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Are there any other animals that become attached to a non-living object?
Do any animals become psychologically attached to any non-living object that is not useful to the animal for any of its physical needs, like some children do to stuffed animals? Some children are so attached to their toys that they take them with them whenever possible, and are upset when the toy goes missing or is taken by another.

My cat loves her laundry basket. Needs it, sleeps in it, plays in it, bathes herself in it, and is usually always in it. If there is laundry in it she always tips in over it's crazy.

So, this is psychological attachment. From the question alone, I thought of physical attachment.
If you provide stuffed animals and human children, then I'd offer the television remote, a chair/sofa and the cellphone for human adults. In general, many adults are far too sedentary for their own health.
Some non-human primates have exhibited behavior similar to that which you describe with the stuffed animals-children example.
In terms of an inanimate object, you can add the Internet. Certain behaviors like over-indulgence in alcohol, sex, gambling, hand-washing, and the like, could, broadly speaking, fit within the question as posed.

Have you a reference for the statement about non-human primates?

This doesn't really answer the question, it gives more examples of human attachment and a vague reference to non-human primates. I think it would have been better as a comment.


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How do fungi react to being grown in a tissue culture?
I know how plant cells and animal cells react to being cultured and grown this way, but what about mushrooms? Would they respond like plants, and result in embryos growing off the mass? Or does the mass just grow indefinitely as in animals? Has anyone done this? How do they react when grown this way?

Generally, fungi are cultured on agar with a food source such as malt extract. One way to do this is to clone a mushroom from the fruitbody of a mushroom or from colonized substrate (e.g. rotting wood). Another approach is to germinate spores.
The fungus will grow as vegetative mycelia until it runs out of food. At that time, some species will grow tiny fruitbodies or sporulate before entering a more dormant phase, dying out. Unless refrigerated, standard agar plates dehydrate. Also, fungi may take on different textures: wispy, bumpy, root-like (rhizomorphic), leathery, powdery, and may darken or change color as they age.
Some cultures start to adapt their metabolism to the media after a large number of transfers (based on observation and discussed in Stamets' "The Mushroom Cultivator".) at this point, cultures may also start to grow more slowly.
The mycelia can be transferred from one plate to another or to another media (substrate) such as a log, 'fortified sawdust' (sawdust with ~30% w/w wheat bran), or pasteurized compost. With the appropriate nutrition and environmental stimuli (CO2 levels, temperature, moisture, light, etc), the mycelia will fruit, creating mushrooms - generally after fully colonizing the substrate.
Here is a figure of 35 agar plates with 16 different fungal cultures that I isolated from the wild (soil, wood, mushrooms, as described in Allison et. al, 2009; LeBauer, 2010), and have transferred from a mature culture (about a 2 months old) to a new plate, which are about two weeks old in this picture. Parent cultures are in the first and third row, with children below (they are genetic clones; instead of counting generations, I count number of transfers.

You can also find cultures of fungi (Yeast) in unfiltered beer.
I have used many techniques to isolate and culture fungi (Isikhuemhen and LeBauer, 2004; LeBauer, 2010) but I would recommend the books "The Mushroom Cultivator" and "Growing Gourmet and Medicinal Mushrooms" by Paul Stamets for more information on sterile culture techniques used in mushroom cultivation.

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Is the appendix a vestigial structure in all vertebrates?
In humans the Appendix is a vestigial organ. Does it serve no apparent purpose in all the vertebrates that have one?

I don't think the appendix is vestigial in humans.

Smith et al. (2009) provide a survey of the morphology of the cecal appendix. One current hypothesis is that the appendix provides "safe harbor" for symbiotic gut bacteria. Among mammals, there is a vast array of cecal appendices:

In summary:

A comparative anatomical approach reveals three apparent morphotypes
  of the cecal appendix, as well as appendix-like structures in some
  species that lack a true cecal appendix. Cladistic analyses indicate
  that the appendix has evolved independently at least twice (at least
  once in diprotodont marsupials and at least once in Euarchontoglires),
  shows a highly significant (P < 0.0001) phylogenetic signal in its
  distribution, and has been maintained in mammalian evolution for 80
  million years or longer.

Aside from humans, it is largely rodents and most notably rabbits that have an appendix.  Therefore, using rabbits as my example:
In rabbits, the appendix is thought to have a key role in the development of the immune system.  Specifically it has been shown experimentally that when neonatal rabbits are given an appendectomy levels of Immunoglobulin A and G (IgA/IgG) fall dramatically. Both these polypeptides are prominent antibodies - IgA plays a key role in mucosal immunity whilst IgGs in humoral immunity.  These effects were localised to the small intestine of the rabbits, however were statistically significant. 1
In infants, the rabbit appendix resembles the chicken bursa and sheep ileal Peyer's patch (both performing similar functions as described above).2
This has led to some ongoing research as to whether the human appendix has a similar properties in having function in infants 3:

If the human appendix functions as a primary lymphoid organ, it may occur during the first few months of age when the GC T-cell density is low.

1Neonatal appendectomy impairs mucosal immunity in rabbits. Cell Immunol. 1997 Nov 25;182(1):29-37
2The appendix functions as a mammalian bursal equivalent in the developing rabbit. Adv Exp Med Biol. 1994;355:249-53.
3A morphological and immunohistological study of the human and rabbit appendix for comparison with the avian bursa. Dev Comp Immunol. 2000 Dec;24(8):797-814.

The appendix was thought to be vestigial in humans until recently. Now it appears that, like rabbits, it is a safe harbour for symbiotic bacteria in the intestines.
Source: Bollinger, Barbas, Bush, et al. J Theor Biol. 2007 Dec 21;249(4):826-31. Epub 2007 Sep 7.

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Do larger multicellular organisms have an increased risk of mutation and thus cancer?
So I was thinking that if each cell has P(X) of becoming cancerous, then the chance of cancer is 1-((1-P(X))^n) where n is the number of cells in the organism.
Since larger organisms have more cells than smaller organisms (I'm guessing that larger organisms simply have more cells than smaller organisms as you can't have larger cells since there is an optimum surface area to volume ratio), does this mean then that larger creatures are more likely to have cancer cause they have more cells?

I would say that the question is more complicated since it really depends on the number of generations of cells. For instance muscle cells rarely get cancel but they also rarely divide.

You also have to take into account that a lot of larger organisms have a large genome with a low percentage actually encoding exons.

@GWW: Is there actually a correlation between body size and fraction of coding DNA?

As mentioned in the comments, this question is quite complicated. If the chance of a single cell from different organisms getting cancer was the same, then you would be correct, but this is not the case.
Different organisms have evolved to live different lengths of time. This is rather obvious when you think about it: mice have a maximum lifespan of ~3 years, humans ~80years (these figures are of course massive generalizations - but it doesn't really matter). Yet 'old' mice (> 2 years) still get age-related diseases such as cardiovascular disease, and cancer. It should be fairly clear that the risk of a 2 year old mouse getting (age-related) cancer is much higher than a 2 year old human.
The explanation for this isn't exactly concrete, but it goes something like this; mice invest a lot more resources in growing very fast and reaching a reproductive age very early, whereas humans develop much more slowly, and invest a higher proportion of their resources in maintaining tissue function, thereby reaching reproductive maturity much later than the mouse. The Hayflick limit for a mouse is about 10, whereas for humans this is closer to 60.
Thus the rate of aging in humans is much lower than that of the mouse, and it comes back to evolution: mortality in the wild is very high for the mouse, and thus mice that invest heavily in reaching early reproductive maturity are selected for - and those that invest in anti-cancer mechanisms take longer to reach reproductive maturity, and thus have less chance of actually doing it!
So to answer your question - smaller organisms tend to have higher risks of getting cancer because their lifespans are comparatively shorter, and thus they 'age' at a faster rate and invest less resources in maintaining function (e.g. genome integrity).

Would the OPs logic apply in the case of organisms from the same species?  For example would larger humans have a higher risk of cancer than smaller ones?

@Mew interesting question. Had a quick search and could not find a systematic study. The closest I could find is a report suggesting that BMI is positively associated with some adult cancers in humans (PMID: 18280327), however this could be confounded by a number of issues (>BMI could indicate unhealthy lifestyle? inactivity, smoking, drinking... only suggestions, but you can see what I mean). I can see that the logic of "large people have more cells" would imply higher cancer rates, but I don't see any evidence for this.


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Providing small molecules to cells on a filter plate
Lets imagine that I have mammalian cells that I've immobilized on a filter. Now I want to keep providing small molecules to these immobilized cells without resolubilizing the cells.
The caveat is that I would like to do so without fixing the cells or waiting for them to adhere to the filter. The small molecules are small enough to diffuse through the filter.

perhaps you can dip the filter plate in a medium containing the small molecules.. and then keep changing the bath after few days.. btw you want a batch or continuous system??

@WYSIWYG, Batch should be fine. The question is what would be the setup to do so. Would it be as simple as reversing a 96 well lid over and placing the filter plate on top? What about the wetting?

I am not very sure but you may try the plates used for growing ES cells over feeder layers separated by a membrane

Perhaps you're looking for these hanging inserts, for example: "Millicells"

Can you elaborate a bit more on why this meets the OP's requirements?

The original poster would like to feed his immobilized cells small molecules, without fixing or waiting for adherence. The inserts contain a membrane, which forms a permeable barrier, to allow diffusion of small molecules, and site for attachment. The insert itself is free to move and hang in different culture media/wells, so no need to trypsinize or resolubilize them, and provides containment of the non-attached cells.


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How do we know the brain flips images projected on the retina back around?
Why do we turn images upside down again rather than dealing with them directly, still vertically rotated after passing through our lens?
I don't see how that would cause any problems, and how we'd ever be able to figure out if we are presented with flipped images after getting used to interacting based on visual input, whether flipped or not.
What am I missing?

My head of Biology has regularly mentioned an experiment where individuals were given glasses that inverted their vision - after a period of time their brain compensated and re-inverted the image (presumably the same happened when the glasses were removed).  Interesting stuff - I'll see if I can find a link.

That'd be appreciated :).

So, what is the exact question you are asking? The title asks something different from the question's body...

The body merely adds the 'why' aspect, the question as stated in the title is also in there: 'I don't see (...) and how we'd ever be able to figure out if...' - Both are interesting and very much related.

@Chris Some preliminary experiments on vision without inversion of the retinal image - the original article from 1896.  More recently (and for me disappointingly :L) a lot of doubt has been put onto the thought that the field of vision was corrected - people were still very much aware that the image was inverted even if they could deal with it The myth of upright vision. A psychophysical and functional imaging study of adaptation to inverting spectacles

Thank you for your efforts. This article seems to point out we can function normally despite inverted vision, i.e. without (the return of) upright vision. So as stated in my first post, why bother with flipping images after the retina if we can deal with the input either way? And how do we know we do?

Closely related question on CogSci.SE

The question assumes there is something like a little projection screen inside the brain -- something that has an "up" and a "down".  It's not like that; there are just an array of retinal cells transmitting pulses to a set of neurons.  Retinal cell A talks to neuron 1, cell B to neuron 2, etc.  neurons 1 and 2 are not physically arranged in space in a way that matters to image perception.  There is no little man in there watching a little screen.  See the CogSci question that jonsca linked to.

@mgkrebbs: the retinotopic mapping of images in the visual cortex is very precise. There is no projection screen in the brain but the image is processed in a very precise spatial manner.

@nico: Of course the neurons maintain precise connection relationships with neurons carrying signals from spatially adjacent areas of the retina. Nevertheless, there is nothing about the arrangement that makes it "upside down" and thus requires further processing to "flip" it.

@mgkrebbs: OK, we agree. I just misunderstood your previous comment :).

The basis of this question is a common misconception, and unfortunately the accepted answer by @CHM is also based on this common misconception. The misconception is based on the homunculus falacy: the tendency for people to think that the image that lands on the retina is somehow 'assembled' and presented for something (the 'consciousness') to view. This is not the case.
As the comment by @mgkrebbs explains, there is no orientation (up or down) in the brain, there is only neural firing. The information of the visual scene is distributed over the brain, and information does not have physical properties like orientation. Although as @nico pointed out the neurons that process the information do have a spatial structure that mimics that of the retina, this is a topological property (i.e. stimuli that are close on the retina are processes by neurons that are close in V1) and such a topological property does not induce an orientation.
The root of the problem is really that the question "How do we know the brain flips images projected on the retina back around?" is a pseudo-question. Although it is grammatically well-formed, it makes no semantic sense. When the image is 'in the' (i.e. being processed by the) brain it no longer has physical properties like orientation. Thus you cannot ask if it has been flipped or not.

So is the retinotopic arrangement inverse top-to-bottom of the input from the retina? In that case it's still a valid question why the pathways from one half would at some point cross over with those from the other half and not just stay on the side they are.

@Armatus: that is a different question from the "upside down" problem though (which, by the way, on the retina is a purely physical issue do the lens that turns the image upside-down).

@Armatus The cross-over is a good question, and you should ask it on CogSci.SE. However, I feel that the question (and the accepted 'answer') was instead about the lenses vertical and the common misconception of orientation of images in the brain, not about why we have opposite hemispheric mapping..

You can talk about a perceived image without invoking the homunculus fallacy. The brain certainly re-orients (or perhaps orients) the image that is projected on the retina, but it is a complex integration of retinal and extra-retinal stimuli. See my answer.

I think you're oversimplifying the problem. Think about gravitation.
Take this informal example: at any point on a massive sphere, you can define "bottom" such that any massive object with weight less than that of the sphere is subject to an attractive force towards that point. The direction of the force points in the direction of the "bottom".
Assuming this holds true for every massive object, the following is logical: for the purpose of orientation, it is a lot more energy efficient for an organism to simply invert the image using brain circuitry than invert every single sensory input to effectively reverse the definition of "bottom", which follows from physical laws to which the organism is invariably bound.

My answer was initially posted in response to this duplicate question. Since this post was made earlier, the question I answered will likely be closed as a duplicate. I think my answer has something useful to add, so I've added it here, with a little more discussion in response to the other answers:

How do we know the brain flips images projected on the retina back around?

You examine your own visual sense and, possibly, if you're examining patients on a neurology ward, examine theirs as well. Here @CHM's answer is on point, as our sense of gravity (through the vestibular system) is one of the senses integrated into our ability to visually perceive up as up and down as down. It also reflects the confusion expressed by a particular patient with Reversal of Vision Metamorphopsia (see below) when an upside down cup of tea didn't spill out. This doesn't require anyone to invoke a little man watching a video projected somewhere in the occipital lobe. You just ask yourself (and the stroke patient) to describe the world around them. If it's upside down, if people seem to be standing on their heads, you present them with a series of letters with a different orientation and ask them to identify the normal (right side up) letters.
Here is the bulk of my answer to the earlier question, which describes the various inputs the brain integrates in order to produce a visual perception of a right side up (and left-side left) world.
Your retina is presented with an inverted image, but a healthy brain  (re)orients the image. I would note that you can talk about the image an individual perceives without invoking a video playing in the brain.
The spatial orientation of a perceived image is a complex process that seems to involve integration of information about the relative position of objects from the light perceived by the retina, about the position of the eyes from the muscles of the eyes, and about the position of the head from the vestibular system and muscles of the neck. It may or may not involve other body position information from the cerebellum and proprioceptive cortex.
As with much of our knowledge about the localization of function in the human brain, the evidence for the importance of these various streams of information comes from cases with lesions at a number of different locations that produce brief disruption of the integration of this information, a syndrome called Reversal of Vision Metamorphopsia.
For one patient:

He saw people walking on their heads, and the floor next to his bed appeared to be over his head

For another:

People were seen walking on their heads, the windows close to the ceiling were within reach of his hands, and a cup stood "upside down" on the shelf but the "tea did not spill out" (all the objects including the shelf were upside down).

Typically this (Reversal of Vision Metamorphopsia) is the perception of a completely inverted image as in C above (left becomes right, up becomes down), but other reversals have been reported (A, D, and E above).

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Effect of spaying on the female cat organism and health
Veterinarians often recommend spaying a female cat if the owner does not want her to have kittens. What does biology know about the effect of spaying on female cats' organism and health (apart from lack of fertility, of course)?

From the standpoint of the skeletal system, spaying is definitely not good for her health. Removal of the ovaries mimics what happens at menopause, when circulating estrogen levels fall. Estrogen is necessary for maintenance of bone mineralization. Without estrogen, bones start to demineralize (the same process that happens in human females after menopause, leading to osteoporosis).
Then again, some animals, if they do not get pregnant, will cycle indefinitely until they get anemic and die. Ferrets are an example. So it's better to have these spayed.

"Then again, some animals, if they do get pregnant, will cycle indefinitely until they get anemic" - did you mean "if they don't get pregnant"?

Do these animals include cats? I've heard that cats go in heat more often than dogs.

I asked something similar: https://biology.stackexchange.com/questions/70223/cat-pregnancy-vs-cancer-risk


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Spatial resolutions in optical microscopy
I have read that different optical imaging techniques such as  such as wide-field microscopy, confocal microscopy or STED microscopy can theoretically achieve a different spatial resolution.
However, I was only able to find information about the STED microscopy's spatial resolution (5.8 nm) on Wikipedia.
Does anybody know of any references or recommended reading (preferably free) where I can learn more about different optical microscopy methods and how the cope with the diffraction limit?

Super-resolution light microscopy will give you a spatial resolution on the order of FRET interaction distance (~10 nm) which is phenomenal considering the threshold was thought to be the limited by the diffraction limit. Conventional optical microscopy techniques can typically resolve down to ~200 nm.

The theoretical resolution for an optical microscope depends on the wavelength used, but is close to 0.22 um (220 nm). Confocal microscopy does not greatly improve axial resolution; it dramatically improves the in-plane resolution (x and y directions, by excluding extraneous light). Theres not a lot to do to "cope" with that using those techniques. If you need more resolution, you can use the super-resolution techniques you mention, or the good old TEM.
There is some more information on the Nikon website: http://www.microscopyu.com/articles/formulas/formulasresolution.html
and on Olympus website: http://www.olympusconfocal.com/theory/resolutionintro.html

You could also have a look at Leica Microsystems' Science Lab. You will find lots of articles and tutorials on the different microscopy methods, ranging from basic microscopy knowledge to specific know-how, including latest information on STED: www.leica-microsystems.com/science-lab
For example:
gCW-STED Microscopy: When the Arrival Time of a Photon Matters
http://www.leica-microsystems.com/science-lab/gcw-sted-microscopy-when-the-arrival-time-of-a-photon-matters/
From Molecules to Tissues – Optical Tools for Cancer Research
http://www.leica-microsystems.com/science-lab/from-molecules-to-tissues-optical-tools-for-cancer-research/
(Disclosure: I have been involved in the launch of Leica Science Lab)

A couple of review articles you could read up on.
1) Leung BO, Chou KC. Review of super-resolution fluorescence microscopy for biology. Appl Spectrosc. 2011 Sep;65(9):967-80.
2) Huang B, Bates M, Zhuang X. Super-resolution fluorescence microscopy. Annu Rev Biochem. 2009;78:993-1016.

Might this not be better as a comment? :)

Perhaps, but roseck did ask for some references to read, so I provided some appropriate articles.


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Quantum mechanics in biology
There is a growing interest in the applications of non-equilibrium quantum dynamics to describe biological processes (I'm not talking here about Penrose's old theories, but new stuff -- quantum coherence in light harvesting, magnetoreception etc.). What is the biologists' take on this? Is this just a whim of physicists looking for grants, or a serious part of biological research?

Have you been listening to Bob McDonald on the CBC? ;)

Absolutely a serious part of research - quantum mechanics defines chemical structure and reactivity. Whenever you see a headline like 'Scientists find quantum effects important in protein activity, weird huh?', read it as 'Scientists find pragmatic classical approximations inadequate in describing protein activity'.
In protein structure, for example, classical molecular dynamics/mechanics are important in generating computationally tractable problems, however they represent a tacit and streamlined parameterisation of underlying quantum mechanics. QM protein structures are usually too gnarly to compute (at least historically speaking), except in regions of interest like an active site, where a model fine-tuned for sequences of amino acids will probably fail badly anyway. As a concrete example, the group that I'm in is in part interested in computationally modelling the active site of plant photosystem II, which contains a cluster of spin-coupled manganese atoms. To glean any useful understanding of how this cluster functions via a computational model, an explicit quantum mechanical level of theory that takes into account electron exchange and correlation must be used. This requirement can probably be extended to any metalloenzyme.
And this isn't touching upon the resonance hole transfer that oxidises the active site, the Davydov solitons that manifest in protein alpha helices, or indeed the quantum electrodynamical origins of the Van der Waals interaction that causes everything to tend to stick to everything else.
Hope this is interesting :D
(note: I am not involved with PetaChem, I just think it's freaking awesome.)

Extremely interesting! Can you provide some links to papers about the Mn clusters?

@quant_dev - unfortunately there's very little that isn't behind a paywall, but if you don't have an institutional subscription and are happy reading abstracts, this is a decent start. IIRC the authors looked at the active site and proximate protein environment of PSII using a QM simulation (spin-unrestricted density functional theory) embedded in a molecular mechanics simulation. This paper indicates that elements of PSII WOC kinetics are affected by the Jahn-Teller activity of Mn sites.

Do you know about some out-of-equilibrium stuff as well?

@quant_dev - please elaborate on what you mean

I mean the cases when quantum mechanics is used to describe non-equlibrium dynamics, not the groundstate or some other stationary state of the system. For example, energy or charge transport.

@quant_dev - That link from petachem shows the time evolution of a protein at an ab initio level of theory. I'm not well acquainted with the state of the art, but Car-Parinello molecular dynamics is a type of density functional theory that can handle potentially large molecules.

Don't forget about deuteriating drugs!


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Effect of histidine on the binding affinity of HisP
I was asked the following question by my teacher:

A gene regulatory protein called HisP regulates the enzymes for
  histidine biosynthesis in the bacterium E. Coli.  HisP is a protein
  whoes activity is modulated by histidine.  Upon binding histidine,
  HisP alters its conformation, dramatically changing its affinity for
  the regulatory sequences in the promoters of the genes for the
  histidine biosynthetic enzymes.
If HisP function sas a transcriptional repressor, would you expect
  that HisP would bind more tightly or less tightly to regulatory
  sequences when histidine is abundant? Why?

My own attempt at a solution:
Less tightly.  If histidine is abundant, HisP's job is to stop the histadine pathway as a "repressor."  If HisP binds less tightly to promotors, the pathway should not produce as much histadine.

Still if you change your question as (If histidine is abundant, HisP's job is to stop the histidine pathway as a "repressor." If HisP binds less tightly to promotors, the pathway should not produce as much histidine.)
Then it should be under another assumption that what is the effect of HisP binding promoter of enzyme's gene. Is it suppressing the transcription or amplifying the transcription.
If it suppresses transcription then answer is more tightly, if it amplifies the transcription then answer is less tightly. I suggest you put this clearly in your answer, as the question is not quest accurate.

I guess your answer might be wrong.
The question should be under another assumption that how does this protein HisP regulate histidine biosynthesis. positiver or negative feedback regulation.
Generally, amino acids synthesis is regulated by negative feedback loops so that cells could control the amount of amino acids they want. In this case, the answer should be more tightly. As it functions as a repressor then it should bind promoter more tightly so that to repress the transcription more which then generate less histidine synthesis enzyme. (I believe this is what your teacher want you to answer)
In the other case, biosystems sometimes have the positive feedback regulation so that they can amplify the sensitivity to the environment noise or generate bistability (phenotypic switching). In that case, the protein bind promoter less tightly in order to generate more histidine.


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How are there alternative initiation codons?
According to wikipedia and the original complete sequence of the K-12 genome, there are multiple non-AUG start codons such as GUG and UUG. How is this possible? I'm particularly curious about the mechanism of translation initiation in the absence of the canonical tRNAfMet.

Actually, the start codon, no matter whether it is AUG or GUG/UGG, always encodes for Met. So the translation is initiated by tRNAfMet (prokaryotic translation). The 30s ribosome subunit binds to the Shine-Dalgarno sequence and then it scans the dowstream mRNA sequence for AUG and the tRNA loaded with Met, which has the CAU anticodon form the most stable interaction. But apparently, only two-bases-interaction between the start codon (GUG, UUG) and the fMet-tRNA anticodon are sufficient for the initiation of translation (1). I will look more into the literature.
1. Initiation of translation in prokaryotes and eukaryotes

Leave it to Marilyn to clarify what everyone else jumbles. I'm seeing some suggestions that there are novel tRNAs with CAC/CAA anticodons. We'll get to the bottom of this.


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Does the Parasympathetic Tract of Colon Sigmoideum Travel with Nervus Vagus and its Nucleus Dorsalis Nervi Vagi?
I have the following tractus now:

nucleus parasymphaticus sacrales -> nervus splanchnic -> ganglion
  terminalis -> colon sigmoideum

The tract is parasympathetic.
It suggests me that it should travel along CN 9 or CN 10, most likely with CN 10.
Does tractus colon sigmoideum travel with CN 10 and its nucleus dorsalis nervi vagi?

I found the following from Wikipedia:

Pelvic splanchnic nerves are the primary source for parasympathetic innervation [for Sigmoid colon].

The non-cranial nerve is extending the scope of the cranial nerve by a synapse between the two neurons. The neurons are transmitting the electrical impulse from one neuron to another.
So this way the splanchnic nerve does not need to be with CN 10 in the region of impact.
The parasympathetic tract of colon sigmoideum can travel with nervus vagus by having a synapse between pelvic splanchnic nerve and CN 10. I verified this from my professor.


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Electricity generated by the body and its applications?
I recently came across this article from Nature. In it, it states that the snails have "tiny biofuel cells that extract electrical power from the glucose and oxygen in the snail’s blood", and that the power obtained is dependent on "how quickly sugar and oxygen can be taken from the creatures' blood". They go on to say that the power obtained decreases over time, and that these implants could power future pacemakers in humans.
Would this application in humans require that a patient eats more and "breathes more" than average? Why does the power output decrease over time, and couldn't that potentially lead to the malfunctioning of a pacemaker?

References

Van Noorden, Richard. “Cyborg Snails Power Up.” Nature (March 12, 2012). http://www.nature.com/doifinder/10.1038/nature.2012.10210.

You'd think if such devices were used in humans, they wouldn't require a change of lifestyle.
They don't say the power always decreases over time:

Katz’s snails, for example, produced up to 7.45 microwatts, but after
  45 minutes, that power had decreased by 80%. To draw continuous power,
  Katz’s team had to ramp down the power they extracted to 0.16
  microwatts.

This is really a chemistry question. The glucose has to be brought to the fuel cell some way. In this case, the glucose is oxydized directly in the hemolymph. As oxygen PP in the hemolymph is always greater than glucose concentration(1), your limiting rate (which is related to the power you can get from the device) is that of glucose intake at the fuel cell. Therefore, the more you oxidize glucose per unit time, the greater intake you need to keep the output from dropping.
The glucose intake at the fuel cell is a function of biological parameters such as quantity eaten, metabolic efficiency, metabolic speed, blood flow, but also diffusion. The kinetics of glucose intake at the fuel cell are such that you can't ask for too much power for too long.
I suggest you read the article to get a more detailed answer. Nature news is good, but there's nothing like reading the real paper.
1 http://pubs.acs.org/doi/full/10.1021/ja211714w

Would this application in humans require that a patient eats more and "breathes more" than average?

From the cellular standview, each glucose and O2 molecule that you substract to the cell for use in a second futile cycle, should be replaced. However, I doubt that the amount of glucose/O2 required per hour will be so important to require additional food intake.
By the way, each cell in the body normally generates electricity from glucose and O2: just think at the electron transport chain during the mitochondrial cellular respiration.


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Are CN3, CN7, CN9 and CN10 the only Parasympathetic Cranial Nerves?
It has been my thought for a long time that this is the case, but I am unsure currently, since the parasympathetic tract of colon sigmoideum does not seem to have connection with CN 10. It connects with pelvic splanchnic nerves.
Discussion about it here.
If there is no connection from pelvic splanchnic nerves to CN 10, like CN 10 running within the nerves, then my though must be wrong.
Are CN3, CN7, CN9 and CN10 the only Parasympathetic Cranial Nerves?

Yes, only III, VII, IX, and X are cranial nerves that carry parasympathetic autonomic neurons. The key phrase is "cranial." Pelvic splanchnic nerves also carry parasympathetics, but they arise from the pelvis, not the brain.

Thank you! I was confused by the definition of the word itself "cranial". Parasympathetic Cranial Nerve only means parasympathetic neurons that arise from the brain. So the elements of brainstem like the lower parts of Medulla Oblongata still belongs to the brain.


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Why do people dying of immune deficiency diseases appear sick?
Please forgive the obviously silly appearance of this question, and/or of the tenor which may come across as flippant or dismissive of real world suffering. My intention is none of the above.
As a layperson, I have always understood that the expression of our various colds/flus etc, while frequently mis-understood as being caused by the virus, are actually just manifestations of our own immunity fighting same.  In other words, all the snot, and fever and inflammation are not caused *by the virus, they are a reaction *to the virus, as we fight it off.
My question then is why do people with AIDS (or similar immunity destroying affliction) appear sick?  If they have weak or non-existent immune systems, following the above logic, would one expect to see them passing away while looking entirely healthy?

Let me see if I understand you correctly. You are asking why people suffering from AIDS show symptoms of being sick, when the body doesn't formulate any response to the virus?

@Gabriel Fair, yes, that's my question.  What brings on the "sick", given that what we experience as illness (the simptoms) is entirely the effect of our auto-immune response, and not the virus' effects, themselves.

This is arguing semantics. Viruses cause flu symptoms. That they cause them indirectly by way of several body reactions, some of them from the immune system, is just a way of viewing this. All actions and reactions in our body are mediated in some way or other. This doesn’t make them less real or causal.

@Kondrad, I beg to differ. If a person gets shot, it is not semantical to investigate what actually killed them. "The bullet" is a useless answer, though clearly semantically correct; Did they bleed to death? Did some specific organ get destroyed? etc. It is *more useful to say that a person died of blood loss, following a bullet wound. So, similarly, to say "the virus is causing the sickness" is meaningless. The virus is provoking a reaction, but the mucous is being created by the immune response. My question is what symptoms do patients exhibit who have no immune response.

Many of the symptoms of disease are indeed related to inflammation, but inflammation depends heavily (though not solely) on the innate immune response.  Patients with AIDS and some of the other immunodeficiencies lose their adaptive immune response, not their innate response.  Therefore they are capable of mounting an inflammatory response that is not effective in clearing pathogens (because it doesn't have help from the adaptive immune system) but can still cause symptoms.
More importantly, many symptoms of disease are not caused by the inflammatory response, but are related to organ and tissue damage caused by the infection.  A patient with pneumonia may have a reduced inflammatory response but will still have difficulty breathing and signs of reduced oxygen supply simply because the lung tissue has been damaged by the pathogen.

that's a much better answer than the one that had originally been given the green check mark... I'm switching to yours.

@iayork good answer. But i think a citation  or two would be appropriate and appreciated.

They appear sick because they are sick, but with other, opportunistic infections. The "immune deficiency" part of AIDS means that the immune system is not functioning normally and, thus, is unable to protect them. Typical illnesses that are more found more frequently in AIDS patients are pneumocystis pneumonia and Kaposi's sarcoma.

I'm sorry, but that's not really an answer. You don't appear sick because you are sick, you appear sick because as a response to the presence of a virus, the body starts to do all sorts of things which manifest themselves as symptoms. You develop a fever, you produce mucous, you cough, etc.  But people afflicted with immune deficiency wouldn't have such a response, right? That's the nature of their illness. So, what symptoms do patients suffering from such illness exhibit? And why?

@Dr.Dredel: Kaposi's Sarcoma gives cutaneous lesions, Pneumocystis Pneumonia gives fever, tachypnea, and respiratory distress in immunodeficient people.

@nico, So, are you saying that these illnesses have their own (non immune related) symptoms that the patient experiences, and that all the while they are *not coughing and sneezing and all the other stuff we get when we are fighting off a cold?

@Dr.Dredel: Kaposi's sarcoma is a type of cancer, one can get it even without having an HIV infection. What you may be missing is that AIDS patients have a compromised immune system, but they still have an immune system.


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Why do some fruits have a much wider range of acceptable sizes than others?
Some fruits such as pumpkins can grow to be 100 lbs. Under different conditions, the same variety of pumpkin can produce a 15 lb. fruit. Both plants are healthy, and look the same except for their size difference. If I took two red apple trees and planted them in extreme opposite conditions, the fruit size would be nearly the same. The fruit quantity would be lowered in the tree grown under poor conditions. Why do fruits have such a variable range of acceptable sizes?

Very interesting question, but this can be likened to asking "why are there more than one different animal species?". I hope someone can come up with a nice and specific answer, other than "evolution".

@chm maybe a good answer could address "R vs K selected species"

Some kinds of apples also have wide range of fruit size. The tree in my grandparents garden have fruits varying from 3 to 12 cm in diameter (when they are ripe).

This is also essentially two questions in one. We could be asking "What can explain the size difference in pumpkins", and "Why are all apples of similar size".

It's fine as one question. Each aspect of jmusser poses here informs the other. It's all related.

Pumpkins, squashes in general, grow on vines, while apples grow on trees. Vines are fast growing and trees are not. Zucchini can be quite large; cucumbers, too. Pears, plums, peaches and other tree fruits do have a reduced variation in fruit size. While I do not know the answer to your question, my background in plant biology tells me that this is an important part of the reason. For example, a watermelon or pumpkin rests on the earth, but a tree fruit hangs. If that fruit is too heavy it falls from the ground before it is ripe - before the seeds are fully differentiated that is. So, while "evolution" might be an answer, it is important to discuss what aspects are at play.
I think it has to do with vine vs tree, and how the fruit is attached and hangs/lays.

If you grow a melon on a trellis, it will grow and fall off under its own weight.

grapes grow on vines, but they are closer to apples in acceptable fruit sizes.

but grape bunches come in a wide variety of sizes.

Does that mean if some external support is provided to say an apple, will it grow to a bigger size? Has there any such experiment done?

Bigger pumpkins have more seeds than smaller pumpkins. When they get ideal nutrition the plant tries to make as many seeds as it can to take advantage of the windfall. Many of these vines with big fruit potential grow in compost and rotting material. So they are more opportunistic a pumpkin seed "in the wild" could land in a barren area or in a heap of rotting material-- if it hits the jackpot it meeds to quickly use those nutrients to make more seeds.
PLants with more consistent fruit sizes don't respond as well to "jack pot" levels of rotting material-- they like more consistent nourishment. I think this is another difference.
Also one large pumpkin is a more efficient way to enclose seeds than lots of little pumpkins.

I suspect the answer to this, is that in looking at agricultural fruits you are looking at plants that have been the subject of artificial selection, and the tree vs vine thing is a practical limit, but not the driving factor... for instance a jack fruit grows on tree and is watermelon sized...
I think if you look at something like a pumpkin, you will likely see that pumpkins have 3 traits:

Indeterminate growth ... they will produce as many fruit as the season will let them.
Individual fruit will try to complete growth and ripen before winter
Vines with fewer fruit can devote more resources per fruit, and therefor larger fruit.

Even in apples; if all of the blooms go to fruit the apples will be smaller (commercially apples are thinned to make market acceptable sized fruit): http://homeorchard.ucdavis.edu/8047.pdf
So I think the real issue is less tree vs vine, and more about growth patterns... it may be possible to have a watermelon sized apple, but the tree will have to be sturdy enough to support the fruit: so it isn't a non-issue, but support is a limiting factor.

Well... If I support an apple, it will still mature at the same size.

that is a non sequitur ... if an apple were to grow very much larger it would require more support.

Yes, but is that the only restriction on size variability within a species?

No it is only a limiting factor... apples are highly variable, there is a good segment on them on "The Botany of Desire" (TV show, probably book)... I think you can sort of generalize it as a distance = Rate * Time problem (it really isn't linear, I assume)... Rate is made up of how the plant responds to the level of growth hormones that it produces with the amount of nutrients it can provide, and the time is the time that it is in the part of the growth cycle that it is actually growing.


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Does GFAJ-1 use Adenosine triarsenate as its energy currency?
Regarding the bacteria found in Mono Lake, CA that scientists believe uses or can use arsenic in its DNA backbone where life as we know it uses phosphorus (according to their experiments depriving the microbes of phosphorus and providing much arsenic), have researchers conjectured and tested whether the energy currency molecule used is also arsenic-based instead of ATP?

Those results have been heavily criticized (see also this related question of mine on Skeptics), the answer might be that those bacteria just don't incorporate arsenic into their DNA.

I'd have to agree that it's highly improbably that the GFAJ-1 strain used nucleoside triarsenates as an energy source. There are three main lines of evidence pointed out in the Science reviews that were published after the initial publication of the paper.

The incorporation of arsenate ions into NTAs is not a plug-and-play process, per se. Arsenate does not simply replace phosphate ions from molecules. In order for an NTA to form, it must arsenylate (like phosphorylate) a ribose molecule, then have the purine/pyrmidine ring form (and be attached to the ribose), and then two more arsenates have to be linked via ester bond to the other first arsenate. Mind you, this all happens in water. Arsenate esters are notoriously unstable in water, so it's difficult to imagine an NTA forming stably.
The original team in Felisa Wolfe-Simon's lab didn't intentionally add phosphate ions to their growth media; instead, the approximate amount of phosphate impurity was measured and reported. The lab compared this level of phosphate with the minimal levels reported in E. coli from another paper and basically said, "There isn't enough phosphate in our growth media for our GFAJ-1 strain to grow solely on phosphorous." Well, that logic is a little non sequitur  because GFAJ-1 is a halomonad (they said so themselves) and there is literature pointing to a species within Halomonadaceae that can grow on phosphate levels lower than that of the impurities reported.
Although the Wolfe-Simon team added arsenate into their growth media, it's unlikely that any biologically-useful arsenic ended up in the cells at all. Under physiological electrochemical conditions, arsenate gets reduced to arsenite. Phosphate ions, on the other hand, are stable at physiological potentials.

All in all, there's a reason why life chose phosphorous instead of arsenic. Although both elements have ions with a propensity to make ester bonds, maybe arsenic just doesn't fit into our anthropocentric view of what life is.

Welcome to Biology.SE! Thanks for the excellent answer!

This is a cool topic/question.
To answer your question.  The hypothesis was based on the conjecture that there was so little phosphorus in the culture medium that phosphorous would have been replaced by arsenic in all its roles in the cell.  IF they had found arsenate DNA, it would have been derived from NTAs (nucleotide tri-arsenates) or a hybrid Phosphorous/Arsenic analog of the compound as DNA polymerase consumes NTPs to create DNA.  If there were only NTAs to drive DNA biosynthesis, then the cell's energy cycle would also have had to use ATA.
BUT
The primary evidence was that the mono lake strain grew in a fermentor (culture) with lots of arsenic (which is impressive) and very little phosphorous. how little? 3 micromolar. The investigators say that they did add a little phosphorus (3-5 micromolar), which, after some more careful accounting, appears to be enough to keep the bacteria growing at the observed rate without using arsenate nucleotides (submitted to Science).
This is not completely surprising as the original publication in 2010 of a preliminary finding in Science Express which only had x-ray abosorbtion fine edge spectroscopy work consistant with an arsenate like that found in a phosphorus backbone.  Given that they did not produce a more direct reading of the compounds such as mass spec or an NMR experiment, this looked pretty iffy in the first place.
You an see why arsenic life was so improbable - a dozen (or more) vital pathways in the cell would have to adapt to use NTAs - pretty much all at once.  If they had I suspect Mono lake would be full of those suckers.
Its sort of a bummer, for those of us who want to discover new forms of life, but you can't find what isn't there.

In my mind, this is definitively debunked in episode 32 of This Week in Microbiology. In short, no, GFAJ-1 does not use adenosine triarsenate as an energy currency, nor does not seem to incorporate any arsenic in its genetic material at all. One of the two well written answers above deserves the accepted status, but I thought I'd draw your attention to a scientific discussion behind this work.


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Is there a biophysical causation from local field potential (LFP) to spikes?
Many experiments showed that neurons tend to fire at some phase (usually trough) of local field potential (LFP) oscillations, such as theta or gamma rhythm. LFP is supposedly generated by a population of neurons with coherent currents induced by spikes. So there is a causal link from spiking activity to LFPs. Is there also a significant influence on the spikes directly from LFP (not via the hidden spikes that generated the LFP)?
Is it just an epiphenomenon, and or is there a possibility that it is partly a serious mechanism for neural computation?

I am not sure that kind of action would be a "significant influence", but the general understanding is that LFP and spike frequency are inter-correlated (1, 2). An interesting recent publication on the topic (3), however, doubts this correlation as the nature of LFP recording and signal processing might introduce some artifacts to the recordings.
It would be interesting to see a correlation between the spike shapes and LFP, but I failed to find a relevant paper here.
References:

 Belitski A, Gretton A, Magri C, Murayama Y, Montemurro MA, Logothetis NK, Panzeri S. 2008. Low-frequency local field potentials and spikes in primary visual cortex convey independent visual information. The Journal of neuroscience : the official journal of the Society for Neuroscience 28: 5696–709.
 Rasch MJ, Gretton A, Murayama Y, Maass W, Logothetis NK. 2008. Inferring spike trains from local field potentials. Journal of neurophysiology 99: 1461–76.
 Zanos TP, Mineault PJ, Pack CC. 2011. Removal of spurious correlations between spikes and local field potentials. Journal of neurophysiology 105: 474–86.

Some evidence from external field modulations:

F. Fröhlich and D. A. McCormick, “Endogenous Electric Fields May Guide Neocortical Network Activity,” Neuron, vol. 67, no. 1, pp. 129–143, Jul. 2010.
S. Ozen et al., “Transcranial Electric Stimulation Entrains Cortical Neuronal Populations in Rats,” J. Neurosci., vol. 30, no. 34, pp. 11476–11485, Aug. 2010.


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Are there differences in DNA between humans of today and humans from 2000 years ago?
Are there any significant differences in our genome compared to the genes of our ancestors from 1000-2000 years ago?
And if there are significant differences, do they result in significant differences in phenotypic traits?

It's a huge leap from "differences in DNA" to "differences in traits."

I don't understand the negative votes: there is some confusion in the DNA vs trait, but the question is still interesting

Exactly, I wouldn't understand down votes either. "[D]ifferences in the genome" is a legitimate question. While one may at first think of sequence changes, and some mitochondrial and Y-chromosome haplogroups may have arisen within about 2000 yrs ago, changes at the level of methylation, acetylation and other levels fits the question.

The larger differences are most likely in epigenetic marks on the DNA. The environment is a lot different today than it was 2000 years ago and those differences are stronger determinants of epigenetic change than sequence change.
2000 years is only about 40 generations and that is not very much to see great differences in DNA sequence or allele frequencies - once founder populations are removed from the analysis.
Height is highly influenced by genetics, but can be masked by environment - notably diet. Diets higher in protein content are more likely to elicit the expression of the "height alleles" but only to a point as too much protein is also unhealthy.
Added in Edit 4 Apr 2012: I should add that my response is written from the perspective of frequency of alleles or epigenetic marks across a population.

Not all enviromental influences are inheritable through epigenetic marks. Have you any evidence of epigenetic changes in human population?

I did not imply that the epigenetic changes are heritable. The environment changed over the last 2000 yrs and some of those changes are constantly acting upon the genomes of successive generations. The question asked about a comparison of a current human genome with one from 2000 yrs ago. Because the environment is different, I expect that population-wide we would see differences in epigenetic marks.

In the literature, there are examples of DNA analysis from very old specimen. For instance, look at the analysis of both nuclear and mitochondrial DNA from 62 buried humans exhumed from a Mongolian cemetery dating from 2,000 years ago, as described by Keyser-Traqui et al. 2003, Am J Hum Genet 73(2): 247–260. Despite, the publication is open-access, the DNA sequences are not available, and no comparison with current mongolian DNA has been described in the study, but for sure your question should be answerable.

It depends on what you define as significant.
The mutation rate in human that I manage to find is given as about 140bp per genome per generation
http://sandwalk.blogspot.com/2015/04/human-mutation-rates-whats-right-number.html
2000 year ago is 40 generations. So that is about 5600 bp on average in a genome of 3200 million basepairs..... 0.000175% as calculate. Next to impossible to find.
Is that significant?
Functionally... most mutation that are inheritable though multiple generations are silent mutation.. which have neither negative or positive effects. (Negative mutations are weeded out relatively fast).
So are all these mutation silent? No, some actually do things... and these are mutations are usually related to the immune system... better able to survive disease like measles, black plague, smallpox, etc.
So they these changes significant? Well.. yes... in that if you don't have those DNA changes you would likely die. Yet those changes are minor structural changes to the proteins receptors that those pathogens use to get into a cell. So extremely minor. THe proteins are still able to do their natural function but are just different enough that pathogens do not have a free pass like smallpox had with the native americans.


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Why is coffee a laxative?
How does caffeine (or any additional agents) act as a laxative when ingested? I'm interested in the metabolic/signaling pathway.

As someone who has serious digestive issues,I can testify that coffee has far more strong of an effect on motility than water does. In fact, I have found that coffee works better than otc laxatives too,at least in my case, and much faster. I imagine there are a lot of ibs sufferers out there who don't realize this and wonder why they have such bad problems in the mornings

https://www.quora.com/What-happens-when-you-water-plants-with-coffee-or-tea

Coffee does have an effect on the peristaltic movement in the bowel.

Coffee increases rectosigmoid motor activity within 4 min after ingestion in some people. Its effects on the colon are found to be comparable to those of a 1000 kCal meal. Since coffee contains no calories, and its effects on the gastrointestinal tract cannot be ascribed to its volume load, acidity or osmolality, it must have pharmacological effects. Caffeine cannot solely account for these gastrointestinal effects.

Effectively, decaf and regular coffee stimulate peristaltic movement in the colon as effectively as a meal does. Caffeine is not the active agent then, but some other compound in coffee.
Source: Boekema PJ, Samsom M, et al. Coffee and gastrointestinal function: facts and fiction. A review. Scand J Gastroenterol Suppl. 1999;230:35-9. PMID 10499460.

Thanks, I'll check the paper. Does it mention the candidate substances causing the effect instead of caffeine?

I don't know because I can't access the article myself. Work done at the same time, by another group found that caffeinated coffee was 23% stronger than decaf, implying that most of the effect is not derived from caffeine. The source (PMID: 9581985; Rao, Welcher, et al. Eur J Gastroenterol Hepatol. 1998 Feb;10(2):113-8.).

It is accepted that unless 500 mg of caffeine is consumed at once, it is equivalent to drinking water for hydration purposes. From this and the results of these two papers, I speculate that water accounts for ~40% of the effect, caffeine for a further ~20%, and the remaining ~40% is an unaccounted coffee effect.

@leonardo: the effect of water would very much depend on the coffee. A cup of Italian coffee and a cup of American coffee have extremely different volumes.

Yes, this is true. For hydration purposes, coffee is as effective as tap water. The effect on gut motility is strongest with caffeinated coffee, then decaf, then water, with both coffee types equal to a 1000 kcal meal. I've  speculated how much of the effect they are able to  attribute to the individual components (caffeine, coffee, water) based on their experimental results. What you suggest nico is a comparison now of two kinds of coffee, of which they would expect the differences seen from an espresso vs cup of coffee.

To address your American coffee vs espresso comparison, based on these results the greatest variation would be a result of the water volumes and the other extracts from coffee (since caffeine content of 1 oz espresso is about equal to one 8-oz cup of coffee).

This is all voodoo. It's simply the volume of whatever you drink, the more the stronger effect. Try it yourself, it's my experience anyway. Reason: the internal pressure is increased by anything you eat or drink. Therefore, the same urge after eating.

@rwst I'm sorry but you are incorrect. That source directly concludes that coffee's effect "[...] cannot be ascribed to its volume load, acidity or osmolality, it must have pharmacological effects." While also finding that these effects are not solely the effect of caffeine.

Caffeine alone certainly does have increased motility effects, speaking personally as someone who has gut issues (Crohn's and irritable bowel) and has experimented on the effects of drinking coffee/espresso vs. various doses of OTC caffeine pills (NoDoz, for those in the US). Just drinking water alone does not affect my motility, while caffeine alone or drinks containing it do.

I have noticed that other stimulants (Ritalin, Adderal) also have laxative effects which supports the pharmacological explanation. I've long assumed that similar mechanisms cause motor tremors and increased peristalsis.

It's not valid to compare anecdotal (or real, for that matter) effects of those drugs you mention to a specific effect of caffeine just because they are broadly classed as stimulant drugs. Those two drugs all have distinct mechanisms of action to how they work. However, if they increase gut motility (e.g., peristalsis) then it may coincidentally also increase defecation.


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Why is maintaining a circadian rhythm important?
What are the real consequences of never maintaining a circadian rhythm?
How is circadian rhythm important for health and function? Where did it arise in evolution?

A similar question http://biology.stackexchange.com/q/1113/238

Note that your body maintains a circadian rhythm whether you want it or not! You may perturb it (e.g. by not sleeping or flying in another time zone etc.), but the molecular basis of circadian rhythm is always there (although animal models where is not there anymore do exist).

In theory, having a circadian rhythm should help anticipating daily environmental changes (light, temperature etc.) so that the metabolic performance is maximized.
In practice, mice chronically exposed to environmental light-dark cycles with a period length dramatically shorter or longer than that of their circadian clock are prone to become obese. Moreover, animals kept under short cycles die earlier than mice kept under normal or extended cycles. So, chronic circadian disturbance by a shortened light-dark cycle increases mortality (at least in mice). In humans, shift workers are likely the population that is more susceptible to circadian cycle derangements.
Ref: Park et al., Neurobiol Aging. 2011

Note that this is probably tied to the fact that most, if not all, of the hormonal system in our body work in a pulsatile way, which is controlled by the circadian clock.


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Will the "frog in boiling water not jumping out" work on warm blooded animals
There is the famous saying about a frog that is put in water that are slowly boiling will not jump out until it's too late. I realize it happens because of the frog's cold blood that adjusts to the temperature change until it's too late.
Will this work as well on an animal with warm blood, or will the animal jump out ones it gets hot, but not hot enough to cause permanent damage?
Edit due to comments:
Cold blooded animals, like the frog, can adjust easier to their surrounding when the surrounding changes temperature gradually as their body temperature adjusts with the surroundings. Will the same happen to a warm bodied creature, and will it find it easier to adjust to the surrounding if the change is gradual.
For example, I don't like saunas, when I get in them I have problem breathing and I can't stand the heat, which means that I can be in a sauna for a very short time until I have had enough and get out. Will putting me in a sauna at room temperature and then turning it on to gradually begin to heat until its destination temperature will allow me to fill more comfortable and stay longer inside once it's at the normal sauna temperature?

"There is the famous saying"... which holds the answer to your question! :)

The frog part is true. According to Wikipedia:"An 1872 experiment by Heinzmann demonstrated that a normal frog would not attempt to escape if the water was heated slowly enough" and later it states that if water are heated at a rate of 1.1 C degrees per minute or faster frogs will jump out, which infers that if heated slower they will not jump. references are given in the Wikipedia article (http://en.wikipedia.org/wiki/Boiling_frog)

You should also read Poincaré's La Science et l'Hypothèse. If I remember correctly, he does mention such an experiment when discussing the fact that sensible perception is not continuous, but discrete: I can't make a difference between a 1kg and 1.1kg weight, but I sure can tell between a 1kg and a 2kg weight.

Concerning that wikipedia article, it seems to me you're cherry-picking your "evidence". I could post an answer copy-pasting parts of that article, but that'd be too easy.

My question regards the affect of gradual temperature change on warm blooded animals. The frog adjusts fairly easily (at start) to the temperature change fairly easy and can adjust its body temperature to that of the water so that it'll fill comfortable.
Warm blooded animals can't change the temperature of their body, but have other mechanisms of coping with temperature difference. So will a worm bodied animal will sit in the water and adjust it self with the gradual change, or will it just say at one point or will it get more and more uncomfortable until it'll get out?

One could make a joke about us not noticing global warming

This answer belongs on Skeptics. Sorry to disappoint, but the "boiled frog" phenomenon is an "old folk warning". This essentially negates your original question altogether. Neither a cold-blooded animal (such as a frog) or warm-blooded animal will boil to death under the conditions implied by the warning (i.e. escape is permitted and water is heated very gradually).
1897 research by German scientist E. W. Scripture, upon which the fable may have first been based, has been deemed flawed by scientists:

From Scripture's research: “. . . a live frog can actually be boiled without a
  movement if the water is heated slowly enough; in one experiment, the
  temperature was raised at the rate of 0.002 degrees Celsius per
  second, and the frog was found dead at the end of 2.5 hours without
  having moved."
According to Dr. Karl S. Kruszelnicki (Australian scientist): "[T]he numbers just don’t seem right. If the water comes to a boil,
  that means a final temperature of 100 degrees Celsius. In that case,
  the frog would have to have been put into the water at 82 degrees
  Celsius. Surely, the frog would have died immediately."
According to Dr. Victor H. Hutchinson (Herpetologist and Zoology Professor at University of Oklahoma):
  "The legend is entirely incorrect! The 'critical thermal maxima' of many species of frogs have been
  determined by several investigators. In this procedure, the water in
  which a frog is submerged is heated gradually at about 2 degrees
  Fahrenheit per minute.  As the temperature of the water is gradually
  increased, the frog will eventually become more and more active in
  attempts to escape the heated water.  If the container size and
  opening allow the frog to jump out, it will do so."

Whit Gibbons (University of Georgia) says that there is an important message behind the false legend:

So where does that leave us with the boiling frog as a metaphor for
  the human response to economic change or environmental degradation?
  Well, it's not true that you can induce a frog to willingly remain in
  boiling water by starting it off in cold water. But that does not
  diminish the truth of the message that the accumulation of
  imperceptible changes can have a significant effect on the economy and
  the environment. We need to be aware of what changes are occurring and
  to respond to them in a timely fashion. The metaphor lies in the
  frog's ability to escape from the container: if there's no way out,
  then the frog's fate is a foregone conclusion.

Actually, it is already on Skeptics: http://skeptics.stackexchange.com/questions/5402/can-a-frog-be-slowly-boiled-alive-without-it-noticing


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Fish "coming back to life" after being frozen
I've encountered a clip on Youtube showing a goldfish thrown in liquid nitrogen and immediately after to normal water and swimming normally. In the explanation to the clip it says:

For everyone that is worried about the goldfish, it survived and was perfectly fine until we fed him and a few of his friends to our turtles. (Which is what they were bought for in the first place!)

I am wondering now as to several issues.
If the goldfish wasn't fed to the turtles and was allowed to live out its life, would it suffer any long term damages from the act?
Is time an issue here, if the fish was kept frozen for a longer time, would it suffer more damage and would it be able to be revived?
Is the size and nature of the fish's body a factor? Would a larger animal or an animal with better resistance to frost that would take more time to completely freeze have damage due to gradual freezing of body and systems?
Does the fact that fish have cold blood affect the result of the experiment?

As a kid ice fishing in Michigan, I would catch yellow perch and throw them on the ice. They would flop a few times and freeze solid. Temp. was around zero. Some time later, 1/2 to 1 hour I carried them home in my pockets and put them in tap water so they could be scaled. Much too my surprise after about 1/2-3/4 hr. they started thawing out and started swimming around, some advanced stages of others. True Story many years ago. I have no knowledge if they had Drain Bamage as I eventually ate them. True story many years ago!!! Walter Sharp

Well, as and you can see the fish just "froze" for max 2 seconds. It is normal to live because it didnt die from cold.

I have no idea what's the real reason for the survival of the poor fish, but I would guess this is all in the timing. I know for certain ;-) that one can submerge a hand in liquid nitrogen for a short time or in general one can pour liquid nitrogen on the skin with no harm done whatsoever.
The reason is that the difference in temperature that interface (-180 deg C or so for liquid nitrogen and 20-30 for the skin surface) is so large that nitrogen vaporizes instantly and does not penetrate/affect the tissue. The demonstrator could have pulled the fish with bare hands.
I think that for the goldfish the time was too short and while it was cooled/shocked a bit, it might have been too short to do any serious damage. But -
As a scientist, I can't help but notice that we don't really know the condition of the fish before or after the liquid nitrogen 'treatment'. We only see it flapping for a few seconds when back in water. I wonder what happened to the eyes and the mouth, both quite sensitive tissues for such a shock. Also, the water the fish was in was a factor probably, providing additional buffer between the fish and the liquid nitrogen.
Last but not least, the ethical committee quite certainly did not approve that demonstration.

Of course we do not really know whether liquid nitrogen was really in the other pot... we just see smoke


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Why do the sick and unhealthy trees leaf out first in spring?
It's spring. The time of year that trees start to leaf out. I have been watching them, and noticed an interesting pattern. The unhealthy trees of a species leafs out first. I've noticed this especially with the wild black cherries. The hollow and damaged trees and the ones in poor conditions leaf out a week ahead of the good ones. The last ones to leaf out are the strongest in the area. This is not just a casual observation, and I have kept careful track of it. What causes this?

-1 for use of the ambiguous (and unscientific) term "trashy trees"

The question is not clear. How a species of tree would be better than another? Why would a willow be worst than a oak or a black walnut? I think you're mixing two things: sick vs non-sick trees and trees of different species with different leafing times.

Be cautious about drawing conclusions from casual observation. There may be within-species variability in the timing of leaf-out. It is possible that trees that leaf out first are more likely to be infected (or to have been infected in previous years).

@nico No. My question is Why the softer and lower quality trees, especially of the same species, Leaf out before the healthier trees. I am not asking why they are different. I think many people will agree that an old oak tree is of higher quality than a willow scrub.

I clarified my question for you who didn't get the meaning the first time.

@jmusser: the market value of the wood of a tree has nothing to do with its leafing time. A 1 year old willow may be as good to its environment as a 300 years old oak tree: we may find it more valuable, but that is economy, not biology. I suspect that the pattern you are seeing there has to do with age rather than "wood quality".

How about the same species? Why do the unhealthy or rotted ones leaf out first?

Can you be more specific than "I have kept careful track of it"? Have you kept records? How do you quantify tree health? How many trees? Are they all approximately the same size? Do they grow in similar soil and light environments?

Trees that have been dormant over the winter exist on nutrients stored in their roots during fall. When a tree has been damaged or diseased, it may not have been able to store enough nutrients before winter, or may not have enough stored to heal the damage/disease. If the damaged/diseased tree has depleted its winter root stores, it must leaf out (earlier than others of its species) and resume photosynthesis in order to have enough energy to attempt healing itself.

This seems reasonable - do you have any references to support your answer?

Agree with @RoryM, it seems a reasonable theory, but I am not at all sure that this is true. It could be just as much about rising sap in the spring, carrying resources, reaching the terminal buds quicker, as there is less distance to travel, and so initiating bud burst earlier.  Also trees can't 'heal' themselves, as they grow they may occlude wounds and cavities, and compartmentalise decay to stop it spreading.


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Are cells really the basic unit of all life?
Please see comments as to the appropriateness of this question on biology SE.
All known life on Earth is made up of cells. It is thus safe to say that all known life is characterized by the presence of cells. But is having cells as a basic unit a requirement for life?
I'm thus asking if life is currently existent and/or possible without biomembranes, and to what degree cells actually matter in our present understanding of life.
An all-encompassing, comprehensive and cited answer would be very much appreciated.

You're basically asking for the definition of "life".

I'm asking whether or not cells are part of the definition of life as we know it, or all potential life. Is that a bad thing? Clearly related to biology.

And in some respects, the question is similar to this one:http://biology.stackexchange.com/questions/90/life-without-dna

I think it's a fair question - perhaps very closely related to "life without membranes".

Well at the moment, there isn't a question related to what is the definition of life. Meanwhile, I think that most evolution of life specialist will say that no, cells are not the basic unit.

Maybe I should ask another question about the definition of life ahah! Although I feel that it'd be more of a debate than anything...

@bobthejoe: and what they would say it is then?

The impression I get is that the inquirer hasn't put much thought into his question. If you were a kid, I wouldn't mind of such a question, but you're not. It's exactly because there's no clear cut definition of life that your question is in fact not a question.

@CHM, just because a question does not have a clear-cut answer, it doesn't mean it isn't a valid question. Exploring such questions and explaining why or how is what scientific thinking is about.

I've flagged this as off-topic. I could go on and explain the reasons, but I think it should be pretty clear.

@LanceLafontaine: I do not think lack of a clear-cut answer is a problem per se. The impossibility of giving a proper scientific answer is, though (for questions on this website, that is). Calling on the possibility of undiscovered extraterrestrial life which is not cell based is like claiming you have an invisible, incorporeal, floating dragon who spits heatless fire in your garage...

@nico and CHM, I can see your points. I'll go ahead and edit the question for it to read something less fantasy/science-fiction based ahah.

Lance, I don't think you're getting the point of my objections. This is not about you or your question: its about maintaining this stack's purpose and quality. You will not get an "all encompassing, comprehensive" answer from anyone - discussion is all that can be done about it. Before even drafting an answer, you'd have to define life. I suggest to close this question and move discussion to the chatroom. I also suggest you go talk with your professors, I'm sure they'll have things to say. Again, don't think this is not interesting, it's just inconsistent with this site's purpose.

As a point of community management and education: This question is not appropriate for THIS type of Q&A. It may be an interesting discussion and even educational, but we forgo these types of question to preserve the purpose of building a canonical knowledge base. Questions should be specific problems you might encounter in your day to day work. But the question above is really a "discussion starter" likely to solicit extended discussions, opinions, and debates. That type of activity is better left to the chat rooms and discussion forums, and not really what we do here.

According to Gerry Joyce: "Life is a self-sustained chemical system capable of undergoing Darwinian evolution."
From a meta-analysis of 123 definitions of life: "Life is metabolizing material informational system with ability of self-reproduction with changes (evolution), which requires energy and suitable environment."
According to Alexander Oparin: “Any system capable of replication and mutation is alive”.
At hand are some key elements in order to match these criteria. Maintaining a Darwinian cycle requires replication, mutation, and selection. Thus, we can break down the above into 5 criteria (personal communication with Gerry Joyce).

Life stores information
Life reproduces its information
Life alters that information
Life does something with that information (uses energy)
Life does all of this in a self-sustained manner

I would point out that the above criteria is quite different from what is currently on wikipedia described by metabolism and homeostasis. There are certainly additional criteria that certainly raise the threshold for what may be considered life. The common discussion revolves around viruses which do many of these things but not in a self-sustained way.
The question at hand then asks if cells are the minimum unit of life? What makes a cell a cell is that there is compartmentalization. The underlying reason behind this compartment is due to the necessity of tying the phenotype to the genotype. Paraphrasing using our definition of life, it links the information with the function that the information carries out. In the modern biological scheme, it keeps the proteins (phenotype) with the DNA (genotype).
The necessity of compartmentalization is negated when the phenotype is already linked with the genotype. The most frequent example is RNA where the material that carries the information is also the material that carries out its function. It tend, is reasonable to hypothesize that life can be made entirely with RNA without the need for compartmentalization (although compartmentalization certainly helps see Paegal and Joyce and Chen and Szostak).
Recent experiments by Gerry Joyce and others have been able to satisfy several of the requirements of life. The have self-replicating RNAs, that store information, that reproduce their information, that introduce alterations to their information, and do it in a self-sustained manner. What Gerry and his colleagues agree on is that their current self-replication Ribozyme system doesn't do anything particularly novel. However, by introducing a larger variety of functional elements to their ribozymes perhaps they will.

I disagree with your conclusions. Otherwise should we say that a virus or a prion is alive?

Also, please link to the sources of the papers that you mention and give relevant extracts of the authors conclusions about ribozymes being a life form (or otherwise clearly state that that is your personal interpretation of their results, which is absolutely fine, of course).

@nico, I think I have pointed out that viruses do not qualify under the above definition. Likewise as mentioned in http://biology.stackexchange.com/a/96/389, prions are dependent on host factors. Citations will come after I finish my experiments.

sorry I had missed the sentence about viruses

What about self-replicating computer software?

@CHM intriguing. I guess we have to start considering the battle against entropy.

Where are you getting those criteria from?

@Preece Gerry Joyce.

@bobthejoe His website is disappointing :(

@nico, CHM, Preece. You guys better be satisfied.

OK, I am not sure I necessarily agree with their views but your answer now deserves a +1.

@nico: As someone who studies mathematical modeling of ecology and evolution, I see no reason not to consider viruses to be alive. They pass the duck test for it: they replicate like life, they consume resources like life, they evolve like life. True, they depend on a host to do so, but so do all parasites. For that matter, all heterotrophs, including us humans, are just as dependent on other life forms — none of us can live on just water, air and sunlight.

@Ilmari Karonen: there is a subtle difference between a parasite and an obligate parasite

This discussion thread is begging to be closed. The chatroom isn't used, people. Why not move there and have a very interesting talk about this subject, where it belongs?

Life is a physical entity that creates copies of itself,sometimes in a slightly changed form.
That's it.
A cell is not the basic unit of a life but a large number of molecules that have bonded together to reap the benefits of specialization.
Like what is happening today, humans coming together to form a society which collectively starts to function like a single living organism again.
So no, a cell is a far cry from being the basic unit of life, it is a very advanced form of life.
All it takes for life to start is for a single self replicating molecule to form, that's it.
Evolution takes over from there.

Molecules aren't "alive". An intricate synergy of a mind-blowing quantity and variety of molecules can be. Would you consider H2O a self-replicating molecule, since it spontaneously undergoes dissociation to form H+ and OH-, at equilibrium?

Not all molecules are alive, but molecules that produce copies of themselves are. H2O is not alive,when it undergoes dissociation there are no extra copies of it being created.

Agree. This is extremely interesting, but I just feel like it belongs in a forum, not a Q&A, since there's no answer to be had, only discussion. Mind giving some sources where I can read more on self-replicating molecules?

"The Selfish Gene" and "The extended Phenotype" by Richard Dawkins.

Now that I've actually sat down and thought about it, this definition does fit; +1. H2O can't be life since it doesn't add any variation to itself.

Well, that's only partially true - while H2O does not create extra copies of itself after dissociation, there can be a difference in its quantum state before and after the dissociation, which constitutes a variation.


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Why are some bodily fluids more of an infection risk than others?
Whilst on a recent refresher course it was highlighted that when considering risk of exposure to infection from bodily fluids we should be aware of two distinct risk levels:
High Risk:

Blood
Semen
Vaginal Secretions
Diarrhea

Low Risk:

Saliva
Vomit
Urine
CSF (Cerebrospinal fluid)

Why is it that some bodily fluids are a greater infection risk than others?  Is it related to the fluids themselves or the species of pathogen that are located within them?

I feel like sputum / mucus should be on that list.  It's the primary bodily fluid that influenza and other respiratory tract infections are spread with.

Likely because the fluids on the high risk list are commonly exploited routes of viral shedding, bacterial transit, and also the likeliest to pick up other microbes on their exit from the body. Saliva is not sterile, but arguably more so than the others; vomit is highly acidic therefore inhibits microbe presence; urine can be higher risk depending on STD or UTI status; CSF is low risk probably because of the rarity of exposure.

@GWW Yeah it probably should - these were just mentioned specifically by the trainer :)

I would say that diarrhea is a medical condition, not a bodily fluid. I would use the term feces instead (OK, fluid does not apply to that either, maybe "bodily secretion" would be better?)

@nico agree with that comment too, as above I was just mentally copying and pasting from the powerpoint.  I suppose it brings about a sub question as to whether more solidified faeces is a lesser infection risk than diarrhoea?

@Rory M: good point, although I have to say I wouldn't like to be the one who tested that!!! :D

This is just about where the pathogens can be found that are dangerous to people.
Vomit is highly acidic and less accommodating to microbe growth. Similarly saliva has many immune components in it as well as digestive enzymes that keep most microorganisms down.
Urine and CSF are actually quite sterile as they come from environments that are highly filtered - the kidney is an osmotic processor that essentially is a molecular filter and does not allow cells to pass, the spine is highly insulated from the blood and other direct exposure to microorganisms.
Compare that with the 'dangerous' list and you have organs that are open to human pathogens.  Venerial disease like HPV is so common that what - about 1 in 5 people under a certain age carry it.  That is a pretty high expectation of a biohazard.  most infections and viruses are blood bourne - influenza, cold, as well as any bacterial infections.
Feces is always a dangerous thing to handle as the digestive tract is rich in nutrients and essentially directly open to external bacteria and fungi.  (and its not acidified like the stomach).  Also parasites like tape worms and other multicelled animals! yum!
Diarrhea is often caused by an infection of some sort, so its just more likely a hazard, but feces is always a place where you might find a pathogen.
This is not to say that the 'safe' list is totally safe.  Its just less likely to bear disease causing agents.

Largely unrelated question:  if roughly 1 in 5 have HPV or this venereal disease in question before a certain age, wouldn't they continue to do so after that age?  Or is the mortality so high as to bring down the fraction of the (living) population that has it?  Why am I not hearing about this as one would if, say, the plague were going around?


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What evolutionary mechanism caused felines to develop purring?
And why can some felines roar while others meow?

I guess the first question to ask is: "Why do cats purr?". If I remember correctly it is not really clear, so I doubt an evolutionary mechanism for it is known. As for the roaring I suspect that size matters.

Also, are you looking for an ecological answer (as in why cats perform the action of purring), or a physiological/anatomical answer (as in why a cat's purr sounds like it does)?

I just think there's no purpose to purring as far as I can tell. 'meow' seems like a more valid form of communication.

It makes sense that the ability to express your emotions improves the quality of the interaction you have with those around you. If a cat purrs those around it know it's feeling good, which can be useful information for future interaction.
I'm sure there have been cats who had a worse life because they didn't bond as well because they didn't purr, and consequently had a slightly lesser tendency to have their DNA end up in the next generation.
This argument goes for every ability to express emotions.

Indeed, so I suppose that cats use purring to communicate with one another?

I would think so yes.

http://en.wikipedia.org/wiki/Purr#Reasons lists several other possible reasons for purring. I'm not a big fan of antropomorphisation of animal habits, but I guess a clear response is still elusive in this case


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Organ cloning - possible to make a non-antigenic organ?
From a J. Neil Schulman article on Organ Cloning:

Cannibalizing organs from other people also entails the risk of
  rejection because of incompatibilities, not only for tissue-typing but
  also for gross anatomical mismatches. Cloning organs [...] has the
  potential of taking a human being's own genetic material and growing
  perfect replacement organs which are fully compatible with their
  genetic makeup.

The reason for using a person's own DNA, is obviously to avoid an allergic reaction to the antigen markers on a strange organ. But in the blood typing system, there exist types which don't have any trouble-making antigens (such as type O-negative, called a "Universal Donor").

Would it be possible to grow an analogous "universal" internal organ, which didn't have any antigens indicating it was a foreign body? (By editing a DNA sample to remove certain expressed proteins, then growing it into an organ.)

I realize this is technically a science-fiction question :) But - A: it may not be in the near future, and B: I can rephrase it to remove the SF component:
In the blood-typing system, the AB antigens don't appear necessary for proper functioning of red blood cells - are the antigens on a person's own cells, actually needed for any essential functions, or could they be removed, without affecting that person's health?

Would this perhaps satisfy your criteria? ~  Could bone marrow transplants be used to prevent tissue rejection of trans-species organs?

@Pelinore that's interesting, but still doing something differently. More like using drugs to reduce an immune-response. I was asking if the organs could be designed to not have an immune response. The linked method would be specific to one person, whereas no-response organs would be generic, and usable by anyone.

"I was asking if the organs could be designed to not have an immune response" Yup, while my one asks if the patient could be designed to not have an immune response :) I think mine might be easier to achieve (if it wasn't for those darn kids! ~ meaning ethics committees of course).

I'll contradict the answer posted here (ages ago) and say no, it isn't possible. Growing an organ wthout MHC proteins might be achievable, but it would be rejected for not having MHC1. NK cells instruct all cells without MHC1 to perform apoptosis. In this case, MHC1 antigens are required on cells for proper self-identification.
Keeping MHC1-less cells alive could be achieved by

equipping them with whatever is keeping erythrocytes and thrombocytes (also lacking MHC1) from being destroyed on sight. (A good idea, but see next paragraph)
disabling their apoptosis mechanism (Cells with disabled apoptosis mechanisms are commonly referred to as cancer, so we might want to not do this.)

MHC1 also has a function; it presents "peptide shreddings" from proteosomes to T cells; this way T cells can check if the cell contains internal foreign proteins (sign of a virus infection or cancerous transformation). Thus, removing MHC from the cells would make them very liable to become nearly unstoppable virus factories or tumor cells.
(On a side note, while everyone technically can receive 0 Rh negative blood, group-identical blood is used always, except in rare emergency cases. A and B antigens here, as far as I know, do not have function.)


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Soma-soma paired neurons
I'm reading this paper about how neurons can connect. Wikipedia says, typically neurons connect via axon (transmitter) and dendrites (receiver) but there are also special cases where dendrites connect with dendrites, axons with with another axon, neurons with no axon etc.
Now in the paper they refer to the soma-soma paired neurons and their strength of their cholinergic synapse.
Does that now mean that they neurons do directly interact via their soma? If so, how much different is that process to the generic axon->dendrite pathway?

Just for completeness: not all neurons connect to another neuron :)

Yep, the soma-soma synapse in that paper appears to be a chemical synapse between two cell bodies. There are no axons or dendrites in that preparation so the synapse must be between the somas. They are using two snail neurons that are far from each other (in different ganglia) in vivo, but which are known to synapse. This in vivo synapse is long-range and so must be mediated by an axon. In the dish, they can encourage the  synapse to form even without encouraging axons and dendrites to grow.
Note that this is an artificial in vitro preparation and they are, in some sense, forcing a synapse to occur in an unusual way in a cell culture dish. They do this because it makes it easy to study certain aspects of the signalling mechanisms for generating synapses. In your paper, they appear to be using it as an easy preparation for a proof of principle for the interface between a biological neuron and a non-biological semiconductor substrate.
The paper you cited references this paper that outlines the soma-soma preparation with a pretty picture to make things clear: http://www.jneurosci.org/content/19/21/9306

With 'preparation' you mean something like the 'setup'? So they prepare the cells in that manner?
Thanks for the answer, will read that paper! Cheers

Exactly right, they prepare (or setup) the cells in a particular way so that they can study them later. For instance, here they are removing the neurons from the snail and putting them together in a dish. Then they add a solution that encourages the synapse to form. As you might imagine, any given preparation will be good for investigating some things but bad for other things. A major part of experimental design in biology is choosing the right "preparation."


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Analysing the results of real-time PCR
I want to evaluate the level of gene expression by real-time PCR.  I have five controls that are "clinically" the same. I calculated the "fold change" of the target gene regarding each control.
What if the result of "fold change" for my target gene is different for each control? I mean it is up regulated according to three of them and down-regulated according to the rest two.
Is the intervention biased? Or should I consider the average?

I have no experience with RT-PCR in particular, but I'd say that the variations in your controls add to your error. And if they vary too much, you'll have a hard time to measure a significant difference in gene expression. The gene you selected might be influenced by a lot of other processes, leading to those variations.

Please provide more information: fold-change relative to what?
If you did what I think you did (single control gene that you calculated fold change to of your gene of interest) I'd say this is the wrong approach. What you need is a set of genes which have similar expression levels across all your samples (controls and cases) to be able to compare your gene of interest to some common baseline. Selection of such genes should be the first step in the project, and it might be a good idea to use one of the established approaches - I recommend Jo Vandensompele's GeNorm (link to the paper) method. It goes like this: from a panel of potential control genes you select two or three that are most stably expressed across your experimental conditions, and then use these two-three control genes along with your gene of interest in a qRT-PCR. You then normalize the signal from your gene to a mean of the control genes.
It has been repeatedly shown that using a single control gene, even a so-called 'housekeeping gene' is misleading, because those genes do change their expression levels in some conditions. Also, using several control genes protects you against potential problems due to unequal amplification efficiency in different samples/groups. However, if you have multiple gene of interest, they all must have comparable amplification efficiency.

You also probobably need to check if your samples haven't been contaminated with PCR reaction inhibitors, which is very common if you first extract your mRNA, digest remaining DNA and then run a PCR with a less then 10-fold dilution. You need at least a 200 times dilution to get rid of all the artifacts.
Once you've diluted your samples, place a repeats of successive dilutions of your target and baseline mRNA (200xdilution, 1000x dilution, 5000x dilution). Normally you will see a nice regular spacing between curves on your rtPCR plot. If you don't, something went wrong with the reaction.
More generally rtPCR is a pretty tricky experience, and if you want it to be 100% reliable, you've got a certain number of controls to perform. You can find a good and comprehensive guideline over here.


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How do SDS-PAGE gels differ in a Bis-Tris system vs. a Tris-Glycine system?
Protein migrate differently in Bis-Tris and Tris-Glycine gels. I was curious about the actual reasons why. Do certain gel systems result in a tighter resolution than others?

SDS PAGE system rely on the fact that protein is denatured and surrounded by the SDS negatively charged detergent micelle.  This eliminates most of the charge and idiosyncratic solubility differences from one protein to another and gives a reasonable separation based only on size of the protein which is related to the size of the SDS micelle around each molecule.
Bis-Tris and Tris-glycine buffers have quite different charge shielding characteristics.  Bis (also known as 2-[Bis(2-hydroxyethyl)amino]-2-(hydroxymethyl)-1,3-propanediol) has a tertiary amine with a pKa of 6.46 and a pKb of 7.54.  glycine is a zwitterion at any pH between 2.3 and 9.6.  This creates a difference in the way that the buffer shields the SDS PAGE micelles from the rest of the electrical field, slowing down (probably glycine slows things down a bit) the time to resolution, but also giving the micelles more time to migrate.
So for SDS PAGE systems, the resolution of the gel has at least as much to do with the size of the gel pores (based on the acrylamide and bis-acrylamide percentages), the amount of protein you are putting into a given volume of loading well, and the size differences of the bands you are tying to separate. (you need to get pretty lucky to separate a 100.54 kda band from a 100.85 kDa band, but 1.5 to 1.8 kDa is easier 10 to 14 kDa is even easier). Also consider adjusting the current or voltage of the power supply.  The buffer system is only one consideration in planning your experiment and often not the primary factor of quality.