a company called Soylent which has developed a food substituent designed to replace all eating, entirely.  The philosophy of that company is that – food is just a collection of chemicals for the body to process, and that as long as the body gets all of the necessary chemicals, it will survive fine. That is exactly what soylent aims to do – the powdered mix they produced has all the chemicals necessary for human life.

The ingredients in Soylent get its calorific value from rice, oats, soy and other plant products.  As such it doesn't fulfil the criteria of the question asker

Soylent Green is People!

Honey is produced from nectar that does not contain any living cells and carefull beekeeper should be able to take at least some from the hive without killing any bees. However bees themselves will also consume pollen that is alive.
It also may be possible to feed on fruits; while cells there are still alive, they are about to die soon without any prospects of future surviving. If you really do not want to harm the plant in any way, take the seed from the fruit and plant it somewhere. Fruits are for seed propagation only and the plant should really not have any pretensions to you afterwards.
Dead leaves in the autumn may contain the needed materials; unfortunately they are not edible directly and would need some pre-processing technology.


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Are there oligocellular organisms in nature and, if so, what are they like?
I'd think protozoans can be oligocellular, but I haven't found any examples, and I'm curious to know what is the minimum number of cells an organism can have other than a single cell.

Well, do you consider relationships like the Mitochondria and Chloroplasts - who were separate bacteria that became functional organelles - appropriate?

Various colonial and multicellular forms of cyanobacterial species are reviewed in:

Beardall, J et al. (2009) Allometry and stoichiometry of unicellular, colonial and multicellular phytoplankton. New Phytologist 181: 295-309

Nostoc and Volvox are some of the simplest true multicellular organisms known (usually 3-4 cell types), but in both cases the differentiated colonies (filaments in Nostoc, spheres in Volvox) typically consist of hundreds of cells.
The paper below reports the emergence of a colonial form of a unicellular organism. Since there is no evidence that the individual cells within a colony have specialised functions this doesn't really count as 'oligocellular' but it is an interesting angle on the question nevertheless.

Boraas, ME et al. (1998)Phagotrophy by a flagellate selects for colonial prey: A possible origin of multicellularity. Evolutionary Ecology 12: 153-164
Abstract: Predation was a powerful selective force promoting increased morphological complexity in a unicellular prey held in constant environmental conditions. The green alga, Chlorella vulgaris, is a well-studied eukaryote, which has retained its normal unicellular form in cultures in our laboratories for thousands of generations. For the experiments reported here, steady-state unicellular C. vulgaris continuous cultures were inoculated with the predator Ochromonas vallescia, a phagotrophic flagellated protist (`flagellate'). Within less than 100 generations of the prey, a multicellular Chlorella growth form became dominant in the culture (subsequently repeated in other cultures). The prey Chlorella first formed globose clusters of tens to hundreds of cells. After about 10-20 generations in the presence of the phagotroph, eight-celled colonies predominated. These colonies retained the eight-celled form indefinitely in continuous culture and when plated onto agar. These self-replicating, stable colonies were virtually immune to predation by the flagellate, but small enough that each Chlorella cell was exposed directly to the nutrient medium.

Just to add to this, there have now been several other experiments observing transitions form unicellularity to multicellularity in organisms. E.g. see https://doi.org/10.1073/pnas.1115323109. Another article summarizing a number more recent examples of this being experimentally observed is here: https://www.quantamagazine.org/single-cells-evolve-large-multicellular-forms-in-just-two-years-20210922/


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Why did high A+T content create problems for the Plasmodium falciparum genome project?
The main paper for the Plasmodium palciparum genome project (Gardner et al., 2002) repeatedly mentioned that the unusually high A+T content (~80%) of the genome caused problems. For example they imply that it prevented them using a clone-by-clone approach:

Also, high-quality large insert libraries of (A + T)-rich P. falciparum DNA have never been constructed in Escherichia coli, which ruled out a clone-by-clone sequencing strategy.

And that it made gene annotation difficult:

The origin of many candidate organelle-derived genes could not be conclusively determined, in part due to the problems inherent in analysing genes of very high (A + T) content.

Question:
What is the biological significance of high A+T content, and why would it cause problems in genome sequencing?
Ref:
Gardner, M.J., Hall, N., Fung, E., White, O., Berriman, M., Hyman, R.W., Carlton, J.M., Pain, A., Nelson, K.E., Bowman, S., Paulsen, I.T., James, K., Eisen, J.A., Rutherford, K., et al. (2002) Genome sequence of the human malaria parasite Plasmodium falciparum. Nature. 419 (6906), 498–511.

I am not an expert in molecular biology so I will leave this as a comment. I think the problem is the same as for G/C rich regions: if you mostly/only have A and T you have much less possible combinations of nucleotides and you will have many more overlapping sequences in the genome, which will hinder sequencing because it will be difficult to overlap the clones.

Good point nico, so by reducing the complexity you increase the chance of having non-unique ends.

The sequencing technologies that were developed in the last 20 years have a range of optimal use at an average A+T/G+C rate. Both highly AT-rich and GC-rich regions are complicated to process by the different sequencing technologies. Each technology has different ranges of usage, but to name one, Illumina technology prefers sequences in the middle range. If you try to sequence an AT-rich genome with the Illumina standard protocol, you will sequence an incomplete genome, the fragments of which are not a perfect reflection of the original complete genome. Other technologies claim to be completely unbiased to nucleotide content. Pacific Biosciences is one of them, and people seem to agree on that claim, after having analyzed the data that is produced by their machines. Oxford Nanopore Technologies claims that they have almost no biases, but as of today (2012-06-13), there is no confirmation of that by external analyses.
Beyond sequencing problems, the software used to assemble and annotate the sequences may also be prone to errors in AT-rich and GC-rich regions. But many of those problems stem from the incompleteness of the sequencing.

I can't comment on how A+T richness complicates the sequencing process itself, but I can comment on complications that arise when annotating the sequence. Ab initio gene predictors are often based on hidden Markov models that are very sensitive to base composition in the genome (di-nucleotides, tri-nucleotides, etc). These gene finders typically perform very poorly if they are run on a genome that has a much different base composition than the one on which it was trained. This could explain some of the difficulty they has with analyzing genes in the genome.

Often sequencing involves a step of amplification of genomic material. The standard way to perform this is with PCR, but PCR is biased and does not amplify very AT-rich regions well. With multiple rounds of PCR, even low-abundance regions that are not as AT-rich might come to dominate the sample and hide the AT-rich sequences.
This is not only a problem for de novo sequencing, but for many sequencing-based techniques (RNA-seq, ChIP-seq, your-favorite-seq...). Alternative methods have been employed in plasmodium, but they are not as standard (yet?).
See, for example, H2A.Z Demarcates Intergenic Regions of the Plasmodium falciparum Epigenome That Are Dynamically Marked by H3K9ac and H3K4me3 at http://www.plospathogens.org/article/info:doi/10.1371/journal.ppat.1001223

A lot has already been said in previous answers so I am just gonna add briefly two potential issues with strong AT/CG bias:
1) Potential for polymerase slippage due to homopolymers: this introduces errors in general because you may have unwanted indels in the reads as well as purely incorrect bases being incorporated. This is a problem that can happen even with PCR (although there's a lot of choices now if u want to spend). So in general higher error rates and higher read failure.
2) Difficulty of the machine to separate the signals of individual nucleotides for SANGER (it gets all blurred) or calibration errors with next gen sequencing. So higher read failure (bad quality).
3) Assuming everything is now fine, still lower complexity regions can be VERY hard to map, let alone assemble a complete genome from scratch.
Hope this helps!

In the past, before massively parallel sequencing, they made a library of cloned sequences and transformed these into E. coli. High AT sequences are difficult to maintain in E. coli (perhaps due to similarity to promoters?).


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Transplantation of stem cells
During the autologous transplantation of stems cells from bone marrow to produce new blood cells why all the other stem cells other than the one obtained are destroyed?

Autologous stem cell transplants are used to treat individuals who have had their bone marrow destroyed or damaged by diseases such as lymphomas or by irradiation or cancer treatments. As they are damaged and potentially cancerous, they are removed. They are then replaced in the transplant. The whole idea is to destroy all the cells before transplanting the marrow back.

thank you
So the stem cell is obtained from another part of the body and transplanted into the bone marrow and not obtained from the bone marrow itself?

or to make it simple where is the stem cell obtained from ?

Although most of these stem cells are in the bone marrow, there are also some in the blood and these are collected in order to perform an autologous transplant.

What Alan said is not always true, they can be taken from the blood or bone. Certain chemicals can cause the cells to leave the bone marrow to collect them in the blood. They are collected when you are in remission or free of any disease and stored, frozen. Then if the disease comes back, every cell is destroyed (hopefully killing every cancer cell) then the frozen stem cells are transplanted back to reconstitute the immune system. This can be repeated but typically shouldn't need to be.


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Batch convert miRNA names to Accession IDs?
Does anyone know of tools to convert lists of miR names to their miRBase Accession IDs? I know they exist, but my search keeps pulling up gene ID converters.
EDIT: both @rg255 and @shigeta have provided solutions to the underlying issue, but I am curious to know if something exists for miRNAs that is similar to a site like this.
EDIT 2: miRNA names are of the form 'hsa-let-7a' and Accession IDs are of the form 'MI0000060'

in what species? this website looks like it will have them http://www.mirbase.org/cgi-bin/browse.pl?org=hsa If you are trying to connect them to data I'd suggest you find the table you want, save it in to a .txt file and use R to match them up.

Somehow, I completely missed that page. Thanks! (If you wanted to post that as an answer, I'd accept it.)

in what species? this website looks like it will have them mirbase.org/cgi-bin/browse.pl?org=hsa If you are trying to connect them to data I'd suggest you find the table you want, save it in to a .txt file and use R (using the merge() function - df=merge(df1,mirbase,by="miR_names") would be a rough guide) to match them up.
Here is a batch converter - http://atlas.dmi.unict.it/mirandola/tools.php - add the text list to box on the right and it produces a table.

Thanks, especially, for pointing out the merge function; I hadn't considered a solution in R.  (The only issue I see is that this particular table doesn't include mature miRNA IDs, but it's a useful list for other reasons.)

@dd3 see added batch converter tool - but could you post an examples of what "miR name" and "miRBase Accesion ID" typically look like so I can tell when I find the right thing. I.e. are you expecting a sequence of numbers, letters, alphanumeric sequence, symbols, a word, a sentence, or (albeit unlikely) an extract from a Shakespeare text... thanks

This is what I meant. I know this wasn't part of my question, but do you have any idea whether something like this exists for mice?

no idea I'm afraid

Well, thanks for all of your work on this question, especially with the repeated edits. (I'll work on making future questions clearer from the start.)

If you want it all, download the mirRNA.xls.zip file from mirbase here:
ftp://mirbase.org/pub/mirbase/CURRENT/
its a spreadsheet that includes these data as columns and also more information besides - for the entire database.

bulk downloads in columnar format are always the way to go :)

That, and Python. I think I make dictionaries for everything.


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What is in the space between neurons in a brain?
When neuron animations are displayed, there are frequently seen neurons, axons arranged in a lattice with a lot of empty space between. I'm interested if there is indeed empty space in the brain, or if it is filled with some sort of fluid? I've checked an article on cerebrospinal fluid but am not sure that it is present all throughout the brain.
The reason I'm asking is that I'm thinking of neurotransmitters- they are released in synapses, but I'm not sure how they stay there - are they suspended in some liquid as well?

Not so empty, actually.
The human brain has a mass of ~1.5kg, and volume ~1200cc (a little bigger for men, a little smaller for women). So is heavier than water by a good margin.
While it has Cerebrospinal fluid, that only occupies the subarachnoid space (the space below the skull and above the cortex, contained between two layers: pia matter and arachnoid membrane) and the ventricular system (several spaces inside the brain, remnants of the embryological development of the brain).
Neuron density may vary widely, depending mainly on the particular characteristics of neuron cell types and their interconnections. But besides neurons, there's a lot of infrastructure inside the brain. For example:

Astroglia: They are a type of glial cells which participate in the formation of the blood-brain barrier (supporting the endothelial cells), nourishing of neurons, maintenance of ion and neurotransmitter concentrations, among others. They also keep in place most of the tissue.
Microglia: Small cells with immune (phagocitic) functions inside the brain.
Radial glia: A more specialized precursor cell, that also participates in neuronal migration in the brain.
Oligodendrocites: Cells responsible for the insulation (myelination) of axons.
Neuroepithelial cells: The stem cells in the brain.

Neuroglia, which includes the first four cell types above, accounts for ~90% of tissue in human brain (http://classes.biology.ucsd.edu/bipn140.WI13/documents/Gliamorethanjustbrainglue.pdf).
Also, when you collect some billions of axons, they can be quite representative in terms of mass and volume. The ratio between white matter and gray matter is close to one for humans, but lower for smaller mammals (http://www.pnas.org/content/97/10/5621.full.pdf).
About the last part of your question, the synaptic cleft (the space between pre-synaptic and post-synaptic neurons) is a salty solution: water with high concentration of sodium and chloride ions (and also calcium ions, neurotransmitters and a lot more). These ion concentrations are fundamental to the generation of action potentials, neural signaling, and the general dynamics of the brain.

To get an idea of how crowded the brain is, play around with the eyewire project (https://eyewire.org). I always thought the brain was mostly space, like it is in diagrams. But it's more like densely packed spaghetti than a fishing net.

I really wonder which of these special cells (or anything else) is responsible for getting nutritions to the neurons for creating electrical potencial. Or are the ions just freely released into the brain?

The answer here again is water. Please see my answer to the main question. Electrical gradients IN the water is what drives the work done in cells.

Apologies for just referencing Wikipedia, but this is a very old bit of science.
The neuron gap junction - the point where the axon touches the next cell over - is 4 nanometers.
This is actually a controlled channel where the neuro transmitter molecules are transferred from one cell interior to another - its a controlled cellular - cellular channel so they really are as close to touching as they could be.

The reality is a variety of very dense arrangements of axons and neurons:

This image is from the cremi challenge website, where you can find some varieties of neuron maps from different regions.
Here's a video explanation of the process for building the neural images:
https://youtu.be/OoU_GF4fc6w?t=659
There are some efforts to map the neuron circuits of mice and drosophile fruit flies, to be able to add them into computerized physical versions of the animals. It's still many years away for even a fruit fly.
There's a good video of nanometer slices here https://www.simonsfoundation.org/2021/03/22/the-connected-connectome-part-2-beyond-the-fly/#
This pic answers the title of the question, here we see 10 micron wide cell bodies of neurons, the cell bodies are distanced by 15-35 in that region.

The question is what's BETWEEN neurons. Most of these answers don't actually even answer. They just say "it's not very empty". Yes, the gaps between neurites are quite small, but not compared to a water molecule. In the images that I took below, it may appear that there is no spacing, but this is misleading as the tissue and areas shrink quite a bit as a result of the processing required for imaging. If you use cryo-fixation however, you can see the gaps more clearly. These gap sizes are not trivial. While they may only span anywhere from a few nanometers to a few hundred, SOMETHING occupies this space. The answer is water. Water molecules are about 1/4 of a nanometer. If you do an Xray analysis in these spaces (as I have done), you will find that its overwhelmingly filled with oxygen and hydrogen, aka water. I could go on, but that is all the question asks of and I hope I have demonstrated sufficiently that water is indeed the most prevalent substance occupying the space in between neurons.

It's mostly filled with water. But not ordinary water, it's like a fluid liquid crystal, 4th phase water. It's quite dense and the carrier of cellular components. 99% of the molecules are water and the distance between subcellular surfaces is usually only a few nanometers and water occupies those gaps in its sticky viscous state

Hi and welcome to Biology SE! While your answer may be true, it would be helpful to include references to reputable sources such as academic articles. Otherwise, it may be challenged as lacking support.

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How do Opioids Stimulate a Histamine Release?
Histamine is a neurotransmitter that also has peripheral functions such as the regulation of gastric acid secretions, allergic responses, etc. I know that opioids stimulate a release of histamine but I want to know how?
What exactly I would like answered is:

Which of the opioid receptors are involved in the histamine release that opioids stimulate and to what extent are they?
How does the activation of the opioid receptors in question lead to a release of histamine?
Are there any ways of suppressing the histamine release stimulated by opioids without compromising the analgesia they elicit?

I would like an answer, not just links. However I would like you to cite journal articles, although a formal reference list is not required so long as I can easily find the link to the abstract/full article.

This might get you started: consider the references in http://www.acnp.org/g4/GN401000037/CH037.html, especially in the section "modulation of histamine synthesis and release in vivo".  This is not my area of expertise, so I will leave it to someone else to explain things.


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What would need to be discovered to prove there is extraterrestrial life?
Curiosity is on the Martian surface and is equipped with a slew of laboratory equipment. What would Curiosity need to discover to prove there is or has been life on Mars? Would it have to find DNA (or its Martian equivalent)?

I think in a more literal rather than biological sense, life that did not originate on Earth

The definition of 'extraterrestrial' is trivial (unless you subscribe to the 'flat earth' theory, or some such nonsense).  The real question here can be boiled down to 'what is life?' - a somewhat tougher question with no clear answer.

Curiosity is on the Martian surface and is equipped with a slew of laboratory equipment.

But not, incidentally, equipment to detect life.

What would Curiosity need to discover to prove there is or has been life on Mars? Would it have to find DNA …?

No. In fact, DNA would be lousy evidence of life on Mars, it would almost certainly be a contamination from Earth.
Lacking equipment, I’m not even sure how Curiosity would go about finding traces of DNA but assuming that it did (through some sort of chemical assay), it has no way of telling the origin of said DNA.
And even if the genetic material could be sequenced there are a number of scenarios. It could be very similar to what is found in extremophiles on Earth, in which case we wouldn’t necessarily know the origin (but due to the aforementioned contamination risk, the prior probability of it being Earth life would be very high). If it were completely different, that might be compelling enough to consider it extraterrestrial.
But maybe not: estimates for the number of existing species on Earth vary drastically. One thing is certain, though: we’ve only scratched the surface of prokaryotic life in particular. So if we find something new, that wouldn’t even be very surprising.
More interesting would be an alternative genetic material, neither DNA nor RNA. So far, we haven’t discovered anything like this on Earth (despite earlier hopes) so it would be more likely of extraterrestrial origin. But again, as the refuted study shows, we cannot entirely exclude the possibility of such life being found on Earth either.
All this is just to show that proving microbial life to be extraterrestrial is quite hard. It would be much easier if we were to find non-microbial life on Mars (i.e. something multicellular). However, I don’t know of any serious scientist who seriously entertains this possibility.
But the reason to prefer such a discovery is simple: the bigger the life form, the less likely that we haven’t found it yet on Earth, and the smaller its viable niche. So if we find multicellular life adapted to the surface of Mars there aren’t many places on Earth where it could have originated from, never mind the low chance of having survived the ride aboard the probe.

Answer to your title:
ex•tra•ter•res•tri•al [ek-struh-tuh-res-tree-uhl]
adjective

outside, or originating outside, the limits of the earth

Answer to your post:
There is a whole field of study revolving around these questions called astrobiology. It is assumed that extraterrestrial life forms will have some sort of information storage similar to DNA but that it will probably not be identical. Accessible water is considered the most important indicator for the potentiality of life. Oxygen or some kind of reducing element is also considered to be very important.

In the simplest sense, extraterrestrial life is life found beyond the Earth. Defining what life itself is notoriously difficult - perhaps the best is a system which is subject to Darwinian evolution?
However, the term "extraterrestrial life" does not necessarily imply that said life (if found) originated in situ. For example, if we do find (presumably microbial) life on Mars, I would not be completely surprised if it had a DNA/RNA (or PNA or similar) information system.
The amount of material exchange (due primarily to asteroid impacts) between the Earth and Mars is large - significant quantities of Martian rocks have been found on Earth, and the reverse is presumably also true. Earth's higher escape velocity would reduce the amount of material ejected from the surface, but Mars' thinner atmosphere would facilitate the successful "landing" of any ejected rock without being burned up on re-entry beforehand.
So, Mars may have been seeded by Earth life traveling on rocks ejected by impacts. Whether this life could adapt to extreme cold, saline regolith, ionising radiation, dessication etc. is another matter although extremophiles on Earth are seen to (individually) have some of these qualities (psychrophiles, halophiles, "radiophiles", etc. Deinococcus radiodurans actually does quite well in all these areas.
Alternatively, Earth life may  have been seeded by Mars rocks traveling the other way. If Mars was warm and wet in the past as some advocate, this idea may not be so crazy.
Look for "panspermia" and "lithopanspermia" for more information.


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In a vertebrate chimera, are particular organs homogenous genetically?
I have read that a chimera is an organism with two or more sets of DNA, with every cell having one of the sets. Is it possible and common for the two or more sets to be present in the cells of a single organ? I'm confining my question to vertebrates because I don't remember much about the biology of invertebrates from high school, but please don't hesitate to add anything interesting about them.

Chimerism (or genetic mosaicism if the cells come from the same zygote) is possible in the same organ or tissue. I don't think you will see a homogeneous distribution of the chimeric tissue because the tissue in any vertebrate organ is rarely homogeneous to begin with. Microchimerism may occur in a small number of cells. That's about all I know.

Could you add references to your answer?

@roryM, the links don't count?

@bobthejoe I read through them and couldn't find any reference for the chimerism can happen in the same organ/tissue point, plus the second is a wikipedia article, I'd rather see their references directly linked to.