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What are known methods of non-surgically disabling neural tracts/pathways (esp. Corpus Callosum)?
I think I've read something about usage of TTX and optogenetics, but I cannot find the papers for either anymore. Any reference would be much appreciated, especially those concerning mice and the Corpus Callosum.
Edit: By surgical, I mean to say methods that are based on actually cutting through the tract using a surgical knife (or lasers etcetera), as is commonly found in literature.

Welcome to Biology. How exactly do you define surgery? Sticking a needle in a mouse's skull and penetrate the corpus callosum to inject TTX may as well be considered a surgery?

Sorry, yes this was a poor choice. By surgery I mean methods using a surgical knife to cut through the CC which is the standard method. And thanks for welcoming me :)

Can I conclude you are after non-invasive methods of ablating the corpus callosum?

Probably yes. I say probably as I have to admit that I have very limited knowledge about these things. I'm basically interested in any non-standard approach to temporarily or permanently disabling the CC (or other tracts if methods are transferable).

I was able to find one non-invasive method to sever the corpus callosum (callosotomy). This method is referred to as gamma knife radiosurgery (Mathew et al., 2007). Basically, 201 beams of gamma beams are focused on the corpus callosum and where the beams intersect, the energy is high enough to permanently damage the tissue. I doubt this technique is available for routine use in animals, though.
Another interesting technique is photothrombosis. This method is based on the systemic injection of a photosensitive dye named Rose bengal. Subsequent focal illumination of the brain with a cold light source through the intact skull leads to focal cortical infarcts of reproducible size, location and geometry (Schroeter et al., 2002) . Brain damage is induced due to photo-activation of the dye and subsequent endothelial damage with platelet activation and thrombosis, resulting in local blood flow interruption. The light source can be applied on the intact skull with no need of craniotomy, which allows targeting of any cortical area of interest in a reproducible and non-invasive way (Labat-Gest & Tomasi, 2013). However, although the light source penetrates the skull, I don't think the method is useful for the induction of deep-brain lesions, as I was able to locate only studies using it to model cortical lesions.
Having not answered the question, I'd like to say that either surgical sectioning, or chemical ablation using micro-injection of neurotoxins are the most commonly encountered methods to perform a callosotomy.
References
- Labat-Gest & Tomasi, J Vis Exp (2013); 76: 50370
- Schroeter et al., J Neurosci Methods (2002); 117(1): 43–9
- Mathew et al., J Neurosurgery: Pediatrics (2007); 106(4): 312-5

Thanks you very much for your well researched answer. Could you maybe elaborate a on the chemical methods you mentioned at the end?

@JohnSmith - maybe that would better be done in a new question. The comments preferably shouldnt be used to ask new questions. Surgical methods were not the question. If you have questions about those you might consider posting a new one.


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How do I test if microbes have survived after dehydration?
I have a solution containing various bacteria and fungi.
My aim is to place solution on filter paper, and wait until it dries.
I then wish to test if the organisms have survived, either on the dried paper, or by rehydrating it (maybe placing the paper into water).
Can someone provide advice on the type of test(s) I should perform to achieve this result?
Preferably the test would be easily sourced (purchase online?) and relatively cheap and easy as I am quite inexperienced in this area.
Thank you in advance for any advice that you can provide.

I think the fungi are not the problem, they are hardy. I used to revive yeast after freeze-drying the poor buggers. Anyway, good question +1

Is there some reason why blotting them onto culture media wouldn't work?

Hi @AliceD and thanks for the feedback. I'm now a bit more optimistic. Regards

Hi @Resonating it may. The drying part is nescessary, which I guess that media would support. Thanks very much for your help.

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Is there any definition of life which makes viruses undeterminable?
There are many different definitions of life (RNA, something that comes through evolution) but not one I have seen which could not determine wheter viruses are living things (even though there are many definitions both for YES and NO). Are there any such definitions (I'm looking for cases where it's really fundamental debate, not only struggling for the correct dictionary definition)?
Thank you.

Can you please clarify your question? At the moment it is (at least to me) not clear what you are asking about.

There is nothing in knowing whether viruses are alive or not but a struggle over accepting a definition or another. Have a look at why isn't a virus alive? for more info.

Your last sentence is the key: defining life really is just finding a dictionary definition that we can agree upon. Biology is something that defies discrete definitions at times: "What is it to be alive?" "What is a species?" maybe even "What is the wild type allele of a gene?"
I would recommend not looking at viruses as a challenge to determine if they are alive or not so much as an excellent opportunity to discuss what we think are important characteristics of life.
Life can alternately be described as:
"Comprised of self-replicating cells" (a paraphrase of the "Cell Theory of Life"
or
As things that embody at least most of the following characteristics:
1. Self-Replicating
2. Metabolizing
3. Growing
4. Showing signs of adaptation
5. Being organized
6. Respond to their environment
7. Being comprised of cells
I like to think that we should focus on extraterrestrial forms when we define life. i.e. what would we want to see in an extraterrestrial in order to call it 'life'? While some are troubled by calling viruses alive here on earth, the same people might be willing to say that we have found extraterrestrial life on another planet if it was similar (granted, it's hard to imagine this kind of life existing without a host...)
as an aside: You might also ask whether this question is fit for this stack as it can not be supported by literature references (at least none that would actually support a conclusion). So should this be posted as 'Biology' or 'Philosophy'?

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Why a particular species of bacteria give rise to particular type of colony?
Bacterial colony varies in form, elevation, margin, opacity, chromogenesis etc. What gives definite character to a colony and what is the source of all the diversity? Is the reason similar to that of structure of salt crystal (i.e basic elements connect in a very definite way with each other)?
UPDATE (clarification)
On this page, it is observed that colonies can take various shapes, as if they have some internal structure, so that for example, form, elevation and margin differ and can even be described as having a particular shape.
Assuming that bacteria do not have any form of social organization or specification, what factors cause their colonies to have a particular shape, and that shape is well-defined for each species?
Also, for example, this picture on this website clearly shows a bacteria colony that is like ice crystals. If bacteria colony has no inner structure, what makes the bacteria to follow such a crystal-like pattern? Why not a shapeless goo, as one would imagine?

It all depends on the gene expression of the component cells, and their interactions between each other.

Different bacteria types are different species of animals. And different animals can have anything different, so there's no surprise to that. For example, it is obvious that cats have different lives than ants or monkeys, and so on.

@noncom The question is not why bacteria is the way it is rather why it has a distinctive colony? Why is it not random or different in each time?

So you mean that different bacteria form some sort of a macrostructure and that macrostructure is different per bacteria type?  Also, you ask how the form and structure of that colony is influenced by properties of a particular bacteria species? And ask if that formation is akin to how molecules form a crystal, likening bacteria to crystal molecules?

@noncom exactly!

This should not have been closed.

To me, this has gone from an unclear question to a broad question.

@GoodGravy is it hard to sum up the reasons for at least one of the relevant cases? Would it take more than a single paragraph to at least make an overview approach to the answer? It does not seem like if the reason for why bacteria colonies form their shapes is known, it would take more than a normal length answer to make an excursion into that.

@noncom Gauging an appropriate level of detail is tricky. I could simply say: "different environmental stresses causes different gene expression causes different proteins, and the proteins cause the cells to assemble in different ways. Each species reacts differently to their environment (and some will do the same thing in any environment)." A good question in my opinion would ask about a particular species and why it adopts a certain shape.

@GoodGravy I agree, and at the same time what you're saying is actually a rather appropriate answer to the question (imho). The authors main question was if this phenomenon is related to how crystals grow. The growth of a crystal is defined by molecular and atomic properties of the compound, and in case with bacteria you have specified the focus on gene expression and protein workings. Can they be likened to each other? That's a subject for furhter research of course. Also, I agree that asking on a particular case would be easier to answer precisely.


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The mystery of coconut tree
Could anyone please explain to me, why the nail which is nailed in a coconut tree is not raised from ground level, when the tree is growing up?

Could you please expand the informat

Could you please make me understand what you are asking?

Thanks, it's clear from the answer. I just wasn't sure which "rising" you mean.

First it needs to be said that coconut trees are not true trees, but palms, whose trunks are made of stems which grow in a cross woven pattern.
That being said - its true for any plant that no plant grows from the bottom up.  If you make a mark on any plant that mark will not rise much as the plant grows.
Plants grow from buds at the end of their stems.  As the plant grows taller  its because the tissue adds from the ends of its branches/stems.

In this illustration you can see the terminal bud, which is where the plant is growing up and also out into branches.  The palm is more like a bundle of grass stems, so the terminal bud is not obvious, but the leading edge of the grass will grow here.
A tightly wound core of stems in the crown of the palm, called the Heart of Palm is where the palm grows (see "growth point" in picture below).  It is also a terminal bud, but it is not as exposed and is not as obvious.

(figure from The Food and Agriculture Organization of the UN, fao.org)

"if you make a mark on any plant that mark will not rise much as the plant grows". This is not the case for plants with intercalary meristems, e.g. grasses (including bamboo). It should be true for woody plants though, as well as relatively large, established palms (I'm not sure about the growth patterns of palm saplings).


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Absorption of Topical Magnesium
Can Magnesium be absorbed through the skin? Some athletes believe that Homeopathic magnesium lotions can reduce muscle pain. I've tried this and it doesn't work nor can I see how it can.

Homeopathic magnesium lotions don't* contain magnesium, so it seems a little irrelevant whether or not magnesium can be absorbed through the skin. However, magnesium ions can definitely be absorbed through the skin. There's no reason why that should reduce muscle pain(especially because ions would disperse throughout the bloodstream etc etc), but magnesium can be absorbed through the skin fairly efficiently.
*Footnote: they do, but not on purpose. If correctly prepared they would contain zero atoms of magnesium(depending on what 'strength' they are), but that kind of purity is impossible.


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Why and how is DNA synthesis so much faster then RNA synthesis in bacteria?
DNA synthesis in E. coli is 20x faster than RNA synthesis at 1000nt/s vs 50nt/s. (Mirkin'05)
I find that perplexing since DNA polymerization has better proofreading than the RNA variety, which requires extra time as you need to backtrack, excise, and replace. Also, in bacteria there's almost no splicing, so that doesn't slow you down. And the 1000nt/s is a single replication fork. We are not talking about several replisomes together clocking 1knt per second.
Is there an explanation of this or, in the absence of evidence, hypotheses?

(shamelessly unreferenced) hypothesis: DNA synthesis needs to be faster, as you need to replicate huge amounts of DNA relative to a single RNA transcript. I believe that there's only a single origin in prokaryotes (compared to many in eukaryotes), so if there's a selective advantage towards growing/dividing/replicating faster, it makes sense that there's a difference in speed

It makes sense that replication should be fast, but that in itself doesn't mean replication should be faster than transcription.

Good question. As Luigi was suggesting, I would guess it has to do with the amount of nucleic acid that must be synthesized. RNAs are tiny compared to DNA, so there is little selection pressure for speed. Also, multiple RNA polymerases can initiate simultaneously, effectively increasing the synthesis rate.

To throw in another hypothesis: note that mutations in DNA tend to occur when RNA synthesis and DNA replication meet heads-on (antisense) ( http://www.nature.com/nature/journal/v535/n7610/full/nature18316.html ) Ultimately this would suggests that - if the speed of DNA synthesis was similar to the speed of RNA synthesis - there would be more head-on encounters and mutations

I wouldn't call them hypotheses, but the question is intriguing, and, as it seems to be ignored in the literature, I'll make a couple of suggestions.

Perhaps it has something to do with recognition of termination signals in relation to selective pressure for speed in the two processes.

Perhaps if elongation of the RNA chain were any faster it wouldn't be able to respond to the rho-independent termination signals which are thought to be specific stem–loops in the DNA that cause the RNA polymerase to pause and fall off the DNA. The speeding RNA polymerase might disrupt the loops instead. The termination system for DNA replication may have evolved to be much more robust so as to be able to bring faster elongation to a stop. (Note: my suggestion of different ‘robustness’ in termination is not based on any data, it's pure speculation.)
If this were true, it would beg the question of why transcription hasn't evolved a more efficient termination system in concert with the a evolution of a smarter RNA polymerase. Perhaps the answer here is that there is no selective pressure for faster transcription — the rate is clearly sufficient to supply the needs of the cell — whereas the rate of DNA replication determines the time between cell divisions and thus the rate of growth, which is subject to selective pressure.

Perhaps it has something to do with error frequency in relation to selective pressure for speed in the two processes.

First I'll make it clear that I think the proofreading argument in the question is a bit of a red herring. If the rate replication is 20x as fast as transcription, the occasional backtracking will not have much effect on the overall difference. However errors and proofreading could be involved in a different explanation.
RNA transcription does not have proof-reading. The length of RNA transcripts is such that the cell can tolerate the errors that occur. However if the speed transcription were increased it is reasonable to expect an increase in error frequency, which might be detrimental. The current rate of transcription may be a trade-off between efficiency and accuracy. Of course one can imagine a proof-reading system for transcription evolving if it were necessary, but, as discussed above, if the rate of transcription is adequate there would seem to be no selective pressure to produce.

Processivity may be an additional factor. I am not sure about the processivity of RNAP, though.

I want to add an observation. Prokaryotes differ from us in that translation often begins before transcription ends. Prokaryotic translation links 17-21 aa/s, which means 51-63 nt/s are read in mRNA (Wiki). This is within the range of 40-80 nt/s of prokaryotic transcription (BioNumbers). Maybe there is a reason why they match.

Sorry. I just read in (http://book.bionumbers.org/what-is-faster-transcription-or-translation/) that single-molecule microscopy has shown that at least in E. coli, most translation is not coupled with transcription.

@Jagoe — No need to apologize. The source you cite was not known to me and is very pertinent to this kind of question. Like many others, I had thought transcription and translation were coupled in prokaryotes. Selective use of images perhaps. (But I wish they wouldn't keep referring to The Central Dogma all the time.)

This is because of the fact that DNA polymerase does the fast process that is 1000 nu/sec as compared to the RNA polymerase that 1000-2000nu/min because this process is done without discrimination and also DNA pol has exonuclease activity

Welcome to Bio. Could you expand your comment into a full answer by adding references and additional background to it? You might wish to go through the help center on answering questions. There it will become apparent that the SE network is not the place to answer posts with one-liners. -1


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Limits of brain neuronal spatial mapping
It is being claimed that brain maps the world space in (roughly) 1-to-1 correspondance of a place to a neuron (link1, link2).
My question is: as the mapping happens in 1-to-1 manner, then is it logical to assume that the brain loses the ability to map space anymore when it already has each suitable neuron assigned to a place?
From these articles, it is clear that the space unit is not very big, and is a sphere of some size not significantly bigger than the body. If the answer to the question is "yes", then what is the approximate size of the world we can map? (any metric would do, be it a volume in liters or surface area in square meters).
Other than that, if the observations described in the articles are lab simplifications, and in real life the mapping mechanism is more complex, then what is it like?


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What evidence is there that common PCR DNA purification kits can isolate DNA from pathogens engulfed in macrophages?
I have previously asked a more general question about how PCR sequencing reaches all possible DNA targets here. I want to ask more specifically now: what evidence is there that common PCR DNA purification kits can isolate DNA from pathogens engulfed in macrophages?
Specifically what such a KIT would have to achieve is to destroy the double lipid cell membrane of a macrophage and destroy the cell walls of engulfed bacteria or fungi. (The latter of which even contain chitin)
I am looking for as specific evidence as possible proving that if one takes a whole blood sample and employs a purification KIT, any microorganism's DNA engulfed in a macrophage should be isolated. Please allow me to say that I am looking for evidence beyond just the manufacturers specifications. I would like to find publications, book chapters or other written statements that specifically show and discuss how isolation techniques work on the barriers I mentioned or even better how they work on intra-cellular micro organisms. Thank you!

What do you mean by a "PCR DNA purification kit" ? Can you link to such a kit?

Also, colony PCRs routinely work on either colonies of bacteria or isolated mammalian cell culture, so there is no reason bacteria inside mammalian cells won't work. I can't say the same for fungi, since I have not worked with yeast.

@March Ho: the link you asked for, https://www.qiagen.com/de/shop/sample-technologies/dna-sample-technologies/genomic-dna/qiaamp-ucp-pathogen-mini-kit/

@March Ho: so your reasoning ist that since isolation techniques work on mammalian cells and on bacteria, they should also work on one inside the other? That might be the case but does not follow by pure logic! The kit you use on one (bacteria/mammalian cells) might not work on the other and even if you use the same kit for both it might not isolate the dna of bacteria inside mammalian cells for reasons of: too short exposure time or not enough reactants or competitive binding or unforseen reactions or altered cell wall of intracellular bacteria or...

I didn't use a kit, but merely ran a PCR using the cells instead of purified DNA as the template.

@MarchHo : From the manufacturer of the KIT you have linked in my other question I quote: With colony PCR, an initial 5 minute denaturation at 95°C is recommended and Use of high quality, purified DNA templates greatly enhances the success of PCR.
http://www.neb.sg/protocols/1/01/01/taq-dna-polymerase-with-standard-taq-mg-free-buffer-m0320

Of course purified DNA works better, but the point is that it is not necessary for PCR to work

For this problem, I would generate the evidence myself taking the following approach:
Apply the DNA extraction kit to the macrophages with pathogens engulfed. As controls, also use the DNA extraction kit on the macrophages alone (negative control), and the pathogen alone (positive control 1). Additionally get purified genomic DNA of the pathogen for a better positive control.
Now, design primers which specifically amplify pathogen DNA. You should test the primers against the independently purified pathogen gDNA to ensure they are working. I would focus on generating 200 bp fragments, so that your primers can be used for qPCR later. Since it seems you are interested in potentially a high throughput sequencing, you may want to target multiple genes to see if there is a difference in efficiency.
Now use your kit on all the samples (Macrophage + pathogen, Pathogen alone, Macrophage alone) and then run PCR on those purified samples. If you detect pathogen DNA from the macrophage + pathogen sample, this would give you strong evidence that the kit is capable of simultaneously purifying both DNA sequences. Otherwise, it would confirm that this co-purification does not work. You can make the technique better by incorporating qPCR to see if the efficiency of extraction is significantly reduced by having the pathogens inside the macrophages.

This does not provide an answer to the question. Once you have sufficient reputation you will be able to comment on any post; instead, provide answers that don't require clarification from the asker. - From Review

@tyersome I am a new user with a Ph.D. in synthetic biology. Can you elaborate on why your feel this does not answer the question? My procedure would help this user to generate the answer to this question, which I feel would be very valuable to a practicing academic. Additionally, this post had no answer for half a decade. My answer provides something versus nothing. Please let me know why this is inappropriate for Biology Stack exchange.

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What is the mechanism of folic acid deficiency and neural tube defects?
I am having difficulty finding the mechanism by which folic acid reduces the risk of neural tube defects. I know that it does so, but what in particular actually occurs with folic acid deficiency to cause the neural tube defect? Is that completely unknown and merely a strong association, or is there a putative mechanism?

You are having difficulties finding the mechanism because it is as of yet unknown.
Now of course comes the hard part where I need to prove that statement. Often, it's just apparent by papers not saying anything about the mechanism, even though you'd expect then to include a brief section if it was known, for example Folic acid supplementation for pregnant women and those planning pregnancy: 2015 update or the various Cochrane reviews on the topic of how much folic acid supplementation is optimal, or the WHO and CDC documents on the topic
Here's a few relatively recent ones that state it outright:
Folic Acid Supplementation and Pregnancy: More Than Just Neural Tube Defect Prevention, 2011

The mechanism by which folic acid prevents structural anomalies in the fetus is not known, but may involve the regulation of homocysteine metabolism

Folic acid supplementation in pregnancy and implications in health and disease, 2014

as FA deficiency may be a risk factor for NTDs additional studies will be required to determine the mechanistic role of the FA pathway in the onset of neural tube defects

FA = Folic Acid, NTD = Neural Tube Defects
Neural Tube Defects, Folic Acid and Methylation, 2013

To date, animal studies have not provided
  sufficient information to establish the metabolic and/or genomic mechanism(s) underlying human folic acid responsiveness in NTDs.

There are some putative mechanisms to do with folic acids effects on the homocysteine metabolism and its effects on methylation. I can't really tell how well-established those are yet, but maybe this can be a starting point for you.


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What is the shortest mRNA the ribosome can read to produce a peptide?
This question came as a comment on a previous question regarding non-ribosomal peptide synthesis, and why Glutathione cannot be synthesized by the ribosome.
In general, Glutathione has a "gamma" peptide bond, thus cannot be synthesized by the ribosome. However, is there an actual minimal length that ribosome can process?
I understand that the mRNA is more then just the codons, however, does it still require a minimum set of condos, e.g., say 18 nucleotides, to produce a peptide?

Haven't read this yet, but it looks promising: http://www.nature.com/nrg/journal/v15/n3/full/nrg3520.html

prokaryotes or eukaryotes?

Reading the paper linked by @canadianer and its references was pretty illuminating. It's a straightforward paper except for its conclusions, and the most convincing part is the evidence of actual translation. There's some evidence that transcription start sites are used as a regulatory mechanism by displacing other things that might otherwise bind. An unknown fraction, but most(90%+), very short bioinformatically detected ORFs are not translated.
Some, however, are. See this table for the experimentally verified translated micropeptides. The shortest is a nearly unbelievable 6 peptides long.


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Is global life expectancy normally distributed?
I am trying to find out what the world distribution of life expectancy looks like.

Statistician here. The answer would depend on what, exactly, you're asking about. The answer you have now wasn't explicit about what precise question it was answering but seems to be answering "if I randomly chose a country, each with equal probability, and looked up its life expectancy, what would the distribution of that life expectancy look like?". I expect you want something different to that (e.g. perhaps something closer to "if I randomly chose a person from the world, what would their life expectancy at birth have been?"). The most interesting/useful questions may be harder to answer.

Let's see!
I took the most recent WHO data from here and did a quick an dirty analysis in R. Here is the histogram as well as a normal distribution with the same mean and standard deviation as the actual data:

Does not look very normally distributed. In fact, the shapiro test confirms this impression:
Shapiro-Wilk normality test

data:  df$life_expectancy
W = 0.94141, p-value = 4.338e-07

Edit
Commenters requested to weigh the life expectancy by population size.Well...the result is pretty ugly:

Apparently, the large populations of China and India produce disproportionally high bars. However, keep in mind that we are using averaged values which means that all the variation within countries is not represented by the histogram. We would actually have to have data on individual ages of death for a random sample of the world population to finally settle the question. :/

Have you tried weighing by the number of inhabitants? It's true that there's no reason to expect a gaussian. But the distribution you show also seems rather weird :)

Who kills all those people just before they turn 80?

It would definitely be interesting to see how the distribution looks when weighted for population.

I'll see what I can do

Both graphs can't answer the question, since they're done by the mean in each country. So, all people from India and China fall in a single column each, when with real data they would be more spread, and, who knows, make something closer to normal distribution. Though it's probably hard to get the real data.

That's what I said in the last paragraph.

A few people thought it would be interesting to see what the distribution looked like if we plotted the number of people dying at each age, so I took data from the SSA (which admittedly isn't global data, but it's probably fairly reflective of the world overall) and plotted the number of deaths per 100,000 at each age.

This looks like it makes sense - the high death rate at birth, the plateau during the 20-40 range, then the rapid escalation past middle age, and eventual decline shortly after reaching the average life expectancy range.
However, while it looks a lot smoother than plotting the averages of individual countries, it's definitely not normally distributed.
EDIT:
If you extrapolate the above death rates using the global life expectancy of 71.0 instead of US life expectancy, the chart looks roughly the same, but is adjusted to reflect what the death rates of the planet most likely look like.


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What is the difference between fixation and loss of alleles in a population?
When running a simulation in PopG, with parameters:

Population size: 100
AA fitness: 1.0
Aa fitness: 1.0
aa fitness: 1.0
Mutation A to a: 1.0E-6
Mutation a to A: 1.0E-6
Migration rate between populations: 0.001
Initial frequency of A: 0.5
Generations to run: 1000
Populations evolving simultaneously: 100
Random number seed: autogenerate

I get a result of 20 populations being fixed and 10 populations being lost. Obviously, as this is a simulation, these results will vary each run; but what I am having trouble understanding is are lost populations just fixation of the recessive a allele?

I'm voting to close this question as off-topic because the question was specific to the OP and the OP abandoned the question, has provided no feedback to the answerers as to why their answers were not sufficient, and has had no subsequent activity on the site.

I don't think this is a valid closure reason. As irritating as it is for the work to go seemingly unappreciated by the OP, they have no obligation to feedback, and Fileunderwater appears to have grasped the question and given an answer that suits, which is therefore still useful to the site.

Yes, 'lost' seems to be referring to fixation of the a allele in this program, where the statements 'fixed' and 'lost' are specifically referring to the A allele. Conceptually, 'fixed' and 'lost' are describing the same thing in this particular case ( since you only have two alleles in the population) - the loss of one allele in a population.

Note that once the plot of the gene frequency curves reaches the right-hand side of the graph, the program prints there the number of populations that fixed for the A allele (ended up with a frequency of 1.0) and the number that lost this allele.

(my emphasis, from http://evolution.gs.washington.edu/popgen/popg.html)

Lost vs fixed population
I am not sure I understand your question. It seems to be a matter of definition. The term lost and fixed populations sounds quite wrong. I have never used PopG. Is the PopG manual using these terms without defining them?
Probability of loss and probability of fixation
Given your parameters, you will clearly expect that, if fixation occurs, then it is as likely that the allele a fixes than the allele A fixes. In other words, the probability of loss and the probability of fixation for a neutral locus are equal if you start at frequency 0.5.
Did you say recessive allele
Note that there is no recessive allele at least in terms of fitness (but you probably don't have an explicit phenotype that is afterward link to these fitness values anyway) in your simulation as all genotypes have the same fitness.
Extra info: $F_{ST}$
If I understand your parameters correctly, you are simulation an island model with constant migration between any two populations with D=100 populations. In such circumstances, the $F_{ST}$ should be $$F_{ST}=\frac{1}{1+4N(m+\mu)\left(\frac{D}{D-1}\right)^2}$$ which is approximatively equal to $\frac{1}{1+4Nm}$, where $m$ and $\mu$ are the migration and mutation rate respectively.
Because of migration, you wouldn't expect that all population would be fixed for one or another allele at any time point.


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Do lunar rhythms have really impact on plant growth?
It is commonly known that lunar rhythms have influence on plant growth, and there are even lunar calendars to know when planting, pruning, transplanting, harvesting, etc.
I know that the lunar cycles affect the tidal patterns, and this consequently can affect the life of sea organisms like reef corals, fishes, etc., but I am very skeptical that this can affect the growth dynamics or plant physiology.
 I would like to know how it works from a scientific perspective, E.g. the temperature and precipitation are the main limiting factors on plant growth, but I'm curious if the moon light or its magnetic field can also be a limiting factor on plant growth.
Then my question is simple, the lunar rhythms really influence the growth of plants, if so, how?

Great question! I think there is a similar question on Skeptics.SE but I assume you want a more scientific perspective, correct?

@TanMath exactly! I would like to know it from a scientific perspective. I have added more details to my question.

Let me point you towards this 3-part blog post on howplantswork.com. There are quite some references in there. If you ask me personally: I think there is no scientific basis for the widely believed lunar influence on plant growth. Just superstition handed down.

I don't know at all is there any relation between lunar cycle and living world. However once I've read that lunar phase and human menstruation cycle both are of 28 days. However they're  not in synchronous relation, and maybe a mere coincidence. But I assume there could exist some direct relation in marine/ coastal organisms because tide take place there.

Maybe the moon light could put some photoperiodic effect in plants.

Is there any effect of the slow and mild gravitation change on terrestrial organism?

It may be worth linking to the similar question on Skeptics.SE — note that the most voted answer there somehow contradicts the only answer here.

Great question! The way I will do this is by explaining a bit about what moon planting is, then I will go through the articles I have found one at a time, to provide the different persepctives on moon planting, as it is called.
What is moon planting?
Moon planting is a methodology of planting, in which the lunar cycles are used as guides to know when to plant.
How might it work?
The first article is a great article about a gardener who tried to do moon planting, but it did not work for her, until she realized she did it wrong. Then, she found out the logic behind why lunae planting works. It really doesn't have to do with lunar cycles. Here is her explanation:

Let’s look at a possible scenario. Gardener I is a moon planter; Gardener II isn’t. Both gardeners wait till spring to plant their beans. (No sensible cool climate gardener will plant beans in winter. It’s too cold for them to germinate, and many seeds will rot or be taken by ants.) But come the first warm spell Gardener II succumbs to one of the great spring urges and plants the beans at the first hint that spring has arrived. Gardener I, on the other hand, waits till the next good moon planting time before planting the seeds. Early warm spells are usually followed by another cold one… and again seed planted too early may rot. Even if it doesn’t, plants that suffer any set-back when they are young usually don’t do as well as plants that have flourished right from the start. (The set-back can be from cold, boggy soil, snail or scale attack — the effect is the same). So counterintuitively, beans that are planted later in spring will probably do better than beans planted too early.

The opposite works too when planting in autumn. By the lunar planting schedule, it is better to grow earlier, and since the soil is warmer, the plants will grow better.
In the second article, the author reviews the research done on the effect of lunar cycles on reproduction, germination, and more. However, only the work of a researcher, L. Kolisko, shows evidence for the benefits of lunar planting. Therefore, the conclusion was lunar planting are not significant to affect crop yield.
However, in another article, it shows that there are many cycles in plants that are affected by the lunar cycles and that for some organisms, the lunar cycles do affect reproduction, germination, and production of different metabolites. Therefore, lunar planting might have an effect in that way as well.
Conclusion
The conclusion is that lunar planting may actually work, but many scientists are debating about it. So in reality, we aren't 100% percent sure about it, because there is evidence supporting it, and evidence contradicting it.
References

http://danfingerman.com/skeptic/Moon_planting.pdf
http://www.howplantswork.com/wp-content/uploads/2009/07/beeson_1946.pdf
http://www.howplantswork.com/wp-content/uploads/2009/07/schad.pdf

good answer, however the first example is based on temperate ecosystems where the temperature is the first limiting factor, but what about planting in the tropics where the temperatures are almost the same during all year?. I was doing by myself some experiments in the Andean region with good and bad results. I did it because there is a strong ancestral tradition to planting with the moon rhythms, and all farmers do it specially with short-cycle crops (Eg. corn, potatoes, etc.) and also in lowlands with the bananas. but it is curious that has not been done much research in this field.

@DarwinPC good point, by the logic pointed out in the firsf article, then there would be no signficiant effect. However, there are theories about whether or not moonlight could affect plant growth. Do you want articles on that? Also, if you like my answer and it answers your question very well, if you want, you can accept my answer by pressing the checkmark button near my answer.

@DarwinPC Much research has been done, but many are biased. Some of the research papers aren't even true science, and more like pseudoscience with astrology.

The point with the germination timepoint is about timing, not about the influence of the moon.

@TanMath I like your answer but I will wait for other answers, I don't want exactly an articles list, rather more convincing answers based on true science.

Based on your Nature citation (the other one being popular science, the third a rather broad work mostly on animals) I dare say the consensus is there is no effect. if you are specifically interested in moon-planting, the kolisko 1939 citation in the nature paper seems the strongest lead to the contrary.


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What happens to blood after a person dies?
After a human dies, what happens to their blood?  I know that it tends to accumulate in the lower areas of the body, whichever parts are closest to the ground, but I am wondering about coagulation.  Does the blood always coagulate?  How long does this take?  Does it ever "de-coagulate"?  If so, how long does that take?  If it coagulates, then "de-coagulates", does it "re-coagulate"?  How long does that take?
Note:  I'm asking this question because I am a fan of The Walking Dead, but I have always been a bit puzzled by the fact that on that show, the blood of zombies (who are dead) is consistently depicted as being fluid, dark red, and not coagulated at all.  I'm obviously not asking about the particulars of zombie blood, because zombies don't exist (yet).  I'm just curious as to whether it is possible for blood to remain liquid, and similar in appearance to the blood of living people, after death has occurred.  You can see my related question, on SF&F.SE, by clicking here.

Related: http://scifi.stackexchange.com/questions/106691/why-doesnt-zombie-blood-coagulate


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How is the enzyme glycogen synthase regulated?
How is the enzyme glycogen synthase regulated in regards to glycogen synthesis? I think I understand that phosphorylation decreases its activity (through glycogen synthase kinase?), but what role do molecules like insulin, glucagon (or epinephrine), protein kinase A, and Protein phosphatase 1 (PP1) play? Do they activate or inhibit glycogen synthesis, and how so?

The answer to this question can easily be found in standard biochemistry texts, e.g. one available online (albeit an old edition): http://www.ncbi.nlm.nih.gov/books/NBK22444/. Presumably this is why this question has not been answered previously. However I think it worth providing a summary answer in order to stress something that I feel perhaps does not receive enough emphasis in texts, and is ignored in the question.
This is that the regulation of glycogen metabolism (and indeed other aspects of carbohydrate metabolism) differs in different tissues because of the different situations in which its synthesis and breakdown is appropriate in relation to the integrated metabolism of the organism. If we just consider skeletal muscle and liver, the muscle stores glycogen to use itself when it needs to generate ATP to power contraction, whereas the liver stores glycogen so that it can provide other tissues with glucose when they require it either for work (e.g. the skeletal muscle) or in starvation (e.g. erythrocytes and brain).
The appropriate integration is provided in the first instance by the hormones mentioned (so-called first messengers), and the presence or absence of receptors in the tissues so that they will respond to these hormones or be refractory towards them, as appropriate.
Both liver and skeletal muscle have receptors for epinephrine (adrenaline) which is secreted as a stress response. This results in the breakdown of glycogen — used internally by the skeletal muscle and released as glucose by the liver, as already mentioned.
Liver also has receptors for glucagon, the hormone which is secreted in starvation or fasting, and also causes the breakdown of glycogen. The skeletal muscle does not have glucagon receptors because the nutritional state is irrelevant to its energy requirements.
Both liver and skeletal muscle have receptors for insulin, the hormone of the fed state, and respond to this by increasing the synthesis of glycogen to build up supplies to be available when needed.
How do these hormones work?
Glucagon and epinephrine (adrenaline) both work by activating adenyl cyclase (a so-called second messenger) in a G-protein-coupled manner to generate cyclic-AMP. This acts by a phosphorylation cascade to activate glycogen phosphorylase and inhibit glycogen synthase as described in any standard text. (Protein phosphatase 1 is also involved.) Glycogen breakdown is this enhanced.
Insulin acts differently. Binding to its receptor activates the protein's intrinsic tyrosine kinase, and there is a chain of subsequent protein self-phosphorylations culminating in the phosphorylation of protein phosphatase 1. This causes it to dephosphorylate both glycogen synthase and glycogen phosphorylase leading to the activation of the former and the inactivation of the latter. Glycogen synthesis is thus enhanced.
It is important to understand the molecular mechanisms of metabolic control, but it is also important to see them in the context of integrated tissue metabolism. So I will end with a question for the reader. The brain (which is absolutely dependent on glucose for part of its metabolism) stores a small amount of glycogen. How would you expect the brain to respond to the three hormones mentioned, and what would you expect to be the fate of the product of glycogen breakdown? If you have understood the principles above for liver and muscle you should be able to make rational predictions for brain (even should the facts turn out to be more complex).


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All-trans-retinal being converted back to 11-cis-retinal or vitamin A
There are two pathways all-trans-retinal can take after detaching from the scotopsin: (1) it can convert back to 11-cis-retinal, or (2) it can convert to all-trans-retinol (form of vitamin A), which then converts to 11-cis-retinol and then 11-cis-retinal. My question is what factors determine which pathway will occur?
The first sounds like it doesn’t involve vitamin A at all and just recycles the retinal. Hence it wouldn’t be affected by any vitamin A deficiency, yet we know vitamin A deficiency affects the stock of retinal in the eye. Yet I don’t see any disadvantages in simply recycling our retinal; why would we go through the process of converting it to vitamin A and then back to 11-cis-retinal?

Short answer
A complex visual cycle in vertebrates involving vitamin A is useful for storage, re-distribution of retinoids to both rods and cones, to improve photosensitivity and reduce noise in the visual system.
Background
The visual cycle in mammalian rods is depicted in Fig. 1.

Fig. 1. Visual rod cycle. Source: Palczewski (2010)
11-cis-retinal isomerizes to all-trans retinal by absorption of a photon.  Your notion that this pathway can involve direct re-isomerization back to 11-cis-retinal is only true for invertebrates. They simply absorb another photon to back-isomerize all-trans to 11-cis (Saari, 2012).
In vertebrates, however, this bi-stable configuration is replaced by a complex visual cycle (or retinoid cycle, Fig. 1). The reason is that the bi-stable invertebrate system is less sensitive, as photons used for regeneration cannot be used to initiate phototransduction. Moreover, the invertebrate system is more prone to noise, as photons can both start the phototransduction or recycle all-trans retinal (Saari, 2012).
In vertebrates it is thought that the visual cycle only emerged after appearance of the cone system (Saari, 2012). Notably, the visual cycle depends on the retinal pigment epithelum (RPE), as shown if Fig.2.

Fig. 2. Rod and cone visual cycle. Source: Saari (2012)
Fig. 2 shows that vitamin A (all-trans-retinol) is present in the RPE. RPE cells are able to store vitamin A by converting it to fatty acids and store it in oil droplets. Moreover, RPE cells can funnel this stored vitamin A to both rods and cones, another reason why the complex visual cycle and vitamin A conversion makes sense (Palczewski, 2010)
References
- Palczewski Trends Pharmacol Sci (2010); 31(6): 284-95
- Saari, Annu Rev Nutr (2012); 32: 125–45

It's entirely wrong statement about sensitivity. Invertebrate photoreceptors are extremely sensitive compare to vertebrates and they can respond to ideally single photon (Randall et al 2015, Hardie 2001 )

@Dexter - one photon is necessary to regenerate invertebrate photopigment after absorption of the first photon. Efficiency=sensitivity hence reduced by 50%. Vertebrate rods can too respond to a single photon.

You might want to look at this. I remember one review comparing sensitivity of both. I am looking into it. And I don't think "efficiency=sensitivity" is true.

@Dexter the responsiveness of photoreceptors also depends on their stack number, height, concentration of photopigment and what not. The simple fact is that when you use x to convert A to B and x to recycle B to A, it's noisy and inefficient. And using two photons to detect one is per definition less sensitive than detecting one and independently recycling the pigment.

I think it's better to provide reference for claim than fight over different points. Another logical points I can raise is that Calcium channels are being closed in vertebrates in contrast to invertebrates. And opening of channel (which also has strong calcium feedback) is much faster than closing channels (which also has calcium feedback but on 100x slower time scale).

@Dexter - references are provided and I am not fighting. And I have never ever said the vertebrate system is fast. Don't put words in my mouth.

Let us continue this discussion in chat.


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What is the name of this moth found in Virginia USA?

Found in Virginia, USA on Nov 1 2015, 10:34 AM.

Oh, found it. It is called a Euonymus Leaf Notcher Moth. It is an invasive species from Asia. It was first found in Maryland and Virginia in 2001.
http://www.insectid.ento.vt.edu/exotic-pests/euonymus/


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Bacteria resistance to natural antibiotics?
It is a known fact that bacteria develop immunity to antibiotics. Why then did not all bacteria develop immunity to natural antibiotics like penicillin in the fungi?
It is for sure that fungi did not care to continue killing all bacteria so that them won't be able to develop immunity (as we're adviced today to use antibiotics carefully, in order not to develop a superinfection)..
Looking at all the time span that bacteria and fungi exist, it seems unlikely that there'd be any bacteria left not yet immune to penicillin at all. However, that's not the case, the antibiotic is still a rather successful one.

As far as my limited genetics background allows me to assess this question, it is population genetics. Let's not close this well-researched question based on a philosophical community question..

@AliceD hi! I am sorry, I think I don't get your second sentence... could you please say it differently? :)

@noncom - that second sentence was addressed to the community at large. Don't worry about it.

@AliceD however well researched question might be, if it is a case of the CW post, then there is no point repeating the same stuff again and again. Newton's law does not change if you replace a "ball" with a "car". Why did all bacteria not evolve antibiotic resistance is clearly an example of the CW question. Just replace "organism" with "bacteria" and "trait" with "antibiotic resistance". Can you explain why this post is different? Also, that post is not philosophical. We created the post such that all possible relevant scientific points are cited to address the evolution problem.

@noncom many bacteria previously sensitive to the antibiotics are becoming resistant.

@WYSIWYG So, basically, you have marked the question as a duplicate of a question on general trait acquisition/persistance and together with that you give a broader answer in the comments that there actually are bacteria that become resistant, but do not mention if you mean natural or engineered antibiotics. Turns out that you have attributed half of the question as a duplicate of another, but marking the whole question as duplicate, and the other half was simply ignored at first and then briefly touched in the comments. Thus, the question was first broken down, and then its parts mistreated

@WYSIWYG Technically, you are right, the "why" of my question is probably answered in the referred duplicate, but there's more to it, and that "more" is being lost.

@noncom Okay. You can edit your question to focus on the "more" part; add more details so that it is no more yet another example of the CW question. We can have this reopened then.

For a natural immunity to evolve, two things have to happen:

The immunity has to actually occur. That means all the necessary mutations will need to be there to grant this bacterium resistance to penicillin. For penicillin, for example, bacteria that evolved such a resistance evolved to produce the enzyme beta-lactamase.
The immunity has to grant an advantage. Penicillin is produced by Penicillium, which is a mold found in environments with lots of oxygen. Lots of bacterial species have never encountered penicillin and the vast majority (for example anaerobic bacteria that don't infect humans) never will. In the absence of this pressure, a resistance to penicillin, even if it evolves, will likely deteriorate within a few generations because the individuals with the resistance do not have an advantage in survival. Producing an enzyme such as beta-lactamase is not without its costs (protein synthesis).

While bacteria van exchange genetic material in the form of plasmids between different species, so not all species would need to evolve beta-lactamase de novo, this is also only "helpful" if the bacteria a) come in contact with resistant bacteria species, and b) if this resistance confers an advantage for the receiving species.
Origins and Evolution of Antibiotic Resistance
Mechanisms of Bacterial Resistance to Antibiotics

Penicillin is made by Penicillium, not Aspergillus.


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What is this spider, and what is this object that emerged from its rear end?
I was observing this spider (caught in a Petri dish) under my microscope, when I noticed that a small, round object emerged from its rear end. It appeared to be black and white in appearance. I am guessing that it is an egg, but I am not sure whether it is one or not. The diameter of the object is approximately 300µm.

The spider seems to resemble Hasarius adansoni from photos:

The scale bars in the image are 5mm in length. The spider and the object are imaged together in the frame for scale.

Can anyone conclusively identify the spider and the object? The photo was taken in Singapore in November (although the seasons don't really matter in Singapore).

Excellent images. I wish I could say anything conclusively other than, 'wait and see.' Maybe you'll get lucky and the answer will present itself conclusively.

I do not know what species of spider this is, but I think the white ball is actually spider poop.  Unfortunately a quick search did not return many references, but here is a picture for comparison.

Spiders produce uric acid, which is a near-solid and excreted out white.  This is done to minimize water loss. These malpighian tubules drain into an pouch attached to the digestive tract, or stercoral pocket.  The uric acid waste from the is combined and eliminated together with solid waste from the digestive tract.  In your spiders case, this would be undigested insect parts (black) mixed with the uric acid (white).

Actually, I forgot to update this question, but after 3 days the unknown object was found to be liquefied into a spread around 3mm in diameter. This supports the hypothesis that the ball is spider waste.


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Spread of malaria from an infected person
If a person is infected with malaria, how can that person be a part of spreading malaria? As in, if a female anopheles mosquito sucks blood out of that infected individual, how is it possible that malarial schizonts will be only sucked by the mosquito and not pure blood? The point is, out of such a huge volume of blood, how can only malarial parasites enter the suckling mosquito?

With humans infected with malaria, the parasite load in the blood can be quite high. It ranges from 10 to 108 Plasmodium falciparum parasites per ml .
When a female Anopheles mosquito bites an infected human, they take in infected blood, not just the parasite. They take in a few micro liters of blood, which in usually enough to get themselves infected, and the next time they bite a human (about one week later), the infection is spread.
You can learn more at the CDC malaria FAQ and their overview of the malaria transmission cycle.


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Do saltwater fish need to drink?
In my biology class we got the question if saltwater fish need to drink. We need to use the term osmosis, but I cannot think of a valid answer and we were allowed to ask help.

Short answer, yes. The fresh water concentration inside saltwater fish is higher than the surrounding sea water, and the salt concentration inside the fish is lower.  This means that fresh water continuously flows out of the fish through their gills via osmosis.  To combat this loss of fresh water, fish must constantly be drinking sea water to replenish the lost fresh water. This also requires that they pump out the excess salt in the sea water they drink using their kidneys and specialized chloride cells in their gills.

Some more information can be found here, or you can watch a short video on the subject here.

Perfect, me and my classmates loved it. Our teacher gave us an apple pie for the good answer :D i'd bring a piece over if I could!


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Wash adsorbed protein without destroying Biotin-Avidin-Mechanism
I am looking for reliable protocols to wash protein (e.g. Fibronectin) adsorbed onto glass surfaces. According to Protein immobilization literature, people usually use 1% SDS and some incubation time. For me this did not work.
Furthermore, the removal step should not destroy an existing avidin-biotin-mechanism.
Does anyone have experience with that? Or is there some kind of standard protocol, which I am missing?

More detailed process:
I have a quartz coverslip with covalently bound Biotin on some surface area. First I add Avidin (Sigma, 10µg/ml), then biotinylated human plasma Fibronectin (Sigma, 10µg/ml). Now I want to wash adsorbed Avidin/Fibronectin, so I have free "glass" area. This is important for me.
For some reason changing the system is not an option for me.

SDS shouldn't appreciably disrupt avidin-biotin interactions. The complex is extremely stable.

@canadianer SDS will disrupt the avidin-biotin bond at high enough concentrations. 1% is rather high (similar to Laemmli sample buffer), so that may be why the OP's experiment didn't work.

Can you explain what this did not work means in greater detail?

@MattDMo I have put streptavidin in SDS-PAGE loading buffer (2% SDS) and run it in an SDS-PAGE gel with only negligible denaturation. This paper has similar, and more formal, findings. I've also washed streptavidin conjugated chromatography columns with SDS without any leakage of the target protein. That said, it's hard to say if the SDS is or is not affecting the experiment. It would help if the OP gave the protocol and explained why it didn't work.

@canadianer that's really interesting. Did you add a reducing agent (DTT, BME) and/or boil the sample?

@MattDMo I don't remember if I had a reducing agent or not. No boiling though. Boiling + SDS = unfolding

@canadianer Let's continue this in the Biology chat room - it's kind of off-topic here.

@MattDMo Sure..

Sorry guys, time shift. I'll explain in more detail as soon as I'm back on the PC. Avidin biotin was totally stable with sds 1% (actually I used laemmli, 2hrs incubation at 4°C). But none of the adsorbed protein was washed away.

Do you want to wash off the fibronectin?

yes, except the avidin-linked fibronectins.


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Do individual neurons communicate with the origin of thoughts?
When mapping the different neural pathways in the brain, often pictures such as these are drawn:

Or similar versions. Clearly these sketches draw the neural pathways as being a two-sided connection, as can be judged from the double arrows. I was wondering, how such bidirectional pathways work. Specifically, I am interested to know whether individual neurons constitute such a bidirectional pathway between different parts of the brain, or if the bidirectional pathway can be thought of as a 'circuit': a pathway of neurons that eventually comes back to a certain part of the brain.
This question is especially interesting in light of abstract thoughts. Let's make some extremely generalising (and ludicrous) assumptions and assume that our conscious thoughts are governed by our hippocampus only. That is, we assume that thinking about a matter without input from sensory neurons causes the hippocampus to fire an action potential into some specific cluster of neurons (somewhere in the brain). E.g. we assume that thinking about the letter 'A' causes the hippocampus to fire an action potential into the cluster of neurons that represents the letter 'A'. Let's also assume that the memory we have regarding the letter 'A' must be returned to the hippocampus, in order to continue our thought process. For example, I might want to recite the alphabet in my head. Starting with the letter 'A', I then continue to the letter 'B', which arises in my conscious thoughts as a result of the firing of the cluster of neurons that contain information regarding the letter 'B'.
So if we assume the circuit, conscious thoughts $\rightarrow$ cluster of information fires $\rightarrow$ conscious thoughts to exist, then how would its feedback most likely work?
Let's take the example where we think of the letter 'A' and want to think of the letter 'B'. I have sketched two different theories about how the communication between these two clusters of information and the 'governing body of thoughts' (which I assumed to be the hippocampus), might be:

The difference is the following: in the second theory, all individual neurons are expected to be able to communicate directly to the hippocampus. Whereas in the first theory, the feedback to the hippocampus arises only when we have reached our destination: the letter 'B'. Clearly, if we assume that a specific thought process is able to self-induce action potentials (of course, this is highly debatable), at least one of the two theories must be partially true. For which one exists evidence?
My first intuition would be to say that the first theory is more likely, but this is ambiguous under Dale's principle: why would only some cells be connected to the hippocampus? On the other hand, I found it hard to believe that every individual neuron is directly connected to the hippocampus.
So now that I have explained my thought process, my question can be formulated as follows:

How are clusters of neurons that are involved in abstract thoughts bidirectionally connected to the thought-governing-body (whichever actual part(s) of the brain this is)? Can we say that just a single neuron in the cluster provides the feedback to the thought-governing-body, or is every individual neuron that is involved in conscious thought potentially capable of a feedback loop?

Disclaimer: Yes, I'm not up-to-date to all the latest advances in neuroscience. Yes, I'm aware that my question might be ambiguous with respect to all the different types of neurons, connections and theory about neuronal networks and micronetworks. My question, however, is concerning the likelihood of the theories I presented. For which one do we have evidence. Are both wrong? If so, in what way? Are both right? If so, when does their difference play a role? etc.

To give a simple answer to the first part, the feedback generally happens in circuits of at least two neurons. A synapse is generally one way, transmitting information from the presynaptic neuron's axon to the postsynaptic neuron's dendrite. I'm sure there's caveats and exceptions because biology always has that, but that's the norm. A simple feedback loop might look like this: A excites B which excites C. C inhibits A as negative feedback.
The second question relies pretty heavily on the assumption that conscious thought originates from a particular part of the brain, or that one neuron is dedicated to one concept. This doesn't seem to be true. Things like memory and thought appear to be distributed, emergent properties of several circuits and areas. They might be organized or integrated by a particular part of the brain but it's not the same as having one central executive looking at all the inputs deciding what you think.
Think of it like a person working on an Excel spreadsheet. There's all the code for the OS, the software, the formulas in the spreadsheet. Those are all important parts of the process but the user doesn't need to see any of that. All they need to see is the end products of each process, and then they can figure out what to do with those products. So circuits and neurons can be involved in lower processing without connecting directly to the area that organizes and integrates information. Also, because higher level processes like thought are so distributed, there's likely to be multiple centers organizing/integrating information and all giving feedback to each other. Does that make sense?
Side note: I think you might be misunderstanding Dale's principle. When it says that neurons have the same chemical action at every synapse, that means they release the same neurotransmitter(s) but that doesn't mean they have to be connected the same way or that the neurotransmitter release has the same results. For example, say a neuron releases the excitatory neurotransmitter glutamate. If it synapses on another neuron that releases glutamate, that will promote excitation. But if it synapses on an inhibitory neuron that releases GABA, then exciting that neuron will actually result in inhibition.

Thank you for your answer. I understand that the brain processes information in different clusters but I can't grasp the theory that conscious thoughts are distributed over clusters of neurons. Taking the Excel spreadsheet example: even though we don't see the lower-level tasks, we are still presented with the lower-level's output. This is what my question is about: assuming that A and B are such lower-level processing clusters, they must report to some central place in order for the information to enter our conscious thought. Much like when I use an Excel formula, I am given the result.

It makes sense to me that such clusters can intercommunicate, but one of the clusters has to report back to some centralised 'conscious thought'. How else can I think of an abstract principle? Surely, when thinking of this principle a cluster of neurons fires. But is this firing all there is? Is my conscious thought within this cluster of firing neurons or does the cluster communicate to a centralised area (like the hippocampus), where connections to my short- and long-term memory are also present (this seems more likely to me than to say that conscious thought is the firing of neurons alone)?

@Jean-Paul Thanks for the clarification on the question! Unfortunately I'm not sure there's a real satisfactory answer out there, but let me try...
First, it might help if you try to think of higher-level brain activity less like a modular machine and more like an overall  pattern of firing. We talk about areas of the brain being involved in one thing and it's easy to get caught up in that, especially when you're looking at imagine studies where it looks like one area lights up neat and tidy.

The truth is that most of your brain is active most of the time. In order to get that clean picture that you see in the paper, they had to do a lot of statistics and filter out a lot of noise and hope that their baseline was decent. This is a big issue in functional brain imaging, especially fMRI, and it's pretty interesting so I'm going to paste some references at the bottom in case you want to check it out. That's not to say that localization isn't useful! But it has to be taken as one data point, not the whole picture.

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC60127/ An article on issues with fMRI baselines http://journal.frontiersin.org/article/10.3389/fnins.2012.00149/full Another on problems with reliability and data interpretation in fMRI https://mitpress.mit.edu/books/new-phrenology Great book about the limits of localization

Anyway, try to imagine things mapped as patterns of firing. For an oversimplified example, maybe the concept 'dog' isn't stored by cluster A, it's what you get when cluster A is firing at a low rate, cluster B is firing at a higher rate, and cluster C isn't firing beyond random baseline noise. If all 3 clusters fire at a high rate, you might get 'cat.' 'Dog' and 'cat' don't belong to any one of the clusters; they're stored by the pattern of firing from all 3. This is more complex, but it lets you store more concepts. That's why there's such an emphasis on the whole connectome thing right now.

As for where conscious thought comes from, that's kind of out of the scope of neurosceince right now. It's a fascinating question but it's difficult to impossible to study it. How do you define conscious thought? How do you measure it? We can pick at parts of it. The insula, for example, seems involved in self-awareness, and thought can light up areas involved with speech and language. But the overall concept of conscious thought is too abstract for us to handle right now. We need more information and more tools before we even know how to study the origins of conscious thought.

Thank you for your extension! I am starting to grasp the difficulties of investigating the brain. Apparently we still know too little about the problem to make any conclusive statements about such concepts. The information you have presented, however, is extremely educational about our current knowledge of the matter. I am definitely going to read those papers to get a better insight. Thank you!


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What's the technical difference between fainting (and being unconscious) and falling asleep (and sleeping)?
This is actually a popular question along google results but the answers usually sound like:

sleep is voluntary (oh is it?) and healthy
fainting is result of accident and is not normal

I read those answers and I'm like: "You don't say?". So yeah, I know that falling a sleep is a result of some preparation to planned unconscious state, whereas fainting is some defensive reaction trying to protect you from moving (or maybe thinking) when you shouldn't.
But I fainted once and when I woke up it was pretty much like waking up from sleep - including the fact I don't remember the moment I fainted. This gave me an idea that maybe, if you faint in your bed, you'll just fall asleep and wake up in the morning, which would be actually pretty sweet.
Therefore my question is, what's specifically going on when you faint and when you fall asleep. Is there any part when these two situations merge and the final state is the same - you're asleep?
And to my original idea: If you hold your breath to the point where you faint in your bed, what will the result be?

I'm afraid this wont be easy to answer, because, as far is I know, the process of falling asleep is not fully understood by now. But there must be a difference between those two states, because you can actually become conscious while sleeping (this is referred to a lucid dreaming state) And you can even stay conscious while falling asleep, when using a methode called "wake induced lucid dreaming (WILD)". However, fainting is defined as a unconscious state.

Perhaps read the Wiki article on sleep and on your kind of fainting. Falling asleep is typically less fast, in the order of one or a few minutes. Sleep is based on the circadian rhythm and body warmth, so people that faint wake up rather fast, as the brain is not primed to rest at that time. There are three broad categories of causes: heart or blood vessel related, reflex also known as neurally mediated, and orthostatic hypotension.

For this answer I assume that we are talking about sleep in healthy individuals as well as fainting as an isolated event without underlying disease or injury.
The most common form of what we call "fainting" is vasovagal syncope. It is caused by a drop in blood flow to the brain (cerebral hypoperfusion) e.g. by (false) activation of the parasympathetic nervous system and inhibition of the sympathetic system, resulting in low blood pressure or drop in heart rate (reviews 1,2,3). This can be triggered by the Bezold-Janisch reflex. Syncope can also be a symptom of underlying diseases or a side effect of drugs.
The reduced blood flow results in a transient loss of consciousness, a 'shut down' of the brain, which we don't really understand. It is sometimes accompanied by a flattening of an EEG signal, even though the data doesn't seem to be very consistent. Consciousness is defined by two factors, arousal and awareness. The fainted person cannot be 'woken up' and is not aware of the situation (as you said, you don't remember the moment of fainting). But this state normally only lasts for a few seconds or 1-2 minutes.
Sleep, on the other hand, is a mechanism highly regulated by the brain, circadian rhythms and hormones. The brain is thought to switch between the states of sleep and wakefulness by an interplay of different sleep-promoting and wake-promoting areas, including the hypothalamus.
You can argue that sleep is not a state of unconsciousness, since dreaming or even lucid dreaming are connected to a conscious experience. While sleeping lasts longer than the unconsciousness during syncope, it can be reversed by an external stimulus. The sleeping person can be woken up, even though the arousal threshold is increased (loud noises from the alarm are needed). The brain, in fact, is highly active during sleeping (as can be seen in characteristic EEG signals), with energy use close to the state of wakefulness in REM sleep and about 85% during non-REM sleep.
Since these are two different mechanisms, you should not be able to switch between them. After fainting you should regain consciousness very fast. Activation of sleep mechanisms is unlikely in a healthy individual, where sleep regulation is normal and syncope is a rare event.

Most of this is good. I would note, that you don't have to restrict this to vasovagal syncope. The final common pathway of syncope is reduced blood flow to the brain, and the EEG shows a characteristic series of changes (if you manage to record during the loss of consciousness).

Two other suggestions for improvement. There is no need to preface this with a "we don't understand the brain" statement. We understand it well enough to answer this question unequivocally :)

Finally, your last paragraph is a little speculative, though probably partially true. I would consider cutting it. The key (which you've described) is that sleep and fainting are very different brain states, with characteristic patterns on EEG, and behavioral differences (e.g., you can wake someone from sleep). I don't think you need to add a statement about whether it is ever possible to transition from syncope to sleep or sleep to syncope . This is different from the side question of "is fainting a good way to fall asleep?"

This is a nice answer. Fainting is involuntary loss of consciousness. During sleep, there is very little difference in the brain between awake and asleep states in that the brain is quite active.

@anongoodnurse I agree in general, though fainting is a little more specific: transient, involuntary loss of consciousness due to hypoperfusion. Concussion, seizure, anesthesia, other medication or chemical intoxication, hypoglycemia, these all involve involuntary loss of consciousness, but are not fainting. But yes, Frieke has hit the important points here.

@DeNovo I have edited some parts for more information or less speculation. I added the last paragraph since it was part of the question to use fainting as a way to fall asleep. I think that any reported connection between sleep and syncope does refer to 'healthy individuals', which I tried to focus on here. There are a lot of reports about e.g. epilepsy, syncope and sleep, but this is beyond the scope of the question.


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ATP yield of fermentation: study to cite?
Everywhere I find the ATP yields of respiratory and fermentative metabolism of glycolysis. While that of oxidative phosphorilation I could find in Stryer to cite one study where this was addressed (Hinkle 1991 observed 30 ATP/glucose) I cannot find a study where the 2 ATP/glucose was observed and the textbooks I've searched do not provide a citation.
Can anyone please provide a link or citation to a paper where the ATP yield of fermentation (regardless of process) was quantified/estimated?
Thanks

See discussion of this paper.

For glycolysis this is really not so much of an issue, because the ATP yield is fixed by stoichiometry. The early biochemistry work by Embden, Meyerhof, Parnas and other that mapped out the reaction mechanisms of the glycolytic pathway shows that you always obtain exactly 2 ATP per glucose; this is simply the stoichiometry of those reactions. There are a number of primary papers documenting these reaction mechanisms, but it's a large undertaking to go through all of it; the glycolysis chapter of Stryer's Biochemistry is a good summary I think. A brief review of the historical development is described in: "A Fresh View of Glycolysis and Glucokinase Regulation: History and Current Status".
For respiration it's very different, since there is no fixed stoichiometry for chemiosmosis --- the ATP yield depends on the proton gradient across the inner mitochondrial membrane, which in turn depends on a number of factors. So in this case ATP yield will differ between cell types and conditions, and must be measured experimentally.

Interesting paper with the historical background, nice to read.


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How can some animals see ultraviolet or infrared light?
I know that some animals like birds, bees, and fish can see ultraviolet and infrared light. Whether it is to detect flowers that bear nectar, or the urine trails of prey. But what I don't understand is how they see these wavelengths. What is different about their eyes or brain that allows them to see different wavelengths than humans?

Welcome to Biology.SE. UV and IR are by definition wavelength that are outside the range of wavelength that humans can see. There is nothing extraordinary about these other wavelength and therefore the question reduced to How do we see colours?. I think this post will answer your question.

@Remi.b - it doesn't. Hyperspectral vision does warrant a specific answer

@K Gargiulio's answer is correct in that distinct cone cells allow the perception of these wavelengths. You may also be interested in the descriptions of colour vision in http://biology.stackexchange.com/questions/39882/are-some-animals-like-dogs-and-cats-color-blind-and-how-do-we-know-that/39890#39890, for further details.

This is not a duplicate because this question specifically asks about UV and IR molecular-sensors.

You might be interested in the eyes of the mantis shrimp.

Somewhere we should add that a specifically small type of iris is necessary so only relatively tiny animals can see in UV, and I expect they have some kind of lens adaption too.

Yes, they have different photoreceptors as well as the circuitry to interpret the information from those photoreceptors. Humans have 3 types of cones which are tuned to respond best to red, green, or blue light, but it's not an on or off signal. A red or blue cone may still fire in greenish light, it just fires much less often. The brain takes that input and figures out the color based on the relative firing rates of the red/blue/green cones.
So for an animal that can see in UV or infrared, they need both the photoreceptors that respond to that wavelength of light, and the ability to integrate that response into the bigger picture of how all the photoreceptors are firing.

You have still not answered which photoreceptors are those that allow UV sensing. BTW, IR sensing is not similar to that of other photoreceptors even though the perception is finally similar to vision (like in pit vipers). IR does not cause electronic transition; it rather causes activation of temperature regulated channels.

In Drosophila photoreceptor R7 and R8 are UV sensitive while R1 - R6 respond to visible light.

photoreceptors don't fire

Short answer
In mammals dedicated UV cones have been found, as well as photoreceptors with secondary peak-sensitivity in the UV range. In fact, human blue cones are sensitive to near-UV.
Background
In humans, the visible spectrum is generally accepted to range from 390 to 700 nm. Figure 1 shows the spectral sensitivities of the various photoreceptors in humans.

Fig. 1. Spectral sensitivity of the four receptor classes. Source: Wikibooks; Sensory Systems
In invertebrates sensitivity to near-UV is quite common. However, some rodents (mice, gerbils and gophers) also feature a peak in sensitivity at 359 - 511 nm. In these rodents and some marsupials sensitive to UV, it is thought to be attributable to a specific dedicated type of cone sensitive to near-UV (Jacobs et al., 1991; Winter et al, 2003). Near-UV is referred to as UV-A, encompassing 315 - 380 nm.  Likewise, birds seem to feature a dedicated, fourth cone class to detect UV (Benett & Cuthill, 1994).
In the color-blind flower bat, UV sensitivity has been attributed to a photoreceptor with two peak sensitivities - one in the green range and the other around 365 nm and running down to 310 nm (Winter et al, 2003). Hence, UV sensitivity can be conferred by cones with broad sensitivities ranging into the UV range.
In fact, the aphakic human eye (eyes with the lens removed after cataract surgery are aphakic) has been shown to be sensitive to near-UV. As can be seen in Fig.1, the blue cones are actually pretty sensitive to near-UV. It appears that the lens absorbs much of the UV, rendering UV light useless to humans with healthy eyes (Griswold & Stark, 1992).
Infrared (IR) sensitivity in snakes is mediated by pit organs and not via the eyes. Basically they are heat sensors and likely don't mediate vision as such (Newman et al., 1982). I was not able to find any relevant information on IR vision, or how it should be mediated. In fact, I doubt IR is used for vision at all, i.e., to reconstruct the visual scene. IR vision is used more in the form of general heat detection.
References
- Benett & Cuthill, Vis Res (1994); 34(11): 1471–8
- Griswold & Stark, Vis Res (1992); 32(9):1739-43
- Jacobs et al., Nature (1991); 353: 655-6
- Newman et al., Sci Am (1982); 246(3): 116-27
- Winter et al, Nature (2003); 425: 612-4

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


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Plasmid Expression Vector
If I am going to transform a plasmid into a bacterium, which will then be fed to a C. elegans, the expression vector needs to be bacterial correct? The other option is to have a worm expression vector, but I just wanted to make sure that I was correct in my thinking. Thank you.

Are you trying to express the plasmid's contents in C. elegans, so that its cells are producing the gene product, or do you want the bacteria to produce the gene product so that C. elegans can consume the protein?

I am trying to express the plasmid's contents in c. Elegans so it's cells are producing the product

C. elegans do not express the genes of organisms they eat. To create  transgenic worms you either need to microinject purified DNA, or use biolistic transformation (using microparticles coated with DNA). Ingestion does work if you are trying to use RNAi to knockdown expression of a C. elegans gene, but in that case the double-stranded RNA is expressed from a bacterial expression vector. You can also synthesize dsRNA in vitro and soak the worms in that, which I believe also enters when the worms "eat."

You are trying to express the plasmid in C. elegans, so it should be a worm expression vector and promoter. Otherwise, it will be expressed in the host bacteria, but not in the worm, so you won't get the phenotype you're looking for.
One thing you can do is add a bacterial origin of replication to the vector (if one isn't already present) so the bacteria produce multiple copies of the plasmid after transformation. Otherwise, the amount of plasmid consumed by the worms will be rather low.

Perfect, thanks a lot for your advice, I appreciate it.


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What's the purpose of Cdk activity having more than one method of becoming inactive?
Cdk becomes partially active once its bound to cyclin and then gets phosphorylated and fully active once a Cdk-activating kinase (CAK) phosphorylates the partially active Cdk. This fully activated Cdk complex can be inactivated through a Wee1 kinase which phosphorylated the Cdk at a different site or through the binding of a Cdk Inhibitor protein (CKI).
Why would the cell need more than one way to inactivated this complex? Are there two methods in case one of them should "fail?" (i.e. the kinase not phosphorylate the Cdk complex in the proper spot) or is there some alternative reason?


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What plant is this?
It was all along a fence in a downtown core in Ottawa, flowering in November.

I didn't get a better close-up of the flower itself, I had thought the leaves would be pretty important.

where was the picture taken (Down Under November is mid-summer) and a close up of the flower is in place

My bad - I'm new at naming species and what is needed to identify a plant. I'll add a close-up. It's actually in Ottawa, so November can be a tad nippy, hence my surprise.

@SQLiteNoob Can you add the information to the question? Information given in the comments may be missed. Also, it is good if the question is complete in itself.

@SQLiteNoob This is an example of an acceptable species ID question, while your others are not acceptable. This image has a clear single plant species visible (or otherwise pointed out), and you provided information about the location and time the photo was taken. In the future, you should provide these information if you want your plant to be more easily identified.

Given what I can guess of the flower organization and the type of leaves I see on the first photo, they could belong to the Ranunculaceae or Rosaceae family.
Edit
The example of Asteraceae provided by RHA seems more likely to be close to the correct answer, although it seems to me that the leaves don't look exactly the same as the one showed in Wikipedia for Tanacetum parthenium:
https://en.wikipedia.org/wiki/Tanacetum_parthenium#/media/File:Tanacetum_parthenium_Blatt.JPG

Really? It looks like a composite to me

True, it could also be an Asteraceae, but the texture of the yellow part, the low number and the almost-round shape of the white petal-like parts somehow make me prefer the other hypotheses.

thanks so much for the input. It was along a fence, so I was myself trying to determine if it is a spontaneous weed or deliberately planted - it's just that there was nothing else around it that looked to be on purpose

I disagree with @bli. I am pretty sure it is an Asteraceae, and I think I even know what species. It is Matricaria parthenium, also known as Chrysanthemun parthenium or Tanacetum parthenium. It is indigenous in Europe (Palearctic species) and it is also grown in gardens often. It is said to be a medicinal plant that works against fever and migraine. For more info see Wikipedia

This seems to be the correct answer.


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Why do telomere lengths not predict differences in life spans among species?
We read that ageing is related to cell death when we run out of telomeres at the end of our DNA molecules. Humans live roughly for 70 years - the traditional three-score years and ten. This compares with the great apes, such as chimps and gorillas, which live for about 40 years. So we would expect the great apes to have fewer telomeres than humans. In fact the reverse is the case. Humans have telomeres of about 10 kilobases in length whereas the equivalent length in chimps and other great apes is about 23 kilobases. So what is going on? Why do we live longer?

Great question. However, a few references that contain the numbers would help people answer. +1

I think the problem is that you mix up the ageing of a cell with the ageing (or life span) of an organism. Of course the maximal lifespan in a perfect environment could be based on telomere length, but there are other factors shortening this life span as health care, general safety, behaviour,...

In response to Skymingen's comment, in captivity chimps live on average for 31.7 yrs (m) to 38.7 yrs (f). I suppose 'captivity' is the equivalent of good nutrition and health care in humans, which still leaves a huge 'longevity gap'.  If cells die off in large numbers, isn't that the main cause of ageing?

Just remember the life expectancy of Mice is about 3 years, but they have really long telomeres. http://learn.genetics.utah.edu/content/chromosomes/telomeres/ I think a lot of the claims on here are absurd, but it gives a general overview.

You are incorrect about your figures. Chimpanzees live up to 60 years of age in captivity. The blog you are quoting is wrong. This is detail from the University of Wisconsin's National Primate Research Center (http://pin.primate.wisc.edu/factsheets/entry/chimpanzee).

Besides being wrong about telomeres, you are also forgetting the fact that through the 19th century, where we saw public sanitation for the first time and the advent of modern medicine, human life expectancy was between 35-40 years. Prior to the Renaissance and Industrial Revolutions, it was more like 30. So we had similar life expectancies to our cousins up until the point where we figured out the Germ Theory of Disease.

As a side note: titles starting with Please explain...,  question about... or help for...  are not very helpful. A better title would be Why isn't life expectancy correlated with telomere length?

The answer should be obvious: Telomeres do not determine an organism's longevity.
There's only a vague correlation between telomere length and a species' lifespan.  See Comparative biology of mammalian telomeres: hypotheses on ancestral states and the roles of telomeres in longevity determination for a starting point.  Telomeres are a part of the longevity story, but probably a fairly small part.
The Hayflick limit is generally associated with telomere length. Human telomeres are a little on the long side as species go, but are not extraordinary. Many species of mice, and other rodents, have far longer telomeres than humans, for example, and obviously have much shorter lifespans. There's also such a thing as a "mega-telomere", found in a number of bird species, which can hundreds of times longer than human telomeres.

Absolutely. One of the likely culprits is Mitochondria no longer being able to perform their roles properly. Though to improve upon your answer, you should probably paraphrase and reference the paraphrases to the relevant primary literature on aging.

Please could you provide references in your answer

It's not really necessary to give references, because as I say it's trivially obvious -- as the original question shows -- that telomere length isn't connected with aging.  It would make more sense that the bizarre belief that telomeres are associated with organism aging -- which defies these well known and simple observations -- should support itself.

Telomere length is linked to aging - there's a number of links here: https://www.google.se/search?q=telomere+length+aging&oq=telomere+length+agi&aqs=chrome.1.69i57j0l3.9980j0j4&client=ms-android-samsung&sourceid=chrome-mobile&ie=UTF-8 @iayork

I asked the question because I am an Earth scientist, not a biologist, and I am not familiar with the primary literature. So what is 'trivially obvious' to iayork isn't obvious to me. As I understand it, with each death and replacement of a cell, the telomere shortens. After multiple cell regenerations there are no telomeres left, and the cell dies. The death of millions of cells effectively results in ageing. Maybe I phrased the question badly, but the question still stands: why don't chimps, who have more telomeres, live longer than humans?

@rg255 Most recent research on neurodegeneration point to the formation of amyloid plaques due to misfolded proteins being able to nucleate the misfolding in normally folded forms of those proteins. The plaques accumulate and are toxic to the cell. Many of these diseases are associated with aging and they have nothing to do with the length of telomeres.

@iayork I just think being so dismissive of the link between telomeres and ageing is misleading, while telomere length does not determine ageing entirely that does not mean they are unrelated to ageing - http://www.nature.com/nrg/journal/v6/n8/full/nrg1656.html and http://www.gizmag.com/telomerase-aging-harvard-reverse-process-telomeres/17107/ - besides that discussion, I was only asking for references because that is the normal standards we set on biology SE, which you might not be familiar with as you seem to be fairly new, just trying to be helpful

Perhaps you could modify your answer to say that between-species the telomere length appears to explain little to none of the variance in ageing, while they appear to some of the variance in ageing within-species, I think this would be a more accurate interpretation and answer to the question.

There is not one simple cause of aging, like short telomeres, and the fact is that it hasn't even been settled whether aging is caused by evolution failing to evolve good enough repair mechanisms, or whether it evolved with a purpose, it might be that the genes of an organism are better spread if that organism doesn't live too long for example. For more details on the latter debate see this previous issue of Current Aging Science (all the articles are free).


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Favored Conditions of Bacterial Growth
I have read that bacteria "thrive" in warm places. Naturally, I am very interested in why this is the case. Humans for instance thrive also in relatively warm conditions if it's too cold or too warm we die. However why would this also apply to bacteria?

The idea that bacteria thrive in warm places is mostly biased from a human perspective. Human researchers will tend to care more about bacteria that cause human disease. These pathogenic bacteria can replicate in/on humans at ~37 °C (which is warm). As Dexter points out, bacteria can grow at other temperatures.
But I'd go deeper and consider proteins (and other macromolecules) in the cell. For example, the enzymes that carry out many important processes for the bacteria (such as DNA polymerases that build the DNA) are most active at certain temperatures: in E. coli or humans or dogs that's ~37 °C; for a thermophile it's warmer. See below:

Actually it's not true. It depends on species of bacteria you are talking about. Bacteria can 'thrive*' in very wide range of temperature. They can be mainly categorized according to temperature,

Psychrophiles : live in very cold temperature. Reported lowest** temperature in which specific bacteria can 'thrive' is $-20^oC$ .
Mesophiles : live in moderate temperature
Thermophiles : live in very high temperature. These can 'thrive' at very high temperature like $+121^o C$

*By 'thrive' I mean they are actively dividing and metabolic process are not ceased.
**People store at bacteria at $-80^0C$ also but there they are not 'thriving' they are alive but freezed.


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Why are segments/parasegments in fruit fly embryos staggered?
I'm reading my developmental biology textbook and I don't understand this concept. I can see how concentrations of Eve and Ftz determine each parasegment. However, I don't understand why the length of one parasegment isn't equal to the length of one segment on the actual embryo. Parasegments and segments are staggered from eachother.
Could anyone clarify?
Edit: I've gone back and re-read a bit. Is this staggering because parasegments are established while the embryo is still syncytial? So parasements are established, and afterwards cell division begins. But the daughter cells cant line up perfectly with the parasegments so segments and parasegments end up a bit staggered.
Edit2: Bit more reading. I think I got it. After parasegment establishment by Ftz/Eve, further segment polarity genes Engrailed and Wingless are expressed, with Engrailed expression being induced by either eve/ftz. The posterior side of the first engrailed cell determines where the boundary for a segment will be determined.
Can anyone confirm?


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Why is warm water comfortable, but warm air uncomfortable?
I friend of mine tried floating, where you lay in a bath kept at body temperature (98.6 degrees F).  He said after a while you don't feel the water at all.
This made me wonder why being in warm water (bathtub, spa, etc) is comforting, but a hot weather feels miserable.  Can someone explain the difference?

I think it is subjective phenomenon.

I don't know about you, but I can walk around in only a T-shirt when the air temperature is 10°C, but jumping into 10°C water is going to be a world of pain... This should really be a chemistry or physics question about specific heat capacity.

You constantly generate heat from metabolism.  The ability of this heat to be transferred to your surroundings from your skin is tremendously different in air vs. water. This is known as thermal conductivity.
The ability of water to remove heat from your skin is roughly 24 times that of air. See list of materials and their thermal conductivity rates here
In water of close to body temp, you can still bleed off heat to water. Your ability to do so in air that is close to body temperature is greatly reduced, so much so that in order to keep up, you sweat and increase the cooling ability through the evaporation of that sweat at temperatures well below 98.6F.

Hot air generally has lesser moisture hence increasing the loss of moisture from our skin. Note that a sauna bath does not feel as uncomfortable.
Also while conductivity of water is grossly more than air (thermal) One has to take into account convection of hot air which may increase the total heat transfer from air to the body.

In case of floating. The question. Is where does the 90 watts of basal heat go... Obviously conduction does not take place without temp gradient...Prespiration .... Will it be possible ?

The specific heat capacity of water is also huge...If you were in a tank with 100's of gallons at exactly 98.6, and it was perfectly thermally insulated to not decrease...it still would take a long time for your 90 watts to raise the temperature appreciably. And even if it was exactly 98.6, and your body temp raised to 99 because of no gradient...voila, now have a gradient.