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Why is the inside of a cell negatively charged
So my teacher asked: "$[K^+]_i$ (k+ on the inside) is about forty times higher than $[K^+]_o$ (k- on the outside). With so many more positively charged potassium ions inside versus outside, why isn’t the interior of the cell positively charged compared to the exterior?"
My Thoughts: I am assuming that there must be enough negative charges inside the cell from other things like chlorine or ATP and proteins that the net coulombs on the inside is lower than the net coulombs on the outside. Does this seem like the correct answer? I am hesitant to use this because so far my teacher has only talked about potentials and not charges. I completely understand that the potential is negative, but potential and charge are two different things.
Edit: posted exact question from teacher as opposed to original summary of question

Since we're just talking about a potential differences, it doesn't have to be additional negative charges inside; it can also be additional positive charges outside. The Na/K ATPase also pumps out a lot of Na+ ions.  See this page:  https://en.wikipedia.org/wiki/Na%2B/K%2B-ATPase

this is a fair point. So Na+ is pumped out and K+ in at a ratio of 3:2 respectively. Therefore is it safe to assume that there are a greater number of Na+ outside than there are K+ inside, hence the greater positive charge on the outside?

That's right.  Now you could answer your own question! :-)

There are anions too, inside the cell. For say in a electrical-chargeless 0.1 (M) NaCl, there is 6.023 * (10^22) particles of Na+ and exact same amount of Cl- particles; and a slight increase of Cl- concentration at the same-time at certain place, could give rise to overall negative charge. Also, not only mineral ions, large-biomolecules contain carboxyl residues (COO-).

Net Potential on a cell surface is always measured in comparison to the extracellular media...so it is a relative parameter. So inside of the cell membrane is negative implies that there is more negative charges inside or more positive changes outside compared to the respective opposite side of the membrane. As we do not deal with the "absolute potential" we need not calculate the values of them.
K+ concentration is more inside the cell compared to outside...but there are other ions in and outside cells...e.g. Na+, Ca+,  proteins, Cl- etc...all of them together determine the potential difference across cell membrane.


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Biological significance of correlation between the radius of gyration and number of layers of convex hull of protein structure
While going through the paper titled "GEOMETRIC ANALYSIS OF THE CONFORMATIONAL FEATURES OF PROTEIN STRUCTURES" by Manish Dutt, I came to know that there is a correlation between the radius of gyration and the number of layers of convex hull of each proteins 3D structure (convex hull layers are formed by forming the convex hull of a set of points, which forms the first layer, then removing them, and recalculating another set of boundary points, i.i., second convex hull, which form the second layer).
Now my questions is, what is the biological significance of this correlation? Or is there any?

What is a 'layer' of a convex hull? As far as I know, there is just one hull layer (the minimal bounding surface containing all the points)

Never mind I'm guessing that you can nest hulls by removing the points on the outer hull and re-calculating. Still worth describing this in your question, I think

@gilleain I have edited the question. Hope you can understand it now...

From reading the paper, I don't see any obvious biological significance. The abstract says:

Proteins exhibit intriguing diversity in their three-dimensional conformations that enables them to perform different functions

Which is great, but there is no connection in this paper between conformation and function - not surprisingly as this is a large part of structural protein analysis!
The way I look at this work is similar to the idea of a "descriptor" from the field of Cheminformatics. The radius of gyration is a descriptor, and so is this hull number. The author claims a correlation between these two descriptors, so... is one easier to calculate than the other?
This is interesting work, but I'm not sure at this point what the significance of hull number is for protein structural analysis. However I can say that the correlation between these two descriptors is not biologically significant - it's just a geometric relationship that would presumably hold for any set of 3D points.

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Why do we have such a wide range of responses to pathogens and carcinogens?
I was reading an article recently debunking the idea of 'boosting' your immune system. It occurred to me that - presuming it's right - our immune systems are all pretty much the same (with the exception of the immunocompromised). Given this, I wondered why there is such a disparity in how people respond to pathogens or carcinogens.
Most people would be quite happy, for example, to say that poor food hygiene causes food poisoning or that smoking causes cancer, but in actual fact, most of the time they don't. People who have poor food hygiene standards have them every day, but they're not sick every day, they're sick once in a while. Only 25% of heavy smokers actually get lung cancer, even with something like Asbestos, only 1 in 10 former Asbestos workers actually get Mesothelioma.
What is it that protects most people from these diseases despite definitely encountering the pathogen/carcinogen concerned?
I realise the most obvious answer is the immune system, but that just shifts the question to why this doesn't protect everyone all the time. Presumably the immune system doesn't just have a day off every now and again

It is indeed our immune system. And for cancer it catches most (probably more than 99.9%) of the cells going wild. But still, once in every while one of these cells escapes and causes problems. The same with the stuff in the environment you live in. You are used to it, your immune system is trained on it. Only new pathogens will cause problems. Or you, getting into a new environment.

@Chris. As I said in the question, I'm aware of the role of the immune system. What I'm asking is by what mechanism exactly does it fail from time to time?

This answer will address only cancer.
There is no such thing as standardized exposure to carcinogens in humans; while it would go a long way to answering your question, it would be unethical.
Also, it is unlikely that two people who do consume identical amounts of a carcinogen have identical environments or identical genetics.
Cancer used to be thought of as a carcinogen-host interaction; expose a (rodent, in my studies) to adequate levels of a carcinogen and cancer will occur. We tried to figure out exactly why. Then it was thought of as a host + environment (This was decades ago.)  The immune system was found to play a role; another level of complexity was added.
Mapping the entire human genome has made us aware of how simplistic these (and most) models were. There are tumor-suppressor genes. There are genes that matabolize carcinogens differently from other genes. There are genes that direct repair of DNA better than other genes. The possibilities are just beginning to surface.
To answer your question more directly,

Although many studies have focused on carcinogen metabolism and cancer risk, more recent studies are considering DNA repair.

I would not go so far as to label DNA repair as Immunology.
I don't know why my father, who had a 120 pack year history of smoking, had absolutely no ill effects (not a trace of COPD, and certainly not cancer, no heart disease, CVD or other) and why my mother had COPD at a 40 pack-year history, but I'm sure it was genetic.

Sporadic cancers are caused by genen-environmentn interactions rather than a dominant effect by a specific gene, environmental exposure, or gene-environment interaction. New paradigms, where we categorize genes as caretaker or gatekeeper genes, will allow for new hypotheses to be tested and will require advanced methods of analysis.

And, in another study,

Three meta-analyses report 35% to 50% increases in breast cancer risk for long-term smokers with N-acetyltransferase 2 gene (NAT2) slow acetylation genotypes.

Cancer Risk and Low-Penetrance Susceptibility Genes in Gene-Environment Interactions
Integrative Epidemiology: From Risk Assessment to Outcome Prediction
Active smoking and secondhand smoke increase breast cancer risk: the report of the Canadian Expert Panel on Tobacco Smoke and Breast Cancer Risk (2009)

Thanks for the thorough answer, if I could just ask for clarification on one point. If I understand correctly, you're saying that response to a given dose of carcinogen is a result of - host environment, host immune response and host genetics (discovered in that order). If that's the case, to take lung cancer and smoking for example. Heavy smoking only produces cancer in about 25% of smokers. The genes you've pointed to in your last study give a 35-50% increased risk, that still leaves a huge amount of resistance to cancer unaccounted for, is that correct?

Also, as may be clear from my comments to the last answer, I'm interested in the research into the host response in terms of factors that a host could control. Is the move to genetic studies a result of the general trend in research since the human genome project, or have there been studies actually eliminating other non-genetic host factors?

@Isaacson - Yes, you're correct. There is also the possibility, though, that a cancer-causing mutation will not occur in 100% of the population exposed to a carcinogen. No, none of the other factors have been eliminated, but they have been, say, relatively dwarfed by genetic factors, for example, in breast cancer, the presence of estrogen and progesterone receptors, multiple copies of the HER2 gene, microRNA, DNA methylation, presence of the BRCA1 gene, and mutations in several other important genes. See, e.g. http://www.nature.com/nature/journal/v490/n7418/full/nature11412.html

Intro courses on pathogens often show a triangle representing interactions between host, environment, and pathogen to help explain why outcomes are so diverse.  Each of those parameters is very diverse, so the combination of the three is even more diverse.  At a simple level, you could think about one fit, well-rested person exposed to a low concentration of pathogen, in a warm, comfortable environment, and compare to a stressed, malnourished person in a hot, humid environment, exposed to a large bolus of pathogen.
As well as concentration, pathogens individually vary in their virulence.  Individuals all have unique immune systems, with tremendous diversity (the immune system contains genes that are by far the most variable in human -- or virtually any vertebrate -- populations).  And environmental effects interact with both sides to enhance or reduce susceptibility in many ways.
It's a set of many overlapping complex systems, basically.  Sometimes it's possible to point to a specific combination of causes, but more often we just see a few people getting sick while most remain healthy, and never clearly understand why.

I get most of what you're saying, but your mention of the fit well-rested person seems to suggest that one can, in fact boost your immune system by being fitter, getting rest etc. If that's the case and the figures I mention in the question are accurate, then when people talk about the 'cause' of a disease it would be more correct to say that lack of fitness and stress was the main cause with everything else only secondary.

First, the notion that "lack of fitness and stress was the main cause" is not in my answer; I listed them as among many potential influences, not by any means a main cause; it's telling that you assumed in spite of the phrasing that this is a "main cause", because it ties into a common (misguided) notion that disease has a moral aspect, people get sick because it's their fault, it's a punishment, and recovery is a sign of virtue.

More importantly, it's not a question of "boosting" immunity. People have a normal default level that can be damaged, not a normal level that can be boosted.  You can, to take an obvious example, take immunosuppressive drugs, like catabolic steroids.  Among that common causes of mild to moderate immune suppression, lack of sleep is one well-supported cause; morbid obesity another.

My intention was not to make a moral point, but a statistical one. It's like saying a runner won the race because he turned up. Turning up was certainly a requirement, but it's not why he won because other runners also turned up and they did not win. The thing we ascribe as the cause is what sets that runner apart from the others. I don't see why the same is not true when we ascribe a cause to disease.

The moral point that I would make though is this. If you drive, there is a chance you'll be killed on the road, but engineers do not simply say that driving kills people and leave it at that, they look at each individual case and try to work out what happened and how they can make it safer for others - seatbelts, airbags etc.

Medical research, however, seems to find a generic cause and then leave it at that. Lots of people are, to use my examples above, exposed to asbestos, passive tobacco smoke or poor food hygiene inadvertently. It's no help to these people to say that these things are dangerous and should be avoided. What would help is if they knew how they could ensure they were part of the majority who are exposed to these things and survive, not the minority who don't.

I'm not sure what your issue is.  I tried to indicate that the interactions between host, pathogen, and environment are extremely complicated.  You promptly claimed that "lack of fitness and stress was the main cause", which is exactly the opposite of what I said, and then you're accusing me of oversimplifying and focusing on a generic cause.  As far as looking for why most survive, that is an intense field of research, but I'm not particularly interested in trying to explain it to someone who is trying to hard to force my answers into their own personal agenda.

If you read my comment I'm accusing the medical establishment of focusing on generic causes not you. For evidence, look at the NHS website on lung cancer, mesothelioma or food poisoning (the examples I've used above), any mention of stress, fitness, lack of sleep among the causes? Yet, as you say in your answer these are important factors, hence a perfectly rational conclusion that they are under represented by the medical establishment.

Nonsense.  I'm as much a part of the "medical establishment" as anyone, and I just quoted the consensus opinion in the answer you agree with, so you're obviously wrong.  As I said, my answer is the typical introduction from the very first courses on pathogens, and it's such basic, common knowledge among the "medical establishment" that to argue it's somehow obscure and unknown means you've never even taken the basics, so you can hardly make claims about what they do and don't know.

Please read my comments more carefully before replying. I'm not making any claims about what they do and don't know, I'm talking about what they do and don't say to the general public and I've provided evidence to justify that claim. I've also provided comparative examples from other fields regarding the way people generally use the term "cause", which I think is significantly different enough from the way it is used by the medical establishment to require an explanation. All I have done here is ask for such an explanation, I have yet to receive one.

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Is 8 hours of sleep necessary?
Many studies claim that humans need 8 hours of sleep. During sleep there are several different stages, from stage 1 to 4 as well as REM sleep. However, are all these stages actually necessary? If yes, what are the importance of each stage, if no, which stage(s) are/is insignificant?

Can you give some examples of sources that others can read supporting your claim that we need "8 hours"? It would definitely help strengthen your question.

It's controversial, but there are some indications for the role of different sleep stages by selective restricting these stages on volunteers of sleep studies and looking at the effects the next day. There found many different roles but broadly speaking, the best evidence is that nonREM (stage 1-4) sleep plays a role in memory consolidation (storing of new memories from the previous day) and creating "space" for new memories the following day, while REM sleep has a role in problem solving and mood calibration. The work of Matthew Walker (Berkeley) and Robert Stickgold (Harvard) is particularly

Please add references!

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What is the rationale behind tapering of immunosuppressant dose a while after transplant?
MMF, Cyclosporine, Prednisolone, Tacrolimus the dose of whatever immunosuppressant used is reduced in around 6 months - 1 year after the transplant.
What is the rationale behind this?
Wouldn't any allograft, howsoever old, still remain foreign? Does the body learn to consider the graft self? Or is the response still there but the destruction is reduced?
Why should a new graft elicit more response than an old one?

This is a very interesting question. One of the most important considerations in patients on long-term immunosuppression is the risk of complications, whether infections or (more dangerously) cancer development; because of this if we can taper the dose then we would like to. This paper specifically discusses a lot of those risks. You mention prednisolone which is a glucocorticoid, and the side-effects (see also here) of chronic steroids (due to very wide-ranging immunosuppression) are well-known and always borne in mind when they have to be prescribed. The tapering of corticosteroids in long-term immunosuppression is often early to replace them with other drugs (mentioned here). With regards to the other immunosuppressives you mention, I'll mention mycophenolate mofetil and tacrolimus later with regards to how this is feasible biologically; with regards to cyclosporine, this study (admittedly old) has data illustrating the rates of rejection of renal transplants when patients withdrew from or tapered cyclosporine (here for financial reasons, but this drug also has significant adverse effects) and you can see from Figure 1 in the paper that although the patients who withdrew completely had many allograft rejections, those who tapered did not.
I'll start with answering your question about what clinical evidence we have for being able to do this; there have been quite a few studies which might help to throw some light on this. This study specifically considered kidney transplants, testing patients who were on standard immunosuppression for the 2 years after a transplant, and specifically measuring the quantity of CTLs (cytotoxic T-lymphocytes) reactive against donor cells, and they found that these cells were significantly downregulated in most patients 2 years after the transplant (while activity against third-party cells was mostly preserved). Since they found other T-cell responses to be unimpaired, they concluded that there was specific downregulation of the donor-specific cells occurring.
This paper also has some data which you can have a look at. This study specifically looked at moving patients from cyclosporine to azathioprine and mycophenolate mofetil and then tapering those. I've reproduced one of their graphs below which shows the activity of donor-specific CTLs before transplantation (the no dose group), 1 year after (still on high dose immunosuppression) and 2 years after (on low dose immunosuppression). The units are the ratio of activity of donor T-cells to activity against third-party T-blasts from spleen tissue (i.e. a control). Although you can see that some patients have ended up with increased activity after tapering, most patients appear to have low activities similar to (or even lower than) their pre-immunosuppression values, and these would be the patients considered for this tapering. This means that they now respond less vigorously to allograft cells than to control cells, and the ratio has decreased during treatment (presumably the reason why almost all of them have ratios under 1.0 before treatment is that the donor is not a random individual but matched for a lower immunological response):

And for another comparison with the body's response to non-donor substrates, the same study looked at response to tetanus toxoid. As you can see in the graph below, although the high dose caused the response to drop, it appears to have bounced back up again in most following the taper, similarly to the 3rd-party T-cell response but unlike the allograft response (the y-axis is proliferation of patient spleen cells in response to the toxoid divided by control rate):

As to the immunological reasons that we can taper the immunosuppressant dose, this is not particularly clear but there are known processes which might help to elucidate it. This paper (also on kidney transplants) suggests that there is a specific downregulation of the activity of CTLs directed against antigens presented by the direct pathway, and that this could be caused by anergy, deletion or regulation. The authors suggest that the most likely cause is an effect of the chemotherapeutics (here MMF and azathioprine) on the T-reg cells, and they speculate from the tests they did (the Discussion of the paper has the details) that the cessation of suppression of T-regs that occurs during the taper is what is responsible. They also mention a role for IL-2 signalling (necessary for T-reg function, and some immunosuppressants suppress it leading to rebound on tapering) and dendritic cells (whose costimulatory function may be altered by MMF).
As to the precise mechanism, it is not yet particularly clear, but it is thought that in the interaction between a suppressing T-reg cell and a CD4 effector T-cell, the latter actually induces the T-reg cell through as yet unknown mechanisms, so that continued activity of T-cells (e.g. in chronic inflammation or the presence of an allograft) may upregulate T-regs that suppress them. It is known that T-regs are important in downregulating chronic inflammation (presumably this is responsible for the pattern in the first graph I reproduced above where the activity against donor cells seems to drop more than that against control cells, even on high immunosuppression), through mechanisms which have been hypothesized to include CD4 T-cells undergoing receptor-ligand interactions with T-regs and providing signals to them to upregulate their production of IL-35 (which is important in suppressing all types of T-cells). Given that it is known that upregulated suppressive activity of T-regs in chronic inflammation downregulates the immune responses of all non-T-reg cells, it appears that donor-reactive T-helper cells will induce T-regs which will then downregulate donor-reactive CTLs. This paper I mentioned previously postulates that on release of immunosuppression this population of T-regs would bounce back and greatly downregulate the donor-reactive CTLs and T-helper cells.
This paper also mentions the fact that an introduction of tapered mycophenolate mofetil in liver transplant patients promotes immunological tolerance to allogeneic transplants. They mention the effect of this on T-regs as well as other immune cells.
For interest, this paper presents some interesting alternative speculation on the nature of the T-regs involved in organ transplantation tolerance. In certain cases, self-tolerance may develop to 'new' tissues, and the authors postulate that the main T-regs involved in transplantation tolerance are newly formed in response to the prolonged presence of the allograft, rather than predefined. Because of this, the tolerance might develop to some extent regardless of the chemotherapeutic regimen.
Finally with regards to tacrolimus, this study has data on the immune response during weaning off the drug after an intestinal transplant. They found that patients with a low immune response prior to weaning had a better response to the weaning, and that their immune function remained low after weaning. This is a bit different to the MMF situation I mentioned above where immune function in general seems to return and only donor-reactive immunogenicity remains low (this tacrolimus study doesn't specifically mention the effect on infection rates, but their Figure 7 seems to imply that those patients with low immune function (presumably those weaned) had lower intervention rates). Specifically the authors conclude here also that self-downregulation of the immune system (probably by T-regs) is likely to be the cause.
So in summary it is not yet fully elucidated as to why we can do this, but the upregulation of T-regs that downregulate donor-specific effector cells, and (at least for certain chemotherapeutics) the release of T-reg suppression on tapering may be important.


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What biological specimen is this? Seed? Excrement? Fungal form?

Hundreds of these 1-3 mm "seeds" have been found a couple of times this summer on my deck shaded by a large oak tree. But, they are not seeds with typical seed parts.  Too small to be pollen or spores.  I am baffled. They each have one or more deep crevices or slits longitudinally. Structurally, they appear to be composed of tiny (almost microscopic) wood chips. (Though I am sure this is just the appearance they have.) The first time I found them was after a rain and they had absorbed water and swelled to twice or three times their size and had become gooey and almost gelatinous to the touch. Almost looked like hundreds of little piles of brown poop on our deck. This time the weather was dry and they look as pictured in the photo.  I swept up hundreds in a four-foot diameter area.  Another area of the deck had a similar amount.  None on the rest of our deck or any noticed in other areas under the oak tree. My biologist friend was also baffled.  Please help identify

I meant to say "too large to be pollen or spores."

Interesting mystery! How do they behave if you cut/break it? Also, you can edit you post to include your correction.

Caterpillar defecation

All right, I'll say it if nobody else will.  Insect feces.  The "wood chips" you saw are bits of your oak (or some other over-hanging tree) that have graduated from the arthropod digestive tract, so to speak.  The pellets soak up water because the bugs are on a tight water budget and extract all the water before making a deposit.  Never heard of a gall infestation that produced feces like this, but who knows?  Look for dieing, deformed, or discolored leaves.  Look for bugs on the tree and on fallen leaves.  On the 2nd page of the document linked below is a larger specimen of what you are getting.  http://collier.ifas.ufl.edu/CommHort/CommHortPubs/Stained_sidewalks_under_Oaks.pdf

Welcome to Biology.SE! I think you've probably got it. Worth mentioning that insect faeces are normally called 'frass' (not least because Googling 'frass' then identifies a few images of caterpillar frass that look broadly similar; e.g. http://bugguide.net/node/view/842314).

These could be anthers from your oak tree—they look about the right size and shape.
Oaks produce separate male and female flowers. The female flowers become acorns. The male flowers are produced in a bunch on long strands called catkins.
Here's a fresh one.
Here's one where the anthers have opened to release their pollen.
Here's a close-up of a fresh anther.
This has some shriveled anthers still on the catkin.
Take a look to see if any of the catkin strands are on the ground or still on the tree.
(These photos are all from English white oak, so yours may be a little different. All these photos came from here.)

Since these pellets are found under oak trees, I researched further and found a possible answer on the internet in a different location.  Apparently, they are "galls" caused by insects disturbing the leaf structure of the oak trees.
https://ask.extension.org/questions/157218
Not sure, still, what exactly is raining down in the pellets.  Is it just dead plant material or is it something reproductive for the insects?  I am very familiar with the ping pong ball "galls" that sometimes fall from these trees.
Once they get wet and then dry again, they eventually become very powdery and crumble into dust.

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Does leaving land alone actually help nature conservation?
I like nature conservation - the idea of creating protected areas where nature lives on its own and wilderness is "created" like that. Is is possible to raise the natural value of land only by leaving it on its own - I mean in the way that humans do not touch the land in any way (buildings, roads etc.)?
I know about some "private" protected areas in Europe, where NGOs thought this piece of land should be protected but the authorities failed to do so, so they bought the land and took care of it themselves (restricted public access to help conservation, removed invasive species etc.)
I wonder what does it take to correctly protect an area - is it OK to leave the land alone and never touch it again or is it necessary to take care of it somehow. I mean things like invasive species (I can imagine the normal "unprotected" nature is full of them) like various types of grass, invasive animals etc. I can imagine this may be largely location dependent (some parts of the world are more influenced by humans than others). My location is the Czech Republic.

I think the concept of a 'correct' wilderness is unclear. There are some landscapes which have been suddenly 'left alone' by humans, and a meaningful answer could consider the general ecological trends of being 'left alone' in this way. Examples include the landscape around the Chernobyl, or abandoned farms. But then the question would be 'in the absence of deliberate conservation interventions, what measurable ecological benefits (e.g., changes in invasive-species populations) arise from simply leaving land alone?' Would you be happy to edit your question into that form?

Your question seems to ask exactly the same so what is the reason for rephrasement?

It removes the reference to a 'correct' wilderness. There is no such thing: natural areas may be managed towards specific goals, like maintaining the number of species present in the area, providing habitat for a key high-value species, or protecting key ecosystem services such as water retention. None of these are 'correct', but each outcome is measurable, and a 'desired' outcome can be defined in each case.

Rephrased to "raise the natural value of land" - is that better?

This may be a better fit in [gardening.se]

I'll give you an example, because this question is pretty case specific. In Delhi, my hometown, they kept areas of the forest, the 'Sanjay Van' free from construction and people and only very recently started cleaning it up. As a result, an invasive variety of the Acacia tree (known locally as keekar) more or less took over the forest and has basically wreaked havoc on the wildlife.
I think better than just letting Nature take it's course, humans should help get abandoned areas back to a sustainable point, where it can integrate with the wildlife, but again, it depends on each area.

According to Peterkin, there are three types of naturalness - past natural (the way it was before humans), future natural (the way it would be if humans left it alone), and present natural (the way it would be now if humans had never touched it). How best to conserve a site will depend on what type of naturalness you want to achieve. There's no rational argument to prove any one type is "better" than any other in the long term, but many conservationists take a safe approach and adopt the strategy with the least risk of extinction (this being the only result one cannot undo), it would be a mistake though to presume that this strategy was definitely the best, it's just in some environments we can't afford to find out.

The German Green Belt see here
I give you a another example. The green line in Germany. This is are are where the German Wall was (you know east and west Germany) This area was untouched by humans for 40 years. And now it is a protected area, because now its one of the last places for a lot of animals and plants to live.


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Shape of feces in herbivores
Why do some herbivores like sheep, cow, and others excrete feces in a pellet (or biscuit or other) shape, while other species including humans do not do so? What is the reason for such an adaptation in herbivores? Is it beneficial to them, and if so, how?

perhaps there is role of  microbes as well as whole process of digestion.

Goats are also herbivores but their dung is bead like, and not soft as cow-dung

I think it has something to do with how the different animals move the feces with peristalsis

I don't think it is an adaption, but the that diet plays a dominant role. The feces of cows in intensively fertilized agricultural fields, with grasses rich in protein, has no shape at all. See picture below.

The feces of cows in natural areas has much more structure. (image has copyright, so can only link)

Please have the courtesy to explain your downvote?!


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What is going on in these cells?
Here are some pictures of human iPS cells in culture. After several passages, some cells look really weird, can you help me understand what is going on? What am I looking at? What are those blastocyst-like structures? (bluish picture) and what about that cell full of vacuole-like thing?
P.S. do not pay attention to the scale bar, it's incorrect.

Extra info:
I did not induce them, I got them already dedifferentiated so I can't be specific on that part of the protocol. However, I am growing them in Essential 8 Flex Medium (with supplements as specified from the kit protocol), I add rock inhibitor 4h before passaging them. Passages are done by dissociating colonies using EDTA only (no enzymes). Most of the expanded cultures look normal, some showed the formation of embryonic bodies (the last picture added) but the blastocysts are very different and not really expected.

I am not entirely sure but there is some vacuole formation so maybe they are going towards the apoptosis. However to see clear phase contrast between Feeder layer and iPS cells the light diffraction may give you hallow formation around the radius of the cells. (Source: Dad)

What further changes on them happened later-on?

This question would be easier to give an answer to if you provided specifics on your protocol for inducing and culturing iPS cells, any variations from typical protocols, any experimental treatments, etc. The greatly elevated vacuole formation suggests cytotoxic stress. Elevated autophagy can be cytoprotective if the cell is moderately stressed, but it is a precursor to apoptosis when the stress cannot be alleviated by autophagy. Depending on the scale (please clarify), the blue picture may depict an "embryoid body" (essentially a blastocyst) - see "identity" section in your own wiki link.

I did not induce them, I got them already dedifferentiated so I can't be specific on that part of the protocol. However, I am growing them in Essential 8 Flex Medium (with supplements as the kit specified), I add rock inhibitor 4h before passaging them. Passages are done by dissociating colonies using EDTA only (no enzymes). Most of the expanded cultures look normal, some showed the formation of embryonic bodies (the last picture added) but the blastocysts are very different and not really expected.

Also, I did not continue growing the blastocysts, but I have backed up a few aliquots.

@Alec_djinn can you edit that information into the question please? I would also recommend changing the images to thumbnails (as described here) to improve readability.

@arboviral better?

I'm under the impression that primed or differentiated iPSC regularly exhibit membrane blebbing, based on a quick literature search.

@CMosychuk can you link the literature you are referring to? I couldn't find any reference so far.

@alec_djinn Just a couple examples, though I may be mistaken. (ref) (ref)

overgrow them and thrown some dapi on them, then check fluorescence.  I wouldn't be surprised to see mycoplasma in this culture.

they might be embryoid bodies:
https://en.m.wikipedia.org/wiki/Embryoid_body

looks like it, at least in the last picture.

ips cells fascinate me to no end. I wish I could culture them at home.


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What are the odds of being an albino human and have Down syndrome?
I know the odds of a human to be an albino. In Europe and the US it is 1 in 20,000 people (source) and for Down syndrome it is 1 in 1,250 (source). So that means the chance of giving birth to a child that has both albino and Down syndrome is:
$20,000 \times 1,250 = 25,000,000$
i.e., 1 in 25,000,000 correct?

Probability of independent events
Assuming the albinism and Down syndrome are independent traits, then the probability of having both traits is the product of the probability of having each trait.
For more information see wiki > probability (especially the section on independent events).
Albinism and Down Syndrome
If (and only if) albinism and Down syndrome are independent events (see below), then the probability fo having Down Syndrome is $\frac{1}{20,000}$ and the probability of having albinism is $\frac{1}{1,250}$, therefore the probability of having both is $\frac{1}{20,000} \frac{1}{1,250} = \frac{1}{20,000 \cdot 1,250} = \frac{1}{2.5\cdot 10^{7}} = 2.5\cdot 10^{-7}$.
So, yes you were correct! Good job!
Validity of the assumption of independence
I want to highlight again the importance of the assumption that albinism and Down syndrome are independent traits. If a person with Down Syndrome has a different probability of being albino then a person that does not have Down Syndrome, then the probability of having both traits will NOT be the product of the probability of having each trait. The only way to know whether these traits are independent is to look at empirical data. I failed to find any evidence of such correlation (but I might have missed it). If this is a homework question, you should be fine just stating Assuming the two traits are independent,... at the beginning of your answer.

Thank you very much for your great answer. Do you know if there was ever a human that was born this way?

It is correct if (and only if) albinism and Down syndrome are independent events, that is, if albino people is not more nor less likely to have Down syndrome than non albino people (and vice-versa).
However, doing a quick Google search I can't find any source relating albinism and Down syndrome, and therefore independence seems a reasonable assumption unless more information arises and your numbers are right - at least, as right as the sources you are based in.
But beware that your sources are not very representative of what you want to get, or at least not very consistent:

Your source for albinism (and its reference) gives prevalence, that is, number of albino people in the whole population of living people in Europe and USA. Please notice that proportion in living population may differ from proportion of births since albino people may have a different life expectancy.
Your source for Down syndrome gives a "baseline probability" for a given mother age (young) in some unspecified country. For older ages, probability becames larger.

Then, "the chance of giving birth to a child that has both albino and down syndrome" may differ from that you calculated, specially if you want to use it in circumstances that differ from those your data came from.
Anyway, if you just want a rough estimate, you can use your numbers.

This answer is fascianting. Thank you very much. Do you know any case where a human was born this way?

I'm sorry but I'm not expert in albinism nor Down syndrome - my answer is mostly from statistics. Anyway, according to your numbers we could expect just a few hundred people in the Earth with both, so it's not very likely such cases having been reported.

do you think there are around 100 people or 0 on earth?

Using your rough approximation, 1 out of 25,000,000 means 280 out of 7,000,000,000. Therefore, if albinism and Down syndrome are actually independent and your sources are representative enough, we could expect a few hundred people on Earth with both. 100 seems more likely than 0.

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


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Is there an ecological scenario where terrestrial insect larvae can show food choices?
I have been going through literature on insect food choices. I plan to study the effect of prior experience on food choices in both adults and larvae of the red flour beetle, Tribolium castaneum. There are plenty of studies that focus on larval and adult experience having an effect on adult preference. I would like to look at how larval experience changes larval choice, but only if it has some ecological relevance. However, I could not find a single study that provides an ecological relevance to larvae making food choices.
This appears to be due to the fact that larvae are usually sessile, and since adult females are the ones making the oviposition choices, therefore most studies seem to assume that the choices of the larvae don't matter. (Preference Performance Hypothesis)
Larval food choice might be ecologically relevant under conditions where females make "mistakes" during oviposition, say if the environment is spatially/temporally fluctuating. But if they show limited dispersal (or slower dispersal than adults), then does their choice really matter?
Does anyone know of any examples (published or unpublished) where insect larval food choice is ecologically relevant? It would help me out a lot to design my study.
Thanks in advance!

Welcome to Biology.SE, and congratulations on a great first question! One suggestion: the 'ecological relevance' criterion is a bit unclear - could you clarify what you would or would not consider to meet this criterion?

@arboviral
I see, I'm sorry for being vague. Well, the criterion for 'ecologically relevant' would be -

The larval choice actually occurs under natural conditions.
There are life-history or evolutionary consequences to this behaviour.
EITHER of these criteria would be sufficient to call it 'ecologically relevant'. It would be fantastic if it were both.

The diamondback moth (DBM), Plutella xylostella L. (Lepidoptera: Plutellidae) is one of the most important pests of cruciferous crops in the world.. A strain capable of complete development on sugar pea (Pisum sativum L. var. macrocarpon) has recently appeared. A recent study (Henniges-Janssen, Heckel & Groot (2014), "Preference of Diamondback Moth Larvae for Novel and Original Host Plant after Host Range Expansion"; link) compared the feeding preferences of L4 larvae reared during previous larval instars on cabbage and pea. Pea-reared larvae of this strain preferred peas, while cabbage-reared larvae preferred cabbage. L4 larvae of the original strain preferred cabbage irrespective of their previous diet. I don't think this example has been shown to occur in the field, but the two plants are both fed upon by these caterpillars in the wild.
There is also evidence that larvae of Cydia pomonella (codling moth), a marjo agricultural pest of orchards with a near-global distribution, learn to avoid apple flavoured with saccharine if they have previously encountered saccharine-flavoured noxious plants (Pszczolkowski & Brown, 2005); this probably meets your second criterion for ecological relevance more closely (evidence for learning to avoid odour/flavour cues encountered in a toxic plant, thereby increasing survival) but it's less relevant to a real-world field situation than the first example.
I also found an article on associative learning in insects here that may include some useful examples.

Thanks, @arboviral! The references helped! Unfortunately, I have not yet found examples for the first criterion for 'ecologically relevant'. I guess the second will have to do until someone actually observes larval choices occuring in the field and characterizes conditions leading to that.


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Are all cells organisms?
As the title says, are all cells organisms? Why or why not?
As I understand, not every cell is an organism because some of them -those which aren't organism- require the rest of the organism to live. But arguing with someone about that, he says that, for that matter, every cell needs of others to live in some way or another, or that they can be kept alive and sometimes reproduce in a petri dish, without the need of the organism. So every cell, he says, even those which constitute larger organisms are organisms in themselves. I tell him that saying every cell is an organism is awkward, that would imply that every multi-cellular organism is really a colony, rather than an organism.
Is this only a philosophical question or can we say for sure, for example, that an epidermal stem cell or a lymphocyte are not organisms?

I would say that some cells are considered organisms (e.g. bacteria) but others not. For example, a skin cell wouldn't be considered an organism because it can live by itself, it needs to be part of something bigger.

it is very true the cell is living, but we cant always call it an organism. "Life" and "individual organisms" are 2 different concepts.

MattDMo's argument is that a single cell from within a human, if extracted from the body is not perfectly self sustaining. Would it not apply then to a human extracted from our own environment? The middle of space? We could not survive there. So are we not organisms? I myself couldn't find food or water in space that's for sure. Put me in an all you can eat buffet restaurant however, and I assure you I will not starve. Like I said, not much of an answer, but certainly food for thought.

What is the point of this semantic debate?

Related: http://biology.stackexchange.com/questions/7053/can-you-consider-a-human-as-alive-or-is-it-the-cells-on-the-body-that-are-alive/7054#7054

This semantic nonsense (or as @Superbest more politely puts it debate) was posted two years ago  and I'm the only one that has voted to close.?Come on put it out of its misery and let's focus on "practical problems in biology that people actually face".

Your friend is incorrect. From Wikipedia:

The word organism may broadly be defined as an assembly of molecules functioning as a more or less stable whole that exhibits the properties of life.

(Viruses are specifically excluded, as they depend on a host cell to fulfill all the functions of life.)
While cells extracted from a multicellular organism like a plant or a person may be able to be cultured in vitro for a time, they cannot survive independently - they require the intervention of humans (or very well-trained monkeys) to obtain nutrients and oxygen, and process/remove waste. A unicellular organism like a bacterium, for example, can handle these functions on its own - it can either synthesize or find a source for its own nutrients, and can reproduce on its own to create more organisms.
The key difference is being self-sustaining. An organism needs to be able to feed itself, take care of its waste, reproduce a full version of itself, respond to stimuli, etc. (see the "properties of life" link above). A single cell from a multicellular organism cannot do all that without assistance (kind of like a virus, actually), while a true unicellular organism can.

MattDMo's argument is that a single cell from within a human, if extracted from the body is not perfectly self sustaining. Would it not apply then to a human extracted from our own environment? The middle of space? We could not survive there. So are we not organisms? I myself couldn't find food or water in space that's for sure. Put me in an all you can eat buffet restaurant however, and I assure you I will not starve. Like I said, not much of an answer, but certainly food for thought.

What do you make of this answer.  If it is correct and your answer is correct, it would seem to mean that cells are alive, but they aren't organisms.  But then that would contradict your premise for organism-ness (IE organisms have to be alive).  So this sole-upvoted answer would have to be wrong, or your is wrong?     One thing to note:  a human is no more self-sustaining outside it's environment than a cell is.  So maybe this answer does not stand up to scrutiny, even though at first I agreed with it!

@GreenAsJade This answer is saying that certain cells are alive and not organisms.  The criteria specified in this answer are "stable" and "alive"; those cells meet the second criteria but not the first.  Based on your comment, you appear to be assuming all cells have the same capabilities - but they do not.

@R.Hull this entire thing is really a semantic argument in the truest sense of the phrase, as we are arguing about the meaning of a term that ultimately matters very little to the organisms/cells involved. Yes, your space-extraction argument is true to an extent, but I am assuming that the extracted cells are put into a hospitable environment where they can find food, etc. A sulfur-dependent chemosynthetic bacterium from a deep ocean vent won't survive if you just put it in plain tap water, just like a plant won't survive in complete darkness.

@GreenAsJade Izkata pretty much got it right. Just because something is alive doesn't mean it's an organism, and one could argue that terminally-differentiated keratinocytes (corneocytes) in the skin are not truly "alive" because they can no longer reproduce. Even many types of lymphocytes, to take the OP's example, cannot reproduce at all, or cannot reproduce alone, in the absence of signals sent from other cells (for example, follicular B cells in the spleen require antigen, Tfh cells, and follicular dendritic cells to send the signals to divide and differentiate into plasma cells).

@Izkata thanks for your contribution, you pretty much got what I was trying to say :)

Many large organisms cannot survive without the help of other non-species organisms. For example ~ the ant species "Formica subintegra" cannot survive because they are physiologically unable to forage for and nurse their colony. They must raid other ant colonies to take slave care-givers.
While reading everyone's thoughts & deliberating, I've decided to reject the idea of "life" entirely.
At one stage, life needed to be created from non-life and this process would require the original arrangement of "non living" molecules to have the "properties of life" in order to create life to begin with.
Ex: chemical evolution in lipids.
Let us evaluate a lipid molecule's "properties of life"
(drawing definitions from wikipedia)
Homestasis: Lipids must maintain a molecular balance to be categorized as a lipid, their current state. Like us, this process of seeking balance is largely beyond their "free will" (or conscious awareness). Should either we or they become overcharged with electrons our current state would burn to ash and all functionality as a whole is lost.
Organization: "being structurally composed of one or more cells – the basic units of life"
How is it possible, that cells are established as life and then used to define what life is? I reject this circular thought.
Metabolism: "transformation of energy by converting chemicals and energy into cellular components (anabolism) and decomposing organic matter (catabolism). Living things require energy to maintain internal organization (homeostasis) and to produce the other phenomena associated with life."
Living things require a balance of energy, to be specific. Lipids may not transform energy but they have clear agency that effects 'other' molecules (being polarized) which does include asserting their agency upon the energy within those molecules, we also know they form structures and can create isolated environments for further chemical evolution. Indeed this is a tricky question, but life is a poorly defined concept, queue this forum. <3
Growth, response to stimuli, adaptation, I feel, are answered above. That or I am getting lazy, this took longer than I thought to articulate. I'll stop here and await new thoughts. Thank you for the platform, you're my kind of people, merely by asking this question, regardless of the answer.


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How does sGP of Ebola virus help it to evade host humoral immunity?
During Ebola infection, the viruses secret a lot of sGP. What's its function? Since anti GP antibodies are effective at inhibiting Ebola infection, wouldn't sGP stimulate host immune system to produce more anti GP antibodies? Why does Ebola virus expose its weakness deliberately?


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I need some forearm bone motion pictures
I would like to know how my forearm bones move inside my forearm when I'm twisting my hand. (Also, it would help to see the hand bones action too). "twisting hand" means to me the motion in which the rest of the body is in place except the hand which turns from upside up to downside.
I have the intuition that the bones inside my forearm move between themselves to make my hand twist, but am not sure if that is true.
I would like pictures of the forearm bones before and after twisting. Animations would also be great of course.

I replaced the "I want" and similar expression (that give of answering to the request of a dictator) by "I would like" and other more appropriate expression. In the same logic, in your comment under the current answer i would remove the I will accept your answer if you clarify that [..] part of it. Of course, I don't think you feel like giving orders. It is only a matter of expression. You might as well not be a native english speaker. (I am not either).

@Remi.b yes, thank you for editing, I was experimenting with language. He fulfilled my request and now I gave him his prize. And yes, I'm not native english speaker.

Here is a basic image. Palm up is called supination and is the resting (anatomical) position. The radius and ulna sit parallel. When the forearm is in pronation, the radius crosses the ulna.
You can feel this yourself. Put your fingers on the ulna and move the palm into pronation and supination. You will not feel the ulna rotate. Only the radius pivots during this movement. The wrist is not involved in this movement.

The ulna is unable to rotate at all, because its olecranon process is locked into a groove on the distal end of the humerus. If you put you fingers on your bony "elbow" (olecranon process) and pronate/supinate your hand (without flexing/extending your elbow), you will not feel you ulna moving.

Suppose I rotate my forearm as described, from pronation to supination. My ulna rotates around itself? I see the radius moves, but I want to know if the ulna rotates around itself. I will accept your answer if you clarify that in your answer.

Thank you very much, this is indeed the info I needed! Please feel useful :).


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Why Is Action Potential Propagation Not Described by Telegrapher's But Cable Equation?
In modelling the propagation of action potential in an axon, why is the partial differential equation the cable equation rather than the telegrapher's equation? The difference between the two is that the former does not have inductance while the latter has. Does an axon not have inductance whether it is myelinated or unmyelinated? This is related to my previous question. There the only answer I obtained attributes this choice not to experimental evidence but the deficiency on the part of biologists in mathematical sophistication in dealing with the complication of electromagnetism arising from including inductance.

I am the individual who answered your earlier question.  The answer remains much the same.  The Cable Equation is inappropriate.  It was developed originally as the Heat Equation of Thomson,  While Thomson disowned its application to the axon as a cable, Herman continued to promote the solution within the Biology community.  The problem is the Cable Equation requires as an initial condition that the stimulation of the cable continues until the signal reaches the terminus of the axon by conduction (diffusion).
When exploring the myelinated axon, the Telegrapher's equation must be used.  The formal name for this equation is the General Wave Equation, GWE, of Maxwell. It involves an initial condition that is much more lenient.  The stimulus must only be applied to the axon for long enough to ensure the desired full waveform is represented. Thus the GWE involves propagation and not conduction (or diffusion).  See section 7.4 of Chapter 7 of "Processes in Biological Hearing," PBH, on my website.
Cole & Baker, "Longitudinal Impedance of the Squid Giant Axon", Journal of General Physiology, (1941) vol 24(6) pp 771-783 present their initial measurements of inductance within the large axon of a small squid.  This axon generated "swim waveforms" and not "Action Potentials" as currently defined.  The inductance is much smaller in a non-myelinated axon than in a myelinated axon.  It remains calculable in either case.
I have reviewed the two papers by Lieberstein & Mahrous you cited for my benefit.  The authors are apparently two very good mathematicians without much knowledge of biophysics or the biophysics literature.  They quote a diffusion velocity from Hodgkin & Huxley (1952) that is several orders of magnitude slower than the phase velocity along an axon that is very well documented by Cole and more recently by Smith et al.  I have uploaded a more complete analysis in Section 9.1.1.4.3 of the above citation to chapter 9 of my work, 9SignalTransmission.pdf.
These two papers should not be relied upon until reviewing Section 9.1.1.4.3

Thank you, again, for your answer. Here are two more papers that suggest the existence of induction in an axon, http://jgp.rupress.org/content/jgp/22/5/649.full.pdf,
http://sciencedirect.com/science/article/pii/0025556470900416 and http://jgp.rupress.org/content/jgp/25/1/29.full.pdf. Feel free to incorporate these references into your answer.


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Is differential equation modelling in molecular genetics useful?
I graduated last year with a degree in Applied Mathematics and just this month I started a PhD in molecular genetics. I was accepted into a program specifically for individuals with a quantitative background, though the differences between my program and the general graduate program seems fairly minimal.
The department is fantastic and I'm enjoying learning the experimentation, but I haven't had the opportunity yet to use my actual skills.
The more talks I attend, the more I realize that much of the "computational" side of molecular genetics seems to be split between machine learning, bioinformatics and statistics or some combination of the three. In my undergrad I studied topics such as differential equations (partial and ordinary, extensively), dynamical systems, vector calculus (though I never took any fluids courses, I was more of a systems guy), computational mathematics, control theory and some computer science (about 5 courses).
I've talked to a few of the faculty so far and when I mention the possibility of differential equation modeling, they don't seem comfortable giving me guidance. In addition, I read a review paper today that seems to suggest this kind of modeling is fairly uncommon.
So, my questions are these: Are differential equation models useful to geneticists and biologists? Why are they not done more often? How difficult would it be to create my own project that involves differential equation modeling coupled with experimental parameter finding and model verification?
Nobody seems to be able to give me an answer, so I hope the Stack Exchange community has some insight.
Thanks in advance!

@WYSIWYG This hardly seems a matter of opinion. I cited two seminal papers in biology and genetics that model biological phenomena with differential equations. Clear diff. eq. are useful in biology.

@CharlesE.Grant It is opinion based. OP is seeking opinion on how easy or difficult something would be and whether something would be useful or not. Moreover, it is also broad and not really about a biological question. There are several papers on mathematical models of genetic systems (I personally also work on such problems). This question is off-topic on several grounds.

Differential equation could be applied anywhere, may it be light-and-darks of a picture or taste-distribution in a cone of ice-cream. Just like +, -, * and / they could be applied in so many places. Rather I think it would be troublesome to find a field where diffirential equations does not work in the nature.

Are differential equation models useful to geneticists and biologists?

Well yeah, of course they are. Look up Alan Turing and "The chemical basis of morphogenesis", or look up "differential equations and gene regulatory networks" But folks have to specialize, and not every department studies every aspect of a field. You may just have ended up in a department where nobody is studying an aspect of genetics that can be well modeled by differential equations. At lot of molecular genetics is still figuring out the coarse grained phenomenology of the genome, like "How does a cell figure out which copy of the X chromosome gets condensed into a Barr body?" A lot of these problems involve picking out subtle signals from noisy data, thus the interest in statistics and machine learning.
If diff. eqns. are the passion of your life, you might have to look 'next door', to departments studying biochemistry and population genetics, both of which do huge amounts of modeling using differential equations. There are also applications of differential equations to molecular genetic methods like QPCR and next generation sequencing, but you'll either have to sell your mentor on the topic, or move to a different department.
On the other hand, if it's just a matter of diff. eq. being your undergrad emphasis, you may want to find a biological problem that interests you, branch out beyond diff. eq., and use your general mathematical maturity to pick up the relevant mathematical tools: say statistics, optimization, or dynamic programming.


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Technical term for water entering a semipermeable membrane?
Would the word happen to be diffuse? I have tried imbibtion but that word is invalid because it isn't specific to osmosis.
Research: http://www.majordifferences.com/2013/12/difference-between-osmosis-and.html#.V9xc4fkrLIU

Are you asking about crossing of the water through membrane? or you are telling about when a dry membrane soaks some water?

Why is osmosis not suitable? Do you want a term that can be used to describe osmosis?

Water passes through membrane also in case of reverse-osmosis (basically  a sort of mechanical-pressure-driven flow). But that term also contains osmosis. so using te term osmosis is also ok.

Osmosis is a sort of diffusion where an overall diffusion is seen not in solute (say sugar) but instead the overall diffusion seen in solvent (commonly water in biological context). So the term diffusion could be used.Also passive-transport through cell-membrane sometimes called diffusion.

This is not imbibition, as water molecules don't get absorbed in the semipermeable membranes commonly found in biological structures like Membrane around cells and cellular organelles (I took this example as you asked it in Biology forum). The water molecules pass through biological membranes via protein channels, that may be an active, secondarily active or passive process. Percolation and permeation are also inappropriate.
If the membrane doesn't hinder a particular solvent it can be said to be permeable to that solvent (e.g. Permeable to water etc.). "Osmosis" is also applicable. As osmosis is only a type of diffusion, you can use the term 'diffusion', but it would be too broad or generalized.

I am not quite sure what you are looking for but maybe the term passive transport will satisfy your needs although it is not specific to water.

Passive Transport is a movement of biochemicals and other atomic or molecular substances across cell membranes without need of energy input. Unlike active transport, it does not require an input of cellular energy because it is instead driven by the tendency of the system to grow in entropy.


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What are the obstacles to "refitting" the human body's metabolism?
As a layman, I understand the problem of rising obesity like this:

In the old times, humans could never get enough food, thus they would eat whatever they could get. This "program" is encoded in our genes.
At least in industrial countries, the ubiquity of energy-rich food makes some of us get obese, at least partial because we follow this old "program".

I hope I didn't get it too wrong. Now my question is this:
Would it be possible to somehow "rig" the human body to change the metabolism and make it fit to a rather sedentary lifestyle?
For example: Instead of storing surplus food / energy within the body, it could be excreted, thus keeping humans at their weight even when eating a lot more than they need.
Could this be possible? Which organs/hormones control the utilization of food within the human body and can they be influenced in such a way?

Yes, you got it right. The theory you're referring to is called the thrifty gene hypothesis. There have been several attempts at "rigging" metabolism to reduce the amount of surplus calories stored as fat, as you suggest, and some of them have gone all the way to approved drugs.
One strategy is to block intestinal absorption of nutrients, so that excess food is simply excreted. Perhaps the most well known example is Orlistat, a prescription drug that prevents fat absorption by inhibiting lipases secreted by the pancreas. This has been proven (somewhat) effective in clinical trials, but also causes gastrointestinal problems like oily stool. Most drugs of this type, preventing the gut from doing normal digestion, will probably have this limitation.
There are also ideas about increasing metabolism of absorbed nutrients to "burn" more calories. Generally, utilization of nutrients in the body does not happen on its own; it is a consequence of activating other energy-demanding processes, like muscle contraction, brain activity, immune system function, and so on. And any attempt to increase metabolism, regardless of mechanism, will end up generating more heat. So in order to increase metabolism, it is necessary to turn on some heat-generating function (other than exercise :) Some research groups are experimenting with increasing energy expenditure in brown fat (a type of fat that normally oxidized nutrients to generate heat) to burn off excess nutrients. This is still a long way from medical use though.


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Can Two Opposite Running Action Potential Cross Each Other without Annihilation in One Axon
Can two opposite travelling action potential cross each other annihilation in an axon?
My answer would be affirmative. If the propagation mechanism is linear as described by https://en.wikipedia.org/wiki/Cable_theory or even https://en.wikipedia.org/wiki/Telegrapher%27s_equations with approximately constant coefficients, the waves are then linearly additive and each signal should propagate unperturbed. The refractory period on each end of the axon can not possibly prevent the other end from being excited at the same time since the signal has not arrived yet.
This question is inspired by the question Can a single axon propagate multiple simultaneous action potentials?

When the waves collide they should extinguish each other since the membrane each encounters is depolarized (because of the other's propagation).

@mgkrebbs: How does depolarization lead to extinction of both waves? The equations contradict this claim since the electric (action) potential is additive.

@Hans the waves would extinguish each other because both will lead to depolarization of the membrane. The AP cannot proceed further. AFAIK, the amplitude of the AP would be the same for a certain type of neuron. If they are different then the dynamics may be different. Using a model you may be able to predict the behaviour but I am not sure if anyone has checked this experimentally.

@WYSIWYG: Your first sentences are stated without reason, just like the statement from mgkrebbs. It seems you are making the same analogy for AP to domino as Superbest does in his answer judging from your concern with the amplitude of the opposing AP's. However, if you switch to the wave analogy then the two should cross each other without interference. It sounds very much like speculation with different analogies leading to completely different conclusions with one no more convincing than the other. But please do derive the proposition if you think otherwise and are certain of its validity.

@Hans No it is not like a usual wave. You have to understand the physiology behind that. AP leads to membrane depolarization. An already depolarized section of the membrane cannot conduct AP. Of course it is not as simple as two waves clashing and annihilating each other. That's why I said that a simulation would be useful (there may be non-intuitive behaviour as these are non-linear systems). I would do the derivations if I had the time. I am a bit occupied and can tell you only what I know right now.

@WYSIWYG: Your proposition is "an already depolarized section of the membrane cannot conduct AP". You have not stated why it is the case. Maybe you have not stated your claim in the most rigorous form. As it stands, this can not be true as it leads to contradiction due to the continuum of value of potential a channel can assume. When a channel is depolarized,  Following the front of the AP, when the first channel, is depolarized to a small potential, your claim would have lead to the AP wold have stopped there and propagate no further because that first channel has already been depolarized.

@WYSIWYG: In my latest edition to my answer below, I added a reference on FitzHugh-Nagumo model showing colliding wave crossing, coalescing as well as annihilating behaviors all depending on the parameters chose of the model. Just as I suspected, annihilation is not the necessary outcome.

I completely fail to see the need to propose complicated models without having evidence for the phenomenon in the first place. Since a membrane that was recently depolarised cannot trigger another action potential due to the refractory period effect, I completely agree with WYSIWYG that the recently depolarised membranes would stop the AP from proceeding along the axon. In the absence of evidence for your hypothetical occurrence, I see no reason to assume the APs will in fact cross each other.

@MarchHo: Are you saying FitzHugh-Nagumo model, a special case of Hodgkin-Huxley model is a newly proposed model? On the contrary it is a classical and widely accepted model for action potential. I have been saying "recently depolarised cannot trigger another action potential due to the refractory period effect" is a vague statement in need of logical derivation to deduce the annihilation of colliding waves. WYSIWYG claims he has a derivation but only has no time to write down. I am skeptical. That means at least he acknowledges that statement is not a sufficient reasoning for annihilation.

@MarchHo: WYSIWYG proposed simulation. And simulation here is. This shows precisely that the "recently depolarised" is NOT sufficient to obtain annihilation. There may be other reason for not observing wave crossing experimentally, say, the parameters that do produce depolarization but wave crossing are not present in most experimental settings. The effect of model and mathematical reasoning is to test your hypothesis. In this case, the simulation shows the hypothesis "recently depolarised membrane cannot trigger another action potential" is false (insufficient).

Combining the lecture notes on the interchannel and channel  electric potential leads to a description of the propagation of the action potential $V$. Specifically, substituting in $I_{\text{ion}}=I_{\text{ext}}$ of equation (6) of cable theory by equation (1) of Hodgkin-Huxley model gives the full propagation equation. A linearization of the Hodgkin-Huxley model leads to a system of linear partial differential equations. I will write out the full formulation and the linear approximation later. That allows complete superposition of action potential. The original non-linear system of partial differential equations under a set of functions/parameterizations at least close to the linear version should permit two opposing wave to cross each other though with interference. So it is not true that all parameterizations of the Hodgkin-Huxley model prohibit two-wave-crossing.
It would of course be intriguing to investigate the existence of a particular form/parameterization where the model does extinguish two opposing waves with its initial condition being two pulses close to a dirac delta function at each end of the axon.
Here is a paper M. Argentina, P. Coullet and V. Krinsky, Head-on Collisions of Waves in an Excitable FitzHugh-Nagumo System: a Transition from Wave Annihilation to Classical Wave Behavior a special case of the Hodgkin-Huxley model. Just as I expected, the waves do not always annihilate each other, but rather may cross, annihilate or even coalesce or even coalesce then re-emit, all depending on the particular values of the parameters of the model. Another paper Oleg Aslanidi, O. A. Mornev, Can Colliding Nerve Pulses Be Reflected? on the numerical simulation of a full-blown Hodgkin-Huxley model reporting crossing of colliding waves. This paper Follman et al, Dynamics of Signal Propagation and Collision in Axons reports under their particular set of parameterization of Hodgkin-Huxley model, two colliding waves annihilate. This paper by Alfredo Gonzalez-Perez et al demonstrates Penetration of Action Potentials During Collision in the Median
and Lateral Giant Axons of Invertebrates based on the soliton theory of nervous signal propation as described in On soliton propagation in biomembranes and nerves by Thomas Heimburg and Andrew D. Jackson.
The wikipedia page on autowave has some interesting information including references for propagation and collision of nonlinear waves in excitable media.

This answer is theoretical, and it doesn't convince me that the model is a perfect representation of reality. It would be greatly improved if you linked to experimental results showing this phenomenon.

@MarchHo: The theoretical answer shows the model allows for wave crossing and annihilation, and that the depolarization is NOT sufficient to prevent wave crossing. No model is a perfect representation of reality. This model and numerical simulation precisely refutes the hypothesis "recently polarized membrane" would prevent wave crossing --- as insufficient.

@MarchHo Although I wouldn't personally accept the answer, it's definitely valuable to know that some models permit the phenomenon. It's an answer in case experimental data does not exist.


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Enzyme Inhibition by alpha-2 macroglobulin
Alpha-2 macroglobulin is a plasma protein which acts as an anti-protease. It does so by a "bait mechanism" - the protease cleaves the bait domain, following which a conformational change causes binding of alpha2-macroglobulin with the protease, and consequent irreversible inhibition of the protease.
This seems to be very similar to "suicide inhibition" or "mechanism based inhibition" - when an enzyme catalyses a substrate analog's conversion to an active inhibitor, which subsequently binds strongly to the enzyme to inactivate it.
Is alpha2-macroglobulin's inhibition of proteases a case of suicide inhibition then? If it is, why is not more commonly described as that (I have not come across any description of alpha2-macroglobulin as a suicide inhibitor)?

Lets first see the proper definition of Suicide Inhibition as given by Wikipedia (emphasis mine):

In biochemistry, suicide inhibition, also known as suicide inactivation or mechanism-based inhibition, is an irreversible form of enzyme inhibition that occurs when an enzyme binds $\alpha$ substrate analogue and forms an irreversible complex with it through a covalent bond during the "normal" catalysis reaction. The inhibitor binds to the active site where it is modified by the enzyme to produce a reactive group that reacts irreversibly to form a stable inhibitor-enzyme complex. This usually uses a prosthetic group or a coenzyme, forming electrophilic alpha and beta unsaturated carbonyl compounds and imines.

Now, lets see how $\alpha$-2-Macroglobulin works, again by Wikipedia (emphasis mine):

$\alpha$M protease inhibitors inhibit by steric hindrance. The mechanism involves protease cleavage of the bait region, a segment of the $\alpha$M that is particularly susceptible to proteolytic cleavage, which initiates a conformational change such that the $\alpha$M collapses about the protease. In the resulting $\alpha$M-protease complex, the active site of the protease is sterically shielded, thus substantially decreasing access to protein substrates. Two additional events occur as a consequence of bait region cleavage, namely (i) the h-cysteinyl-g-glutamyl thiol ester becomes highly reactive and (ii) a major conformational change exposes a conserved COOH-terminal receptor binding domain (RBD). RBD exposure allows the $\alpha$M protease complex to bind to clearance receptors and be removed from circulation.

So, clearly, it is not suicide inhibition as:

$\alpha$M protease inhibitor does not form an irreversible complex with the protease, instead it uses steric hindrance to prevent protease from binding any substrate.
this inhibition does not occur during the "normal" catalysis reaction, it is after the protease has catalyzed a reaction that the inhibitor covers it up, more like the consequence of catalysis.
the inhibitor does not bind to protease active site, it covers the active site like a shield.

Putative mechanism of protease entrapment and inhibition by ECAM (Escherichia coli Alpha-2 Macroglobulin)
References:

Suicide Inhibition
$\alpha$-2 Macroglobulin
Structure of protease-cleaved Escherichia coli $\alpha$-2 macroglobulin reveals a putative mechanism of conformational activation for protease entrapment (PDF)


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Determination of the species of a skull
Out here in the mid german woods,  the kids found this skull:

Now we would like to figure out what it is. Started to look at various google image search results for all kinds of animals that came to our mind, but not only due to bad reception this takes long and lead to no result.
So what is a good structured way to start detrmining what this is?

What is the size of the skull? Could you measure it or make a photo with a euro coin next to it? Looking at it's teeth, it looks like a herbivore.

Just to clarify, do you want people here to identify it or do you want to know how to identify an unidentified mammal skull?

@kmm: ideally I would like to have some information that can guide me to do such identification myself in the future; the skull here should serve as a kind of example people could explain some method, so in the end it should be identified here

@RHA: obviously you are right, that information is important. I will try that as soon as I have better network. For now the size is approximately 20cm I length

I usually use an old-fashioned book, but it's in Dutch. I imagine these kind of books exist in English (and German?), but I can't advise you on that.

@kmm If you seek a single question on 'how to identify a specimen from certain group of organism'; it would be too too broad. I think it is appropriate that anyone could upload specimens and experts could take part in identifying what specimen it could be. And obviously, why it is different from certain-other specimens, or in other very-close-specimens what similar things could be found, could be discussed in reasonable-amount of  words.

@PlasmaHH it looks to me like a skull of wild hog. Sorry I've too-little experience in zoology to identify an individual skull with characters.

@AlwaysConfused: fair point being too broad. We could interpret it as identification plus thought process? I really would like to take away more than just the name from it

@PlasmaHH I din not told you question broad. The answer could be as short as only its technical name. I told Kmm that a single question to identify mammalian question is far from too broad. To do it, a big book will be less than enough.

And about results, it must be a young wild boar (Sus scrofa) or a domestic pig (please notice the very small canine).

Can you add photos of the occlusal surfaces of the teeth?

Tag add suggest Osteology

I changed the title of your question for it was in imperative mode. Hope you don't mind.

If you're serious about this (and it appears you are), you'll benefit by starting with a Comparative Osteology book or webiste that discusses all the various characteristics of skulls that give you clues to exactly what you're dealing with.
This page on Amazon has a variety of such books. Pages such as this one begin with the basics and references help you to pursue the subject further.
On your specimen, although the missing teeth would be very helpful, important identifying features include the very large percentage of the cranium given over to the masseters, the eye socket placement, the size, the jaw shape, etc.

Teeth are really important features for mammal identification.
The types of teeth gives an idea of the kind of food they eat.
In the skull you show, I guess that the tooth surface is far from being a "flat" grinder (which would be typical for an herbivorous, especially if old), but neither is there a sharp scissors-like structure (which would be typical of a carnivore). Therefore I will bet the animal is omnivorous.
The size, number, disposition and diversity of the teeth (dental formula) can further help. Some comments pointed to the presence of small nascent canines.
You can then look at a list of mammals that are living in the region of interest, filter it by size, and check what kind of dental formula they have.


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Drinking River Water Unsafe?
I've read that drinking river water is unsafe. Did people in the past drink water from the well exclusively or did they deal with diarrhea constantly?

This is not really a question about biology. I am not sure which SE site this may belong, though; perhaps [history.se] but even then these factors vary geographically a lot. I am afraid this question would be considered too broad in [history.se].

Which river? Unsafe how?

It depends how far in the past you're looking. Post-agriculture but pre modern sanitation, yes diarrhoea is a major problem. Pre-agriculture, however would have been a different matter. The majority of pathogens in river water are derived either from agriculture (e.g. cryptosporidium, giardia) from large human populations (cholera) or rodents associated with human populations (leptospira). There would, therefore have been far fewer disease causing organisms in river water Pre-agriculture. Add to that the effect on the immune system of Post-agriculture diet and lifestyle and it would seem unlikely that the cleanliness of most river water would have been a major problem.

It very much depends on the river and location along that river. if there is a city upstream who is defecating into the river, you'd better not drink from that river. But drinking from the same river upstream of this city could be totally fine.
Disease transmitted through the faeces were very common in the the 19th century especially in cities that had no system of evacuation of wastes. Now, of course the prevalence of such diseases depends on the type of society and therefore on the era and location.
Generally speaking, it is always best to carry tap water (or bottled water) on you. If you have to drink from a river, be cautious, talk to local people, think of what could live upstream (people, cattle, ...) and always use a good filtration system before drinking from any river.


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Protein binds to DNA and just stays there, what will happen next?
If I hypothetically make an inactive version of Cas9 or ZFN (that will bind to the DNA but does not apply the cleavage reaction). What will happen after the protein bound to DNA? Will it be stuck in there forever and disrupt the transcription/translation process? Or will it be self-unbound after a while?

Welcome to Biology SE. You could visit the tour-page for basic informations, the help-page for more detailed informations about what could be asked or could not be. For formatting tasks in command prompt, visit this help sub-page. Thanks

All binding reactions are reversible. The binding and unbinding (association and dissociation) are usually in equilibrium. How much of the protein is bound to the DNA and how much time a single molecule spends in the bound state depends on the kinetic parameters. In case of the non-catalytic Cas, the protein may inhibit transcription if it is bound at the promoter. In fact, such inactive variants have been developed and used for targeted inhibition of transcription (Himeda et al., 2015).
If the CRISPR-Cas is blocking a binding site for a transcriptional activator, then the degree of inhibition would depend on the competition between the activator and the CRISPR-Cas-inhibitor for the binding sites. This competition would be dependent on the kinetic parameters as well as the concentration of the competing species.
Similarly, you can design proteins/RNAs that can bind to mRNAs (at RBS in prokaryotes or Kozak sequences in eukaryotes) and inhibit translation.
Another interesting fact: CRISPR-Cas system has been engineered to work like transcriptional activator, as well (Didovyk et al., 2016).


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Intron sequences in course of evolution
In course of evolution did some exons become intronic  sequences or will introns in some species acts as exons in other species.

There are alternative exons (and cassette exons). See alternative splicing.


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How to incubate freeze dried culture?
I have a freeze dried culture of staphylococcus aureus; how do I incubate it?
Can I just mix it into Luria broth and just keep it in the incubator?

Yes, it's that easy!

Please don't ask the same question repeatedly. You were already given an answer to your previous question, why did you ask again?

Many micro-organisms do not tolerate freeze drying (you should freeze them using cryo-protectants). Apparently Staphylococcus can tolerate it. You don't directly put the dried cells in the medium. First you have to rehydrate the cells using the medium and then transfer them to the culture vessel. See the following instructions from ATCC:

The preferred method for long-term preservation of bacteria and algae
  is freeze-drying; however, some bacteria do not survive freeze-drying
  well and are frozen instead. For freeze dried cultures, using a single
  tube of the recommended media (5 to 6 mL), withdraw approximately 0.5
  to 1.0 mL with a Pasteur or 1.0 mL pipette. Use this to rehydrate the
  entire pellet, and transfer the entire suspension back into the broth
  tube and mix well. The last few drops of this suspension may also be
  transferred to an agar slant. Alternatively, algal cultures must be
  initiated on agar plates. Please note that anaerobic bacterial
  cultures must be rehydrated in an anaerobic environment; the viability
  of the cells decrease rapidly if the vial is rehydrated in an oxygenic
  environment.
Incubate cultures under the appropriate conditions. Given proper
  treatment and conditions, most freeze-dried cultures will grow out in
  a few days. However, some may exhibit a prolonged lag period and
  should be given twice the normal incubation time before discarding as
  nonviable.

If you had received the cells from some repository or a vendor, you would have also got an instruction manual on how to revive the cells and what media to use. It is best to follow the specific instructions given in the manual.

What is special about the rehydration medium? Like what is it made of?

@user2990508 From ATCC manual it appears that is same as the medium in which you are going to grow the cells. If you are buying from a vendor then follow the specific instructions mentioned by them.