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What is the evolutionary reason behind the fragility of teeth?
Almost all organs in the human body have a rather large threshold within which the organ or tissue is capable of repairing itself using materials supplied by the body, whether it's made from organic tissue or structural proteins. Wounds and minor damage to the skin or flesh for example heal by themselves, skin, nails and body hair can grow back if damaged or removed, even most bones can be repaired autonomously by a biological body. Cutting off a significant chunk from the human flesh or removing over 90% of a hair or a nail would cause no permanent injury, and the body is capable of repairing the damage over time with ease. The vast majority of the human body (not counting critical organs such as the heart or the brain) can be "grown back" to an extent by itself, because such parts have a rather large damage threshold.
On the contrary, teeth do not. There is a certain threshold in which tooth enamel can be supplied and "repaired" by the body to an minimal degree, but past that point virtually any damage caused to teeth are permanently irreparable by natural means. Which is quite strange, given how fragile a set of human teeth is, be it chemical or physical damage. Especially if you take more "artificial" causes into account. A moderately heavy object aimed towards a human mouth, for example, can easily render ten to fifteen teeth permanently damaged past the point of recovery within a heartbeat, also causing the said person's digestive process to be heavily impaired.
Another strange fact worth noting, is that the human body is capable of producing two separate set of teeth due to biological growth and size differences, but not more than that. Wouldn't it be beneficial for a biological body to be able to supply new teeth in the place of ones that have been damaged or removed? One could argue that such an action would be too complex and impossible, similarly to growing back an entire limb or a spare heart, but given the material that makes up teeth and its fragile nature, it would be safe to assume that it is biologically possible, especially given the fact that the human body DOES produce two separate set of teeth over its lifespan.
However, even stranger still, is that the only element capable of damaging or deteriorating  teeth by natural means, is the consumed food itself, and the acidic bacteria found within. Several types of edible food consumable by human means are capable of damaging the enamel to critical levels within relatively short periods of time, even non-artificial ones. What happened before the invention of the toothbrush and various dental cleaning methods? Why haven't humans evolved in the past tens of thousands of years to the point where repairing or regrowing teeth by natural means is feasible? Simply put, why don't teeth grow back contrary to hair, nails or skin?
What is the biological and evolutionary reason behind teeth being so fragile and indisposable?

Regarding the replacement of teeth, sharks do this continuously.

I think your premise is wrong - teeth are not fragile and enamel is supposed to be the hardest part of the human body. Also, strictly speaking, humans do not produce two sets of teeth independently. Both sets are produced at the same time (with a very cool looking result): The mouth of a child is a terrifying thing to behold

@RoryM most non-mammals replace teeth continuously mammals are the weird group out with only limited numbers.

I don't recall where I read this, but I believe human teeth cannot be replaced because we require a fairly high-precision bite. Compare this with a shark's mouth where they just need a bunch of teeth in the same general area, making it practical to regrow them at will.

The evolutionary biologist in me would argue that, on average, teeth are exactly as strong as they need to be. In other words, the fitness cost of producing and maintaining teeth is balanced with the the fitness benefits of having teeth.
To address your questions from an evolutionary lens:
Why haven't humans evolved in the past tens of thousands of years to the point where repairing or regrowing teeth by natural means is feasible? Simply put, why don't teeth grow back contrary to hair, nails or skin?
The short answer is that we have evolved the ability to regrow teeth. That's why you lost your baby teeth and a new set grew in their place. And why most folks have wisdom teeth that grow in later in life.
Essentially, we only need enough functional teeth to get us to the point of reproduction. After that, the effects of selection for stronger, more, better teeth wanes.
You may find this review article1 helpful wherein the authors explore the evolution of teeth, and specifically health issues related to teeth from an evolutionary perspective.

[1] Koussoulakou et al. (2009) A curriculum vitae of teeth: evolution, generation, regeneration. Int J Biol Sci; 5(3): 266-243.

you do realize endless teeth is the norm mammals have lost that ability. We have not evolved the ability to grow new teeth, we grow a set number of teeth.

Human teeth and animal teeth are not fragile. It is meant to last a life time, barring physical injury. If anything makes it fragile it is ourselves. The main two causes of tooth loss is dental decay and gum disease. Both are cause by the soft tenacious bacteria filled biofilm called 'Plaque". If there is no plaque then there is no dental caries(cavities) and no periodontal disease(gum disease).
Wild animals don't have both and eskimos did not have these diseases till they were exposed to modern civilization. Raw fibrous food have a terrific cleaning effect and effectively removes plaque. And even if there is plaque, since there is no refined carbohydrates there is no decay.
If you want to prevent dental decay remove plaque completely, by brushing ,flossing and sealing all the pits and fissures where plaque can lodge. Follow this and one can eat all the sugary things without worrying about their teeth if not anything else.

"If there is no plaque then there is no dental caries". I can agree with that, as there must be a method of decay, but is bacteria really the cause? Can a tooth be "healthy" enough to resist the actions of bacteria (which I would think would be present in everyone's mouth, yet some people's teeth don't decay even with no brushing ie eskimos)? An analogy would be that dead animals decay because they're dead. If they decayed because of bacteria, then live animals would decay as well (unless they cleaned the bacteria off 3 times a day, which they don't). I question the accepted cause of caries.

I think the reason for caries is more chemical than biological (ie plaque is a symptom, not the cause). Also, caries are common in all cultures and are present in animals. The diet seems to be the single most prominent factor in the formation of dental caries. On the Eskimo thing, is that from Price?

The sequence is like this: Plaque harbours and protects the acid producing (acidogenic) micro organisms. Acid producing microorganisms metabolise refined carbohydrates to pretty strong acid. This acid easily decalcifies the enamel which is 96% minerals. However the quantity of the acid priduced is minute and its action lasts for 20 minutes to 40 minutes and tapers off. The role of the plaque is to harbour these Microbes in high concentrations close to the enamel or tooth structure and to prevent dilution of

the acid by saliva. The effect of acid in enamel is like acid on marble. Enamel gets damaged even by mild acids like carbonated drinks. These are well established facts readily available in standard text books in Dentistry. In short no plaque no caries.

@RamManoharM I've heard the claim before that indigenous people had no cavities nor gum disease until after European contact. Do you have a reference that evidences this?

human teeth are rather fragile compared to the teeth of other animals, and the material itself is rather weak compared to other hard biomaterials

Because teeth first evolved to be disposable not permanent... then mammals lost the ability to replace them.
There are two questions here, one about regrowth of teeth the other about tooth composition.
Tooth regrowth
The norm for vertebrates is to keep growing new teeth forever, mammals have lost this ability, the current reasoning is that the ancestor of all living mammals were all small nocturnal short lived insectivores. Because of this we are stuck with a bunch of otherwise counterproductive adaptations, limited numbers of teeth is one of them. insectivores benefit greatly from tightly fitted complex teeth which you can't do with endlessly growing teeth (you can dinosaurs found a way but it is not easy) The current understanding is that mammals used (mutated) the genes that let us regenerate growth centers for teeth into genes that control the shape of teeth which is why mammal teeth are so much more complex than any other group of organisms. Since they were short lived this limited number of teeth would not be a hindrance. Because these genes are now used for something else the only way to get them back would be to recreate them from scratch. (two great books on the subject non mammalian teeth and the (evolution of teeth) Mammals don't really grow multiple sets of teeth they grow one set of teeth over an extended time frame, some mammals like elephants only grow a few at a time but still run out eventually. Note there are one group of mammals that does keep regrowing teeth, cetaceans have re-evolved polydont by giving up the differentiated heterodont complex teeth of other mammals, they have lost the genes entirely. So for mammals the choices are extremely simple endless teeth or a set number of different complex teeth.
Why teeth are made of what they are
Tooth enamel and dentin did not originally evolve for eating things, they developed from the external armor of thelodont fish. The inorganic salts teeth are made from were originally a way of storing calcium, then were used in armor, then were used for their electrical properties, only after all this did they start to get used for processing food. Basically early fish used what they already had available, not a material specifically evolved for shear strength, so now we as their descendants are stuck with it. Evolution involves a lot of jerry rigged solutions, teeth happen to be a good example. Snails for instance have "teeth" (radula) made of a much harder material than vertebrates have, it is actually among the strongest natural materials ever found.
Why human teeth are particularly weak
Now humans have fairly weak teeth because we have much less enamel than our relatives (chimps, early hominids, ect) this is believed to be due to to invention of tools and cooking by our ancestors, cooking, among other things, softens foods. Teeth cost a lot in terms of energy and calcium to produce so if they do not need thick heavy enamel to they will naturally evolve to be weaker so those resources can be used elsewhere. On top of that our jaw is much smaller so there would have been considerable pressure ot make teeth smaller as well. For most of human history our teeth were good enough, only now with advances in medicine and sugar rich foods are we regularly exceeding the operational lifetime of our teeth.
To sum it up mammals are using a disposable structure in a permanent capacity.

Human teeth are strongly attached to a socket, which is not true for many other animals. Our teeth are designed to last our lifetime (specifically up until the point we pass on our genes). Most people's teeth last until they are in their 50s, when the majority of people have passed their genes on.
As for food attacking our teeth, this would be fruit juice, sugar etc. These were not the diet of people years ago, in fact refining sugar is more of a recent discovery. And since that time we have been plagued with bad teeth. I think it was queen Victoria that was first introduced to refined sugar and suffered deleterious consequences quite rapidly.

The amount of food (especially more fiber?) and water consumed might also be significant (in this sugar might provide a double-whammy, dense calories as well as more directly encouraging tooth decay). Chewing on (tougher) low-sugar foods might have some direct tooth-cleaning effect and might encourage more salivation from the food being in the mouth longer (which might also help "wash" teeth). Just "reasonable" speculation.

Adding to your answer; for most of our evolutionary history we lived shorter lives and reproduced at an earlier age. Therefore, our teeth have probably served us fine, and there haven't been strong selection for even more durable teeth. I can also imagine a trade off with other parts of the body for the minerals needed to build teeth, especially in a sometimes poor hunter/gatherer diet.

Sugar is water soluble, so it doesn't stick to teeth. The real enemy is starch found in grains.


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Will lipid molecules 'flip-flop' over a membrane without the use of an enzyme?
All of the references to this I can find refer to enzymes like Flippase making it 'easier' or 'more likely' that the translocation will occur, rather than actually make it possible.
The following is from Alberts

In the ER, however, phospholipids equilibrate across the membrane within minutes, which is almost 100,000 times faster than can be accounted for by spontaneous “flip-flop.”

Does this mean that left unattended, any phospholipid membrane will 'flip-flop' spontaneously, just very slowly, and can this be observed?

Bilayer components will 'flip-flop' at measurable rates, but these are very different for different lipid classes. Here are the results of an experiment using fluorescently-labelled analogues.

Bai, JN and Pagano, RE (1997) Measurement of spontaneous transfer and transbilayer movement of BODIPY-labeled lipids in lipid vesicles. Biochemistry 36:8840-8848 DOI: 10.1021/bi970145r

The authors followed the transbilayer (flip-flop) and interbilayer movement of fluorescently-labelled analogues of various membrane lipids: sphingomyelin (C-5-DMB-SM), ceramide (C-5-DMB-Cer), phosphatidylcholine (C-5-DMB-PC) and diacylglycerol (C-5-DMB-DAG) in a system of unilamellar vesicles consisting of 1-palmitoyl-2-oleoyl phosphatidylcholine.
The results were analysed in terms of a model in which the labelled molecules could move between vesicles and between the two monolayers of the bilayer.
half times:
            interbilayer    transbilayer (flip-flop)
C-5-DMB-SM  >21 s           3.3 h
C-5-DMB-Cer 350 s           22 min
C-5-DMB-PC  400 s           7.5 h
C-5-DMB-DAG 100 h           70 ms

So, for the phospholipid tested the half-time for flip-flop was 7.5 hours.

This answer is a good starting point and gives a flavor of the issue. I think it's worth noting though that there is a pretty big variation between different experiments on flip-flop rates. I think there are orders of magnitude changes, and so a more recent reference would be good. (Anyone interested in this could probably look at the 1997 ref. and see what papers cite it in Google Scholar.)

source: Stack Exchange

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DNA replication Okazaki fragments
I understand multiple origin bubbles; DNA polymerase only synthesizes DNA from 5' to 3' and all that. But what I don't understand is why it has to be in fragments. Yes, DNA is anti parallel, and so the DNA elongates in opposite directions, since DNA polymerase can only go one way. But why not go on just like the leading strand? Why not continue happily along the DNA template continuously but in fragments?

So you mean start at the 5' end of the lagging strand and go the whole way along the chain in one?

If I understand the question, this would require that the entire leading strand was copied first, and then the entire lagging strand would be copied using a primer put in at the terminus of leading strand replication. Apart from any considerations of keeping all of that single-stranded DNA safe from harm, this would mean that replication of an entire dsDNA molecule would take twice as long.

I think you may have been misled by graphic representations of the process: The actual replication fork is very small as, like Rex Kerr mentions, it costs a lot of energy to keep DNA single stranded.
Have a watch of https://www.youtube.com/watch?v=yqESR7E4b_8 at minute 1:45, it contains a relatively realistic representation of the replication fork. Of course you have to imagine all of the space around the molecules in this video to be filled with other DNA, RNA, proteins and small molecules zipping about.
On top of this, we like to think of DNA as a lone double strand where occasionally a protein might attach and do something. Realistically however, most of the DNA is constantly being manipulated by all sorts of proteins (mostly histones for compression, but also transcription factors, methylating and demethylating enzymes, DNA repair enzymes,...). DNA replication has to minimise the interruption it causes to all the mechanisms going on around it, and the most effective way to do this is by replicating the lagging strands in fragments which can be zipped up quickly and left to whatever other proteins might do to it.

Thank you everyone else i ask just keeps talking about EFFICIENCY! thanks alot that is very helpful indded :)

It's in fragments for efficiency.  Single-stranded DNA is not very stable without proteins to stabilize it.  If you tried to replicate the entire strand in one go, you'd need to keep the entire strand in single-stranded form one way or another (e.g. start at both ends and meet in the middle would still leave each half as an old/new duplex, plus an old single-stranded copy waiting to be filled in from the other direction).
To avoid needing a chromosome or genome's worth of SSDNA binding proteins, it works in fragments.
(That is: if you had organisms that had to produce that much SSDNA binding protein, they'd be out-competed by organisms that didn't have to.)

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Is it possible to print humans?
According to this news, scientists can use stem cells to print objects. So say theoretically, is there any possibility to print human beings?

This question has been migrated from scifi.stackexchange as it is not a good fit for our stackexchange site. However I believe it is answerable on this site, biology.se.

When a generic-press article about science says "XXX could be used to do YYY" it generally has to be read as "in at least 15-20 years, an extremely improved version of XXX, that will probably not even resemble to XXX anymore, will be able to be used to do a proof-of-concept YYY." :)

The easiest answer to this question is NO. We will not be able to print humans any time soon, if ever. Despite the potential of the technology, it will likely still make more sense to use stem cells to fight genetic diseases, create limited cellular masses such as hearts and other organs, and to do reconstructive surgeries such as skeletal repairs.
The reasons vary but will include:

The human being is not just a single series of cells, we are a complex melange of integrated systems connected together in a predetermined manner by our genetic code.
The standard 3D printing process might be most effective for producing a single type of cells or a simple organ whose structure is simple and whose configuration could be managed with computer aided design to produce the cells needed at the time of the organ's creation. Even an organ such as a liver will need connective tissues, for blood to be provided for the organ and those cells would need to be integrated as well.
Brain tissue would be the most difficult part of this process. Even having the tissue matrix derived from stem cells would not give us the understanding of how to create an actual brain from a printing process, which uses a layering method to deliver the material into a 3D structure.

It is certain that some things we may do in the future may be done by printing output that resembles cellular matter, i.e. bone repair and restructuring.

In the case of fixed materials such as bone, a 3D model could be taken and then replicated on a printer. The replicated material is then integrated into an area of the body and allowed to either grow in place or artificially stimulated to grow to replace the damaged area.
I use bones as an example since they have very limited purposes and once replicated artificially, would be relatively easy to put in place. This would certainly transform the dental industry, perhaps hip replacement surgeries.
If the technology could be applied internally to damaged tissues, perhaps spinal injuries could be repaired and with proper rehabilitation, a person who may have lost mobility due to an injury could have nervous tissue regrown and learn to walk again.

The potential for specific cellular development is outstanding but the method for growing complete humans has had millions of years evolution and not likely to be surpassed by Humanity in the next thirty to one hundred years unless we come to a far greater understanding of the human genome and the genetic/cellular relationships between systems in the human body as a collective whole.

Any biomaterial scientist working on bone will read this and just think "I wish..." :)

No.
The reason is that development is extremely important for getting tissue organized on the appropriate scale.  We can place groups of cells or a scaffold somewhere, but we can't assemble a working cell from component bits, much less make one that has one end in one's toe and the other in the spine (as is the case with sensory neurons for our legs).
So 3d printing of tissue is limited to tissues that have very simple or robustly automatic developmental processes.  This includes things like skin, liver, and bone; it does not include things like muscle, neurons, joints, or blood vessels.
As technology and knowledge of developmental processes advances, we will be able to print more complex things, but it's not clear to me when or if we'll start running into physical limitations that mean that we basically just have to let things grow and develop the way they normally do.


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Is RGB diode lighting okay for the eyes?
Is a light source giving off light composed of red, green and blue lights harmful to the eyes? Does it lack any important qualities that other artificial light sources, such incandescent lamps or white LEDs may have?
Is it alright to use RGB light panels in a room instead of the usual lighting?

At a fundamental level, no, we're fine with LED lighting.  The absorption spectra of our cones are quite broad, and RGB LEDs are chosen to match our color sensitivity reasonably well.  That red+green looks the same to us as light that is actually yellow is because our eyes can't tell the difference since we don't have good enough spectral resolution in our vision.
There could be more subtle emotional or other complex effects, but to a good approximation, if it looks right it is right, and there aren't magical frequencies that we need to avoid e.g. retinal degeneration or something else awful.  (Well, large amounts of UV are bad, but RGB LEDs don't produce a significant amount of UV.)

Plus, all of the wavelengths in RGB LEDs are also present in white light...


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Are there neuronal firing artifacts produced by head movement?
I'm experimenting with a consumer-grade ElectroEncephaloGram (EEG) sensor and have created the image below using the device. Because the sensor on the device does not use a suction cup, there are a lot of motion artifacts when the headband contact is poor (during motion).

This got me thinking - neurons have mass and thus inertia, and they are not glued to each other.  When the person moves (actually rotates) the head around, forces of inertia are applied to neurons/axons. I'm interested if such motion produces any kind of firing artifacts within the brain or how the brain filters out such firing?
This reminded me of this article: (5-HT and motor control: a hypothesis). Could it be that some neurons stop firing in response to movement?

There are certainly head-orientation cells (e.g. in the hippocampus).  But neurons are reasonably immune to the kind of mild physical stresses that come from turning the head around; computing head orientation requires complex analysis of input from e.g. the visual system (optic flow) and vestibular system.
However, the electrical activity of muscles tends to swamp that of (nearby) neurons, so various muscle-related artifacts are often visible in an EEG if not carefully filtered out.  And, of course, if the contact is poor you'll get artifacts from that: you're just measuring the variability in resistance between the sensor and your skin, not anything interesting about what faint potential changes are visible at your skin as a result of neuronal activity.


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Is it possible for a person to become "reinfected" with the same strain of a virus?
If a person contracts a virus, viral conjunctivitis for example, is it possible for the individual to become "reinfected" with the exact same strain of the virus once the person has it treated and the symptoms have gone away? I am a nursing student and am fascinated with virology, but my basic microbiology class did not go very in-depth on the subject.

I think norovirus might be a example. Although patients develop immunity after recovery, the immunity wanes quickly. So a person can contract norovirus for multiple times. I don't know whether it's because of viral mutations.

The nature of infectious agents is that they transmit between organisms. This means that they have reservoirs outside a single host, and hence of course encountering the exact same strain twice is possible if this strain leaves the body and at a later stage is carried back to it. This could typically happen for example with influenza or common cold viruses, spreading from one child to other children at school and later being carried back to the original child through them.
The reason why the child will not develop another illness when being exposed to the same virus again is the adaptive immune response: After the first infection, immune cells specific to a pathogen will proliferate and differentiate both into effector cells to destroy the pathogen, and into memory cells. These can mount a much stronger immune response much faster when they come in contact with the same (or a structurally very similar) pathogen, meaning that a secondary exposure usually does not result in a proper infection and illness. Of course, this mechanism doesn't work properly for anyone with a compromised immune system.
In most cases where a viral disease develops repeatedly, this is due to evasion mechanisms. For example in some viruses, those antigens which tend to be targeted by immune systems have high mutation rates. In this case the "same" virus is actually a mutated strain which causes the same illness, but "looks" different to the immune system, and so the memory cells don't respond. Again, influenza is a great example. The reason why we get flu again winter after winter, is because this virus tends to mutate over the year with relatively low infection prevalence. Then during the winter, when the conditions are favourable for flu infections, typically only a small number of strains cause epidemics - because we were maybe immune to last year's influenza, but this year's has mutated antigens which our immune systems do not recognise yet.

Much better! I'm removing my down vote and deleting the comments you've addressed. I'll upvote if you add some references :) I know it's a pain for answers you pull from your general knowledge, but it's how we keep things honest here!

Exactly that - the Q is asked at best around first-year undergrad level, so I wanted to keep it simple. WP links should suffice for a reader here. Your answer complements this very well with more depth and detail, you're clearly more familiar with this field than me :)

@DeNovo: Actually could you repost the comment regarding winter prevalence of influenza? I had no idea about that (I'm guessing this is more recent than my degree), and thought it was an interesting detail to add on this topic.

i don't remember exactly what I said, but it was probably something about the immune system not being "weaker" in the winter and seasonality being a function of a virus, not the immune system. Influenza has a winter peak because it is more stable in dry cold conditions. Other viral infections (e.g., enteroviruses, arboviruses) have a summer peak.

As discussed in @Armatus's answer, the adaptive immune response can protect against or severely limit the progression of re-infection.
Viruses have a number of ways to escape the adaptive immune response (see Murray Medical Microbiology Ch. 48). They can interfere directly with the immune system (e.g., preventing interferon action or suppressing antigen presentation), they can hide from some parts of the immune system (e.g., by spreading directly from cell to cell, or maintaining a long intracellular latent period). Some viruses are empirically less immunogenic, resulting in waning immunity. A given viral species can have a very large amount of antigenic variability, and/or a high mutation rate for important antigenic sites. Some of these escape mechanisms help maintain an initial infection and some reduce the effectiveness of a memory response on re-infection.
Viral conjunctivitis is caused by one of several serotypes of adenovirus. Generally, infection is believed to produce protective immunity against the same strain (Ch. 52, Murray Medical Microbiology), but there are many different serotypes and, perhaps more importantly key antigens are highly variable. Adenovirus uses a few other strategies to escape the adaptive immune response. The virus can enter a latent intracellular phase (avoiding the humoral response) and block a number of important effectors of cell mediated immunity with small interfering RNAs (avoiding the cell mediated response). Despite this, infection does result in seroconversion, and empirically, protection against reinfection by the same strain (Murray Ch 52 again).

Viruses that mutate quickly (particularly notorious are respiratory viruses such as the flu and common cold) quickly produce new "strains" within the same virus family. While most people should be familiar with the terms "influenza A" and "influenza B", those are merely blanket terms for a large family of viruses with thousands of strains (by surface structure). Immunity against a given strain is no guarantee of immunity to a different strain.
In the general case, reinfection with an exact same strain previously recovered from is possible if the immune system "forgets" the pathogen (which happens with some infections, hence the need for periodic booster shots) or if the person becomes immunodeficient.

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How do sharks and other fish conserve and gain water in marine environments?
With the osmolarity of the average vertebrate being around 300mOsml, and salt water having an osmolarity of 1000mOsml, why does the water from the shark not leave to the salt water around it?
I presume the scales must act as a barrier to stop water form leaving, but with the blood vessels being exposed to the saline water in the gills, why does water not leave the body?

The mechanisms of osmoregulation is different for sharks (and other elasmobranch fishes) and teleost fishes.
In Elasmobranchs the body osmolarity is maintained equal to the seawater by Na⁺ Cl⁻ and urea. Toxicity because of high concentrations of urea (strong chaotrope) is counteracted by high levels of trimethylamine oxide (TMAO). So, the elasmobranchs do not need to drink water to prevent dehydration. But sometimes they do drink water for adapting to different salinity levels [1].
Teleost fishes, however, need to drink water in order to prevent dehydration. Initially Na⁺ and Cl⁻ are absorbed in the esophagus via cotransporters (Na-Cl/Na-K-Cl), thereby reducing the osmolarity of water. The cells that absorb Na⁺ maintain its low concentration by pumping extra Na⁺ in the Extracellular fluid, using Na⁺/K⁺-ATPase. Cl⁻ is also exchanged with Bicarbonate (HCO3⁻) via anion exchangers [2].
.


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How can I view modENCODE data faster?
I am trying to view several data tracks in the modENCODE GBrowse genomic browser. However, the site is so slow, it is practically unworkable. Is there a faster way to explore the data?

I have no experience with this, but apparently you can download it: http://www.modencode.org/publications/faq/#How_do_I_access_modENCODE_data.3F

Download the data and parse locally..

Options:

You can always download the data (as @WYSIWYG has suggested in the comment).
Transfer the data to Galaxy
Convert and export the selection of your choice.

Source: http://modencode.oicr.on.ca/fgb2/gbrowse/fly/


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Does anyone know what marsupial this is?

I know what this is a marsupial, but i'm not quite sure which one. Any thoughts?

Why was this closed? Species identification questions seem to be on topic and this is no more localized than any other such question. @mad-scientist?

I think the OP could have included information like where the photo was taken? But still I am inclined to agree - I have seen many similar questions on here that were not closed.

@terdon I closed it mainly because it was self-answered in a very short time and because the question and the answer don't contain much detail

I had not taken the photo myself; I had received it from lecture notes that did not give any information about the photo. The reason I answered in such a short time after posting it was because I had asked an Australian friend of mine, and he got back to me not long after I had asked the question. So I thought it was best I answer it. As for the detail in the answer, the question was just relating the species, nothing else.

I can see how it looks suspicious though! Sorry!

I've been told it is the marsupial 'Myrmecobius fasciatus' commonly known as the numbat.
http://en.wikipedia.org/wiki/Numbat


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By what mechanism does elevated homocysteine level cause endothelial dysfunction and damage?
It has been stated that elevated homocysteine level causes endothelial dysfunction and damage. By what mechanism does this happen? Why is it the endothel where elevated homocysteine causes problems?

In addition Alan Boyd's answer homocysteine interferes with Glutathione synthesis by reducing the catalytic efficiency of GCL (Glutamate–cysteine ligase), the enzyme which performs the rate-limiting step in GSH synthesis.

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2267299/
Results of the present study are the first to suggest that the relatively high levels of homocysteine that accumulate during aging can interfere with de novo GSH synthesis. Although the precise nature of the underlying mechanism is at present unclear, our results demonstrate that physiological concentrations of free homocysteine can inhibit the efficiency of cysteine utilization by GCL in a competitive manner. Homocysteine has been shown to bind GCLc at the active site in vitro [25] as well as in vivo [35], forming γ-glutamylhomocysteine [36], which is then rapidly degraded enzymatically. An additional mechanism by which an age-related increase in free homocysteine can inhibit the catalytic efficiency of GCL in a competitive manner is described in [35]. It is possible that an aging-related increase in the competition between cysteine and homocysteine for the cysteine binding site of GCL might lead to a decrease in GC synthesis.

Low glutathione means a reduced ability to detoxify and deal with oxidative stress and a more oxidised redox state which has many implications
Further reading:
Inhibition of glutathione synthesis in brain endothelial cells lengthens S-phase transit time in the cell cycle: Implications for proliferation in recovery from oxidative stress and endothelial cell damage
http://www.sciencedirect.com/science/article/pii/S2213231713000244
Glutathione reverses endothelial dysfunction and improves nitric oxide bioavailability
http://content.onlinejacc.org/article.aspx?articleid=1125915

Short answer: homocysteine promotes elevated levels of reactive oxygen species which interfere with signalling via nitric oxide.
There is an extensive literature on this topic: a Web of Science search using [TITLE: endotheli* AND homocysteine] produces 567 hits.
The prevailing view seems to be that homocysteine causes oxidative stress in cells because autooxidation of the sulphydryl group of homocysteine promotes the production of reactive oxygen species (ROS): superoxide, hydrogen peroxide and hydroxide radical. There is also evidence for decreased levels of glutathione (GSH) and glutathione peroxidase (GPX) (McCully, 2009). The classical pathway for dealing with ROS is conversion of the primary species,superoxide, to hydrogen peroxide (by superoxide dismutase) followed by reduction of peroxide to water by GPX using GSH as a reductant. This pathway rapidly destroys ROS and importantly avoids the generation of the damaging hydroxide radical. Reduced glutathione is regenerated at the expense of NADPH.
Endothelial cells use nitric oxide (NO) to signal to surrounding smooth muscle, resulting in vasodilation. ROS react with NO, inactivating it. There is also evidence that NO production by epithial nitric oxide synthase (eNOS) is affected, and Leung et al., 2013 present data indicating that the phosphorylation level of eNOS is reduced by homocysteine. Phosphorylation is a key regulator of eNOS activity (Mount et al., 2007).
Leung SB et al. (2013) Salidroside Improves Homocysteine-Induced Endothelial Dysfunction by Reducing Oxidative Stress. Evidence-Based Complementary and Alternative Medicine 20: Article ID 679635
McCully, KS (2009) Chemical Pathology of Homocysteine. IV. Excitotoxicity, Oxidative Stress, Endothelial Dysfunction, and Inflammation. Annals Clin. Lab. Sci. 39:219-232
Mount, PF et al. (2007) Regulation of endothelial and myocardial NO synthesis by multi-site eNOS phosphorylation. J Molec. Cell. Cardiology 42: 271-279


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By what mechanism does elevated homocysteine level accelerate thrombin formation?
It has been stated that elevated homocysteine level accelerates thrombin formation. By what mechanism does this happen?

According to a heavily-cited paper (below), homocysteine reduces the expression of thrombomodulin on the surface of endothelial cells.
Thrombomodulin binds to thrombin, and the resulting complex does not promote coagulation, but instead activates protein C. Protein C has an anticoagulant effect. Thus reduced levels of thrombomodulin will result in increased levels of free thrombin (promoting coagulation) and in reduced levels of protein C (also promoting coagulation).
I haven't found any evidence that homocysteine has an effect upon thrombin formation directly.

Lentz,SR and Sadler, JE (1991)Inhibition of thrombomodulin surface expression and protein-c activation by the thrombogenic agent homocysteine. J. Clin. Invest. 88:1906-1914
Abstract Elevated levels of plasma homocysteine are associated with both venous and arterial thrombosis. Homocysteine inhibits the function of thrombomodulin, an anticoagulant glycoprotein on the endothelial surface that serves as a cofactor for the activation of protein C by thrombin. The effects of homocysteine on thrombomodulin expression and protein C activation were investigated in cultured human umbilical vein endothelial cells and CV-1(18A) cells that express recombinant human thrombomodulin. Addition of 5 mM homocysteine to endothelial cells produced slight increases in thrombomodulin mRNA and thrombomodulin synthesis without affecting cell viability. In both cell types, thrombomodulin synthesized in the presence of homocysteine remained sensitive to digestion with endoglycosidase H and failed to appear on the cell surface, suggesting impaired transit along the secretory pathway. In a cell-free protein C activation assay, homocysteine irreversibly inactivated both thrombomodulin and protein C in a process that required free thiol groups and was inhibited by the oxidizing agents diamide or N-ethylmaleimide. By inhibiting both thrombomodulin surface expression and protein C activation, homocysteine may contribute to the development of thrombosis in patients with cystathionine beta-synthase deficiency.


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"Oblong to Allantoids" .... Is it valid?
I read on the text book:
The characteristic of Dinemasporium are: superficial, cupulate to Discoid conidiomata with brown satae, Phialid conidiogenous cells that give rise to hyaline, oblong to Allantoids, and Aseptate conidia with an appendage at each end.
My question:
the phrase "oblong to Allantoids"; Is the word oblong valid for this context? if not, what other word would associate?

Oblong is probably correct in this context, but "allantoids" should probably be "allantoid" to be the adjective form. It's describing translucent (hyaline), oval (oblong) to sausage-shaped (allantoid), undivided (aseptate) spore.

Thank you, I should have referred to this link.


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Does the human ear adapt to noise levels?
I have noticed lately that if I go to sleep, when I have my radio running, it is on lowest volume, I still consider it kind of loud.
In the morning, when being on the edge of waking up, I hear the birds, and the tennis balls already being batted on the court nearby, but I do not hear my radio. If I wait a few more minutes, I start to hear the radio, with no changes in the sound levels outside.
I know that the human eye adapts to the light levels (aperture, what cells used), but is there something similar for sound sensitivity?
Note, the radio is on that occasion running all night long, with always the same sound level.

In  this instance, I would say your attention has been adjusted, not your ear's ability to perceive sound. Our ears don't have a control setting or a means of adjusting incoming sound levels (though I'm certain when an ambulance with loud siren drives by, we all wish we did).
What you are experiencing is a prioritization of the sound by your brain in relationship to other sounds.

You put the sound on before you go to sleep. Your brain accepts that incoming sound as non-vital, non-threatening sound. (Radio, meant to soothe, supposed to be there, relegate this sound to innocuous)
Come dawn, new and novel sounds appear. For our brains, the new and novel could indicate a threat, so your brain prioritizes that sound over the known and considered innocuous sound (your radio) which it has heard all night. Birds, tennis balls on courts are distinctive enough your brain would prioritize them even though you know in your conscious mind neither is an actual threat.
As you waken, your brain then reminds you there is still another sound in your environment which is not threatening and yet still prevalent (your radio) prompting you to decide if you want to do anything with the non-threatening sound.

Yes, this is an oversimplification of a very complex process of sound prioritization but most modern science bears this out. As a curiosity, our minds are predisposed to seek out information which may be vital to us, hence the reason conversations held by other people who are on the phone are so distracting because our brains dislike hearing things which may be necessary to our survival but only hearing half of the conversation.
EDIT:
As I was reminded there are some involuntary control elements built into the ear via:

the tensor tympani muscle whose role is to dampen sounds (mainly internal ones such as chewing)
and the stapedius muscle which dampens the ability of the stapes vibration and protects the inner ear from high noise levels, primarily the volume of your own voice.

You can thank the stapedius muscle for making your voice sound so strange to you when you hear it on a recording. You have never truly heard your voice until you hear an external recording and playback of it!

Although I think you are correct about prioritization as the reason behind the described phenomenon, I disagree that "Our ears don't have a control setting or a means of adjusting incoming sound levels". The tensor tympani and stapedius both help attenuate the mechanical response to loud sounds.

Then perhaps the word I should have used was a "conscious" and controllable ability to regulate unwanted sound...I would be completely deaf when my son starts his thrash metal music with the dial at 11...


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What's the difference between shotgun sequencing and clone based sequencing?
In a lecture during  my undergraduate degree we were introduced to the race to complete the human genome. Celera were competing with Sanger and collaborators to sequence the human genome. Celera wanted to patent some sequences, whilst Sanger et al. wanted to keep their findings in the public domain. Celera knew they couldn't compete with Sanger et al. with conventional cloning techniques which required a lot of man-power, "so instead opted for shotgun sequencing".
To me it seems like both clone based sequencing and shotgun sequencing could have been used together, however the lecturers semantics were a bit vague (...okay, I wasn't paying close enough attention!) and I didn't ask for clarification at the time.
Whilst I appreciate this is a large topic, what are the main differences between Celera's shotgun sequencing and Sanger's clone based sequencing during the late 1990s? Are "shotgun cloning" and "clone based sequencing" actually mutually exclusive terms?

Umm, you realize that an answer to this will be quite a few pages long right? Why don't you look up some of the common sequencing technologies on wikipedia and post a more specific question?

What a coincidence, I happen to have had the exact same question, also from a lecture during my undergraduate degree, within the same context of the human genome project. I suppose the lecture notes haven't changed that much...

The v short answer is that in shotgun sequencing, the sequencer is fed a set of random sequences from the target.  This can be done for instance by mechanically shearing DNA and then building a set of shotgun sequencing jobs which are then compiled back together by a genome assembler (i.e. in whole genome sequencing projects) into a full sequence.
In clone based sequencing, the DNA to be sequenced is specifically sectioned off into sequence copied into of plasmids (BACs - bacterial artificial chromosome) to divide the sequencing job into sections- a divide and conquer strategy.  BACs can be 150 kb long just to give you an idea.
These are not mutually exclusive terms; clone-based sequencing projects usually use the large clone libraries to section the project into a set of shotgun sequencing projects.

In short: the basis of the process is the same in both, the difference relies that in the clone based sequencing you make DNA library of the pieces of DNA clones you got from the sequence you used in first place. Like that, data management and the mounting of DNA contigs will be a lot easier computationally speaking.
In shotgun sequencing the same is done but without the cloning and libraries, you directly mount contigs from sequenced sequence pieces, thus better computers are needed.
Also I think your terminology is wrong: shotgun strictly means the sequencing based on the random shearing and consecutive construction of contigs. I think you better mean whole genome shotgun sequencing with "shotgun sequencing"(as the clone based sequencing also is a shotgun sequencing method).

"To me it seems like both clone based sequencing and shotgun sequencing could have been used together,"
I believe they were.  The public project cut up the genome into BACs and shotgunned every BAC, and then put the BACs together, while Venter used some sequence position information from the public effort to help him place his shotgun pieces.
https://en.wikipedia.org/wiki/Human_Genome_Project


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What is solid-phase bridge amplification?
During Illumina sequencing there is a step called bridge amplification by which DNA is amplified by isothermal enzymes. What is this stage, and how does it work?

This stage is after the adsorption of the adapter-ligated fragments on the flow cells.
The fragments are isothermally amplified to generate clusters [1]. The exact nature of the enzyme mix that catalyses this step is not disclosed by Illumina. I assume it must be similar to Helicase mediated isothermal amplification, which uses helicase and single strand-binding proteins (SSB) to denature the template. The polymerization is catalysed by a mesophilic DNA-Pol such as Klenow (E.coli).


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Breeding laboratory mice with cancer; how does this work?
It has recently been brought to my attention that live laboratory mice with specific cancer strains can be readily purchased for medical research.  For example, the Jackson Laboratory sells mice with a wide range of strains of cancer (with price depending heavily on the type of cancer desired).

Question: What is the general process behind breeding laboratory mice with specific cancers for medical research?

I could imagine a) they inject a few cancer cells from an in vitro culture which, being cancer cells, find a niche to proliferate; or b) the genes causing the cancer type are known and they produce a local knockout/knockin/knockdown in order to get the cancer started.

It really depends... for instance we have transgenic mice with a specific mutation in a protein controlling cell cycle that spontaneously develop certain tumours when adult/old. Other tumours can be induced by giving specific substances.

Cancer is a highly genetic disease, and much is known about how different genetic mutations contribute to the generation, growth, proliferation, metastasis, and control of tumors. Jackson Labs (commonly known as Jax in the research community) provides literally thousands of strains of mice, each bred/genetically engineered to have certain genotypes and/or phenotypes, a good proportion of which can be used for various purposes in cancer research.
I'll take a very basic example to walk you through the creation of a "cancer mouse." Say I've been doing research and have found through studying the DNA of many patients that the ABC123 gene seems to be associated with a certain type of cancer (skin, for example). I want to know more how ABC123 works, so one of the first things to do is to find out what (if anything) goes wrong when it isn't there - when it gets "knocked out." Using genetic engineering techniques, I create a sequence of DNA (called a vector) that matches the "wild-type" (WT) or normal mouse ABC123 gene sequence at the ends, but in the middle has a certain selection gene called Neo instead of the rest of the ABC123 sequence:

Neo makes cells that it is in resistant to a certain antibiotic called Neomycin or Geneticin, also called G418. I take my targeting vector and electroporate it into mouse embryonic stem cells (ESCs) that, if implanted into an appropriately-prepared female mouse, could develop into a normal mouse embryo. I then culture these ESCs in the presence of neomycin, which will kill any cells that haven't taken up and incorporated the vector into the genome.
Once I have some cells that I know have taken up the Neo part and are missing the targeted part of the gene (the exons marked 1, 2, and 3), I inject a few cells each into mouse blastocysts, where they divide and differentiate to form various parts of the new mouse.

This is a chimeric mouse, with different cells coming from different origins, either wild-type or ABC123-mutant. I try to generate a number of different chimeras to breed together in the hopes that at least some of my original injected mutant cells went on to form the gonads, and the mutant gene can be passed on to its offspring. I then breed the various chimeric mice to WT mates in hopes of producing heterozygous offspring, which have one copy of the WT-ABC123 gene (from one parent), and one copy of the mutant-ABC123 gene (from the other parent). These mice can then be bred together to produce homozygous "double-knockout" mice, which I can then use to study my gene's effects and its possible relation to skin cancer. This is the type of animal typically sold by Jax, although this depends very strongly on the gene being studied.

Now, there are many issues that can arise along the way, such as the mutation being embryonic-lethal, causing sterility, or other defects that don't allow you to produce true knockout mice. Much can still be learned, though, and scientists have gotten very inventive in producing functional animal models of previously-difficult mutations. For example, it is possible to engineer a strain that only becomes a knockout when you feed it a certain chemical in its water, or is only knocked out in certain cell types or tissues. Some gene functions are only apparent when two (or more!) genes are knocked out at the same time. Genetics is incredibly complex, but fascinating, and more and more complex tools are being developed all the time to assist scientists in their research and ultimately help people overcome illness and disease.

Just a very minor correction: although geneticin and G418 are the same antibiotic, neomycin is a different molecule (although they are both aminoglycosides). Resistance to both is conferred by an aminoglycoside 3' phosphotransferase, and the gene encoding this enzyme is often designated neo


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Storing Apples at 30F?
This article about storing apples for the winter says:

You do not want the apples' temperature to fall below 30°F (-1.1°C), however,
  because that will make them freeze and turn to mush when they're
  thawed. Their cell walls will all collapse.
Therefore, apples are best stored somewhere around 30-35°F (-1.1 to 1.6°C), in a humid environment.

I don't understand why you should keep the apples below the freezing point of water. Why would damage only occur below 30°F (-1.1°C)?
Is the article correct?

This temperature range would be a compromise between a very low temperature needed to limit natural decay or decay triggered by micro-organisms (the lower the temperature, the lesser the decay) and the formation of destructive ice crystals.
Only pure water freezes at 0°C (32°F) under atmospheric pressure. But the content of apple cells and cell walls is a rather complex aqueous solution, containing many natural cryoprotectants, among which the fruit's sugars. Therefore, the freezing point of apples might be as low as 30°F.

OK but when it says "in a humid environment" wouldn't the apple be covered in ice (damaging its skin)?

They would be covered in ice if the air were saturated with water. In this case humid means that a dry environment has to be avoided. e.g. keep 80% relative humidity.


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SNPs mapping into protein
Starting a new project on protein-protein interactions and SNP analysis tool development. I would like to ask how does SNPs is mapped into protein? What does mapping means?

I assume SNP means Single-Nucleotide Polymorphism? I'm confused exactly what your question is - how does one take a SNP and see what effect it has on the protein sequence? Is that it?

Well SNPs are single nucleotide polymorphisms. Some SNPs are in the coding regions of genes and they can result in changes in the resulting protein. For example, the SNP rs1801131 is a human variation where some individuals have a G instead of an A at position 1515 of the gene MTHFR. When the gene is transcribed and then translated into protein, this variation (the presence of the G nucleotide) causes a Glutamate residue at position 429 of the protein to be a Glycine instead.
So, SNP rs1801131 maps to position 429 of the protein MTHFR.

@MattDMo you've got a dirty mind... :)


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Why is Sanger sequencing inferior for detecting SNPs in cancer cells?
I am familiar with Sanger sequencing, but at the level of an undergraduate. A lecturer of mine tried to describe Sanger sequencing as losing the sequence information in noise when used to detect cancer. This paper also says "lacks sufﬁcient sensitivity for detecting mutant alleles in tumor biopsies,"(Thomas et al., 2006). What is it about Sanger that makes it too insensitive for SNP analysis?
Thomas, R.,K., et al. (2006) Sensitive mutation detection in heterogeneous cancer specimens
by massively parallel picoliter reactor sequencing. Nat. Med. 12, 852–855

As I understand, Sanger sequencing has low error rates compared to the NGS. But high throughput and whole genome coverage is difficult.

In the Sanger approach, DNA would be isolated from the biopsy and would contain both normal alleles and mutant alleles of genes associated with the development of the tumour. If, for example, PCR amplification was then used to derive a sample of a target template region, this material would end up being sequenced as a mixed population: the derived sequence would be an average of that population of sequences, and rare alleles would be masked.
The key difference in most next generation approaches is that the template DNA is "cloned" physically (e.g. by sequestering individual molecules into droplets, or by binding them to a surface) so that the sequences of these individual molecules can be determined in parallel. This approach would reveal tumour-associated polymorphisms when the sequences of the individual template molecules were compared.
Added later as supplementary information.
I have now looked at the paper cited in the question. This quotation from the Introduction bears out my main point about sequencing a mixture of templates differing at just a few key positions.

Although commonly used in many clinical settings, dideoxynucleotide chain termination (or ‘Sanger’) sequencing of PCR products often lacks sufficient sensitivity for detecting mutant alleles in tumor biopsies, where the failure rate has reached 75% in some cases. Gain-of-function oncogenic mutations are frequently heterozygous events or may represent a single allele of an amplified gene; thus, the signal for mutated residues is typically reduced relative to neighboring bases. Moreover, the ability to detect single base mutations or small insertions or deletions in biopsy material by Sanger sequencing depends heavily on sample purity (for example, the extent of contaminating stromal DNA) and genomic DNA integrity. Furthermore, resistance to kinase inhibitors may correlate with low-frequency second-site mutations. These observations underscore the challenges for accurate mutation detection in cancer specimens.
A massively parallel sequencing-by-synthesis approach, ‘picotiter plate pyrosequencing,’ provides a new alternative to Sanger sequencing. This approach relies on emulsion PCR-based clonal amplification of a DNA library adapted onto micron-sized beads and subsequent pyrosequencing-by-synthesis of each clonally amplified template in a picotiter plate, generating over 200,000 unique clonal sequencing reads per experiment. Sequence variants that represent a fraction of a complex sample can be vastly oversampled, thus enabling statistically meaningful quantification of low-abundance variants.

Sample issue would be with both sequencing strategies. Sanger sequencing is still used to confirm the de-novo sequences because of its low error rate. Cloning is also involved in both techniques but in Sanger you may need to prepare BAC libraries. The problem of Sanger is only with respect to its amenability to high throughput. [NGS wasn't there when most of the human genome got sequenced]. PS: Sanger is also relatively cheaper.

This is a recent paper in which two unicellular algae were sequenced using Sanger.

@WYSIWYG I'm not sure what either of these comments is adding. There is no question that Sanger sequencing can be used to derive genome sequences, since as you say it  has been so used. My interpretation of this question was that it relates to a scenario in which a mixed sample is to be sequenced, which creates problems for using Sanger sequencing, as I have tried to explain.

I understood the point of this paper. In this paper, I think the comparison is not between the technologies. Genomes from each cell can be separated using the picolitre plate(or other nanofluidic devices) and parallely sequenced. As Sanger sequencing fails to handle high throughput, the choice is sequencing by synthesis.

@AlanBoyd Your answer summarised the information in the paper very nicely. The paper makes sense after reading your answer! I still don't quite understand "Furthermore, resistance to kinase inhibitors may correlate with low-frequency second-site mutations."


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Why do ants dig surface paths?
A few days ago I observed a corridor built and used by ants that went over a path in fields:

Why do they build it? It seems it doesn't bring any considerable protection from the surrounding environment and it certainly costs them a lot of work.
The picture was taken in the morning when the temperature was low so there is no ant activity visible.

How is that "protected"? It looks to me like there is a natural "cliff" which the ants are simply walking along.

@terdon No, I'm quite sure they built it for some reasons. I've seen many of these structures on that place. You're right, I don't know if it's for their protection or for anything else.

I mean I do not see any protection. Since there is no wall on the "southern" side, there must be a difference in altitude between the "north" and "south" areas pictured. If the ants were creating this path by walking down it, there would be walls on both sides. At best, perhaps the ants created the path just by walking down it, if there is a difference in altitude that is exactly what would result with no active effort from the part of the ants other than the act of walking. That is how paths are formed after all.

@terdon The location is completely flat, and the ants walk inside the structure, so they're covered from both sides. Most these structures have only the side walls, but it looks like this one is being covered from the top as well at the ends. I'll try to find the place again to see if they'll eventually cover the whole path.

Well, that's the thing, It can't be flat, if it were there would be no wall or the wall would be higher than the surrounding area which is not the case. The overhang would be created naturally by the ants' walking down the path and does not imply that it was done on purpose.

@terdon The surface that surrounds it flat, the structure is not. I'll try to make a better picture.

I wonder if this might be an extension of nest-building behavior.  the dirt that runs along both sides of the path looks like debris from nest cleaning.

Ants like to keep their routes clean from debris. I think they just overdid it on this one or for some reason the surface itself looked like debris to them.

It kind of looks like there is a wall on the bottom side but it's really hard to see the edge of it as it blends in, making it appear flat.

I don't have it with me, but the book Adventures among Ants by Mark Moffett, which I highly recommend if you're even vaguely interested in ants, describes the creation of paths such as this. Some ants apparently build underground "highways" of a sort, and such a sunken path is indeed an intermediate step in the construction of such. I can't remember the specific reasons given in the book but I expect protection (if not from the elements, then from other insects and rival ants in particular) and efficiency (it minimizes ants wandering around for that bit of their journey) would be involved. Given how short the path in the photo is it might also be an underground path that the ceiling caved in on for a section.
I am not saying that this is what your photo shows, or even that the ants you were looking at typically make such paths, and I realize that I am technically not even answering your question, but I hope that a confirmation that this is a phenomenon that happens and the recommendation of a book that will answer your question is a decent start.
EDIT - Found the book !
The ant species described in this section is the Marauder ant, a species from India so probably not the one you saw. But the motives described in the book could be transferrable. A few quotes from the chapters "Roads" and "Defense":

Marauder colonies maintain a fast, steady, well-protected flow of food and labor on their trails. Whereas small ant colonies, like people in small societies, are able to access and distribute the supplies they need without roads, larger groups depend on an infrastructure so complex that in the marauder ant it rivals human highway systems.(...)
Marauder colonies avoid both gridlock and species confrontations, like that with the Diacamma worker [an encounter described at the beginning of the chapter where killing that errant worker of another species involved major disruption in the flow of traffic], when trails are in good shape. Highway construction efforts are part of the society's logistics, providing supply lines for fresh combatants on the front lines as well as streamlined routes for bringing home the plunder[2]. Trunk trails are well looked after - that's how they can be distinguished from the fleeting paths created by raids

The note after "plunder" points to the following:

The lower cost to ants of sticking to clear paths rather than going over rough ground is addressed in JH Fewell 1988, Energetic and time costs of foraging in harverster ants, Pogonomyrmex occidentalis, Behav. Ecol. Sociobiol. 22:401-408.

A description of the building of the trails, which matches some of how the picture looks like:

Each worker size class participates in the creation of the roadways. All the castes eliminate surface irregularities along a trunk: while the medias[medium-sized caste] and majors[big ones] chisel out embedded roots and pebbles, minor workers[little ones] extract grains of soil, establishing the road's slightly concave shape in cross-section. The dross is discarded along the edges of the trail, where it accumulates in embankments(...). When the ground is moist, the minor and media workers build up the ramparts into a complete soil cover, or thin-roofed arcade, fabricated from soil extracted from the trail surface or from mining shafts - blind-ended tunnels near the trail used specifically as quarries.

Giving some reasons for their existence:

To what use is all this effort? Not, it seems, as protection from the elements. The earthworks fall apart in rain, and disintegrate when the earth is dry. Arcades are thin enough to puncture with a tap of a finger, which means a route is weatherproof only when it travels through an underground tunnel, perhaps dug and then abandoned by other animals. Alternatively, near the nest the ants may make a subterranean route of their own: over time, construction crews can scratch away so much soil from the trail surface that the highway sinks from view, at which point the ants seem to be able to construct a thicker, rainproof cover that becomes flush with the surrounding land.
The main function of this relentless building is defense. Because trunk trails extend for dozen of meters, they travel through territory controlled by other ant species. Marauder ants must therefore be organized to protect the trunk trails from aggressive neighbors or even from hapless passerby such as the Diacamma.(...)
...after an arcade has been completed[,] the Diacamma workers could now walk over the trunk trail, blissfully ignorant of the industry below them. if a trail should sink underground, it is as protected as a passage in an army bunker, safe even from human footfalls.
Bulwarks constructed over trails and provisions prevent battles among competing marauder ant colonies as well. Where they are absent, combat can last a day and engage thousands of minor workers, which pour along the line of contact between the armies.

Are there trees ? The only thing this seems to stop is leave litter and small grains from blocking the path when there is a slight breeze. They build other structures for rain and seem to build less of these where there is shade and more where there is sun and nothing much to eat or hide under. But thats just from a few observations walking larve areas. When ita going to rain they take sticks and thing and make a cone structure around the entrances. Initially the just clear paths and collect food. Thats from the karoo eastern cape south africa, dry lands with large areas that get really hot and some patchs with trees (acacia karoo, thorn tree small leaves) have more ants.


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If Evolution Is In Progress, Why Fight Extinction?
Natural selection is a central tenet of evolution. However, most biologists seem determined to prevent the extinction of the species that have been selected against. Why is this? Preservation of genetic diversity?
I thought evolution was supposed to create diversity not destroy it. What am I missing?

We're not trying to prevent extinction - species go extinct all the time. We're trying to prevent extinction caused by man. One of the big things that sets us apart from other species is how massively we manipulate the environment we live in. Some of those manipulations have a high destructive potential, and we do not understand ecosystems well enough to confidently say that destruction of species caused by us would go without lasting effects that we'd rather avoid.

@Armatus Couldn't the same argument be made for invasive species?

Evolution by natural selection is not progress but adjustment toward a local optimum; the local optimum changes with environment (which includes the biological systems that change to seek a local optimum).  One might also ask why librarians and scholars seek to preserve publications that seem to present outdated ideas; existing biological systems contain historical information and formerly isolated systems present convenient laboratories for improving understanding (much of the anti-extinction effort is compensating for artificially increases mixing).

Yes, hence why they're trying to contain invasive species, or at least protect those species they're threatening. Same reason goes for containment of genetically engineered organisms as well.

@Armatus How does evolution pre-humans deal with the issue of invasive species? Aren't invasive species the "fittest" creatures that evolution through natural selection favours? Doesn't survival of the fittest imply an expense to the less fit aka non-invasive or native species? Why should humans interfere with invasive species? The fittest survive right? Genetic engineering would deserve its own question.

@PaulA.Clayton Doesn't natural selection assume that a local optimum (emerging species) is superior to a more global optimum (aka invasive species)? If it were only about preserving outdated ideas we would merely sequence their genes and let the endangered species die--that would be much cheaper in many cases. You mention "artificially increased mixing," but you ignore the fact that for much of early history the world is believed to have been a single continent, which means "mixing" back then was naturally easier than today and likely comparable to human induced mixing of the present.

Again, invasion may also happen in nature and we are not trying to prevent invasion itself. We are trying to prevent invasion caused (directly or indirectly) by humans, again because we cannot determine the effects it may possibly have on the invaded ecosystems and hence we try to avoid potential problems. The whole idea is that we want to prevent a nature that evolved based on human manipulations.

"Survival of the fittest" is not a central tenet. Scientists strongly prefer the term "natural selection".  Evolution is a very stochastic and opportunistic process, and much of it is not necessarily "progress" in the common sense. Are cows evolutionarily superior to elephants because we breed cows for food but slaughter elephants for their ivory? Or some island species that gets wiped out by a random meteor? Plenty more about it here: http://en.wikipedia.org/wiki/Survival_of_the_fittest

We are still a part of the evolution process though. I'll use the example of beavers creating damns that sometime irreversibly change local habitats. It's (cringe) a natural process to affect their environment as we do to our environment. My interpretation of the question is if a species is made extinct by us, WHY should we care? Money could be spent on preserving our own species instead.

@GoodGravy True, but as I said I think the relevant difference is the extent of manipulation, which is vast for humans. Aside from that, I think it boils down to fear of change.

First, a shorthand definition of Evolution is heritable change and not 'progress' (which is a rather loaded word). Also, evolution is not 'supposed' to do anything, and can lead to both an increase or a decrease in diversity, since (local) diversity is simply the net result of speciation rate and extinction rate (if we exclude colonization of new species from other areas). Therefore, I think the question is framed in the wrong way.
Second, there are many reasons why biologists might want to halt species extinctions, as hinted in the other comments and answers. Most obviously, conservation biologists want to prevent man-made extinctions which are due to how we have influenced/modified/destroyed the natural environments. I don't think conservation biologists in general are determined to halt all 'natural' extinction. However, most of the time it is really hard to pinpoint what would be a 'natural' extinction. Either way, the current rates of extinction, which have been estimated to lie 100-1000 times (IUCN, 2007) above background rates (some say it's closer to 10000 times higher), indicate that most extinctions are man-made.
The rationales people use for preserving biodiversity can however differ. Three distinct categories are:
1) For human survival and/or economy, e.g. through ecosystem services or resources we rely on.
2) For human welfare, e.g. recreation or esthetical reasons.
3) Ethical considerations, e.g. inherent value of species or to preserve the unique evolutionary history of the system.
Another way to structure these is to label 1) & 2) as instrumental values and 3) as inherent values. The instrumental values can then be subcategorized as services, goods/resources, information (e.g. genetic to be used in medical research), and esthetical/spiritual values.
Since the direct value of individual species are often (usually) uncertain (irrespectivly of the direct rationales used) the precautionary principle is often invoked to justify species conservation. Also, numerous examples exist of how aspects of biodiversity are related to human values (some recent examples are Garibaldi et al. 2013 and Gamfeldt et al. 2013), such as production or services, which can also be used to justify both conserving biodiversity or individual species. However, other aspects of biodiversity are functional diversity, which focus on preserving functional groups of species, or phylogenetic diversity, focusing on taxonomic coverage and uniqueness (evolutionary history), instead of 'overall' biodiversity (see e.g. Flynn et al, 2011 for a discussion of these concepts). Under these perspectives less focus is placed on individual species.

In the first paragraph you portray extinction due to invasive species as illegitimate. In the second paragraph you say there is nothing wrong with 'natural' extinction. It would seem that you are re-defining extinction to exclude extinction caused by invasive species, which is what humans are most like. Then you say that "current rates of extinction" are orders of magnitude larger than "background rates." It would seem that by background rates you mean "without invasive species." So instead of answering the question you have re-defined extinction to avoid the messy parts.

I think you have misunderstood some parts of my answer and I have tried to clarify my writing. The first paragraph is only dealing with (in my mind) the rather loaded statements on evolution ('progress' and what evolution is 'supposed' to do). Nothing about invasive species in implied. 'Background rates' is a standard concept referring to "normal" extinction rates pre-modern humans. Nowhere am I redefining extinction, or are implying that invasive species are unimportant or should be excluded (on islands they are one of the main reasons for extinction of native flora/fauna).

Evolution by natural selection requires heritable change but evolution is simply the change in the allele frequency of a population over time.

A change in allele frequency is inherited to the next generation, therefore it is heritable. So what is you point? For natural selection to lead to evolution the trait must be heritable, but that is another question. With genetic drift the allele frequency can also change. Either way, the result is a change in allele frequencies which is inherited to the next generation.

@fileunderwater I agree.  I misinterpreted what was being said on my first reading.

Evolution is simply a change in the allele frequency of a population over time.  It is not progressive nor does it have to create diversity.  Some of the mechanisms of evolution such as genetic drift and stabilizing selection tend to reduce the genetic diversity of populations.
Furthermore evolution and extinction are two independent processes.  Extinction is the complete loss of a unit of genetic diversity (e.g., a species) from the planet.  Evolution and extinction are linked because extinction eliminates a particular evolutionary history that cannot be recovered, but the two processes are affected by different factors within the environment.
Clarifying these definitions we can see that both evolution and extinction are value neutral from the perspective of the biosphere.
Humans tend to ascribe value to biodiversity based on aesthetics, ecosystem services, ethics, etc... and thus we may strive to preserve it for these reasons but this is unrelated to the biological function of evolution and extinction.

I agree with your last two paragraphs, but not the first two. Calling genetic drift a "mechanism of evolution" is inaccurate at best since no new genes are produced.
If evolutionary history cannot be recovered, as you say, then how have various traits "re-evolved" multiple times throughout history? It is only the "inferior" combinations of those traits that (hopefully) will never re-emerge. This is where I fundamentally disagree with evolution. Each creature is majestic in its complexity and to merely call it a "mistake" and "inferior" needing to go extinct for life to march forward is mad.

Genetic drift is a mechanism of evolution - that is a fact. Creation of new alleles and genes is another thing. Also, that traits "re-evole" is generally due to convergent evolution, where similar selective pressures or niche spaces can produce very similar evolutionary outcomes. However, the genetic basis for the reevolved (convergent) traits in different species are (in general) completely different. Therefore, it is not in any way a case of "recovering evolutionary history".

Good question.  Evolution will and does continue.  Mass extinctions have happened in the past and in fact we are the product and beneficiaries of that process; when niches open up from extinctions, other species just move in and take over, eventually they will adapt to take the place of those who have left.  Of course that's a useful perspective since it will happen.  A large number of animals and plants are endangered and while the impact overall can't be estimated since we have never counted all the animals and plants, much less microscopic species, an example of our dire straits can be gleaned from the fact that perhaps half of amphibians are endangered,
There are various arguments that there is lost knowledge - when these animals and plants we have never even cataloged disappear we will lose hundreds of millions of years of biological 'experience', of lost knowledge as well as an aesthetic/ethical argument that this is clearly wrong somehow; like a mass murder of animals and plants.
I think that most people who have never seen these animals and plants, understood how wonderful and awe-inspiring they are, how many odd abilities that evolution has gifted them.  It seems like a nearly universal experience that those who have seen this are pretty strongly in favor of efforts to save them.
But that's not the question at hand; really won't the ecosphere heal and eventually be okay?  Now that we have discovered life so far under the ocean and in the depths of the earth that even nuclear holocaust would probably not touch them.  The answer is yes.  The ecosphere and life will go on.  There are two other useful questions though:
1) will we go on with it? Mass extinctions are the result of changes in the environment - all living things in that environment will sink or swim as it were and humans should not exclude ourselves.  Will the future human race deal with loss of oxygen content, the loss of fresh water and the misery of population explosion?  If the environment just keeps getting worse, will we do well?  We're all assuming that we will figure out how to feed ourselves, find drinking water when both food and water are not really growing to meet our growing population, not to mention the desertification of arable land and the rise in temperature that will impact human geography and economics over the next 100 years or so.  If the environment were to stabilize at least we would not be standing on shifting ground. If you are familiar with Malthus' argument, when there is no food or land left to exploit nature will take its course with us - war, famine etc etc.  That is also a natural state, which we've managed to slowly eliminate.  We may be bringing it back in.
2) How long do we want to wait for the ecosystem to heal? After the mass extinctions of the past, hundreds of millions of years were needed for the species around to re-establish themselves as they are now.  Is that really a good trade off for a few decades of industrial-economic expansion?
Until then, the survivors are not necessarily the ones we'd prefer.
I volunteered at a survey of shellfish in the San Franscisco Bay.  At one time the shellfish here were so plentiful that the natives piled giant shellmounds the size of small hills from their regular diets.  Now because of fertilizer runoff and pollution these shellfish are nearly gone - we didn't see one the entire day looking around the survey area.  Instead they nesting shells were covered with a slimy bunch of sea squirts -  plant-like animals which can grow quickly enough to absorb the nutrients and robust enough to ignore the pollution and chemicals.  I'd probably rather have a bay scallops on my plate rather than a salad of seq squirts.  The Bay is swimmable, but is plenty slimy.
Got to sign off now, but that's the outline of an answer...

There are contradictions in this answer: First we "benefit" from the process of mass extinction, then we "loose knowledge." Some creatures benefit from the extinction of others. However the "loss of knowledge" argument seems hocus pocus since various traits have been shown to have evolved multiple times in different species. While I agree that organisms are majestic etc. I don't see how evolution provides any precedent for preserving diversity. Like you said; the extinction of one species provides room for a superior species to speciate. Human speciation would seem to be the ultimate good.

Your comment about nuclear holocaust is hilarious in its reference to morality for which evolution provides no basis. Your questioning human survival is even more comical since you previously said that humans are "too fit" and must be restrained from dominating other species. Your final joke about waiting for the ecosystem to heal is choice. Human speciation would "heal" the ecosystem, no? Wait! Humans aren't speciating! They are becoming inbreds! New question: how to reconcile speciation with inbreeding?

I can't find the word 'loose' in my writeup...?  Evolution doesn't preserve diversity - but people try to learn from it - if human values mean anything here, which I allow it might not.  Still, what goes away, never comes back.  Superiority is a different question - the superiority of one species over another is similar to questions of the value of diversity - it means nothing in absolute terms, overall, if we hold the mass extinction as fine, then we must also allow our own extinction or changes to our species as similarly valueless - our actions will change us, probably not for the better.

You could just as easily have said that "our actions will change us, probably for the better."

Not really.  Not all changes are improve human happiness or well being - global warming is like everyone moving south a few hundred miles or more, unless they own a house at low altitudes above sea level - then your whole country might disappear.  I see it more as a case of short sighted personal consumption trumping long term planning and rational thought.  Not human beings at their best in my opinion.  Using relativisitic values arguments are probably not going to change my reasoning in this matter.  Sorry.

You might want to try to understand the human tendencies that are at play here - you can look at "Tragedy of the Commons" and "cognitive bias and global warming" e.g. http://rd.springer.com/article/10.1007/s10584-006-9060-3#page-1  I don't think I'm alone in this perspective.

The "fight against global warming" has less chance of succeeding than the "war on drugs." both are fighting economics, which is supposedly the foundation of evolution. I would view an invasive species as "short sighted consumption" at the cost of long term planning, which is why I asked this questions.

That's true - Invasive species from human movements about the world have destroyed millions of acres of forest (pine beetle) and killed most of the grapes in Europe at one point or another.  We spend lots of money to fix those problems, not just give up and let fungus eat all our food and cause famines and the loss of productive forest.  The kind of diversity that is produced from environmental changes are not usually desirable to humans who evolved in the conditions previous to those changes.  Human misery will generally result, if that's worth anything.

Another thing here is that all this is an entirely theoretical argument.  Maybe you can post another question where you walk through a specific case as to what you mean by this theory.  Your question doesn't discuss its motives or what you feel this means should happen. It sort of sounds like 'don't worry be happy' about ecological catastrophe.

I deliberately seek to avoid a specific case, because such a case would constrain the topic to a narrow set of preconditions, which tend to obscure the preconceptions of those engaging in discussion. For example: your answer and comments have shown how it is actually humanism and not evolution that leads us to preserve endangered species. Every point you have made is about how extinction will affect us, not evolutionary progress, which we cannot hope to assist since by interfering with a system we disrupt causality. Please forgive my bluntness.

I do start my answer with a statement that its true that even if there were no people, the planet and life will get along somehow.  I make no bones about it.  Human beings will try to save their own bacon even if we have to evolve a more rational self to do it - that's natural too. Stack exchange is asking me to move this to chat - if you want to continue feel free to pull me into a chat room.

Simply put, evolution through natural selection is a process which occurs naturally. It will occur to any self-duplicating organism with: variations, hereditary traits and threats to propagation (e.g. all life forms we are familiar with). Evolutionary biologists study this, the same way astrophysicists study space, and studying black holes or life forms doesn't indicate anything other then knowing how it works.
Actually, considering that most people in a certain field take interest in it (because logic), it is to be expected that biologists as a whole would rather see life doesn't go extinct then it does - again saying nothing about whether extinctions have or have not happened in the past.

why the downvote?

I doesn't answer the question,


text:
Why is a slow worm not considered a snake?
Slow worms are considered lizards as opposed to snakes, both are reptiles. Now I get that there are traits that distinguish them (eye lids, ears ...). But snake species themselves vary already quite a lot.
The Wikipedia article on snakes states:

Based on comparative anatomy, there is consensus that snakes descended from lizards.

But how comes slow worms are considered lizards despite the loss of their limbs during evolution, whereas the same evidently has happened to snakes?
What's the defining factor here? The time frame when it happened, that it happened independently (like the evolution of, say, an eye)?
Note: I couldn't find any detailed descriptions about the alleged evolution of slow worms, whereas for snakes it is easy to find material.

the defining factor is that the species definition comes from where they species has come from, not only its body plan.  In fact the slow worm has features in its body plan that more resemble lizards than snakes.  The species name is as much a reflection of the history of that animal as it is a description of what may look like.

The number of vertebrae (more than 70, or something like that) is another synapomorphy in snakes (Serpentes). But they are all lizards, in the cladistic sense.

You are correct that the reason is similar to that of convergent evolution of the eye.
Both snakes and legless lizards are lizards (Squamata) that have lost their legs. However they have done so entirely separately much as octopus and human eyes have evolved entirely separately. An easier analogy is between whales and sea cows. Both are legless mammals but as they have evolved separately the must be given separate names.
Unfortunately it seems that the exact position of the snakes in the tree is unknown which makes this explanation less clear.
http://tolweb.org/Squamata/14933
However, the legless lizards (subfamily Anguinae) are within the family Anguidae, most of which have legs. This family is within the Anguimorpha, which includes even more species with legs. Just one small tip of the tree, with around 20 species is legless. On the other side of the tree, separated by many millions of years is the snakes (Serpentes).
A related question is why are snakes given their own name while legless lizards are just considered lizards without legs. This is partially due to the fact that there are so few species of legless lizard while there are thousands of species of snake. It is also probably due to cultural history. As snakes are dangerous to humans and prevalent in most inhabited areas of the world words for snakes are much older than the study of taxonomy. A western example is the snake in the garden of Eden. It is also important in Hinduism
and many other cultures/religions.

thanks a lot for your answer. I am reading through all the links still, but I think it answers what I was asking.

I'd dispute the premise that octopus and human eyes evolved separately! Too many of the molecular mechanisms involved in development are shared in all animals known to have photosensitive organs.

I'd agree that the visual system of cephalopods and vertebrates likely evolved in one common ancestor. However, this was a rudimentary "eye". The modern lens-type eyes of both groups almost certainly evolved independently from this common ancestral organ.

Slow worms share many characteristics with other lizards, such as the presence of eyelids, which no snake has. Leglessness in slow worms evolved separately than in snakes, as can be seen by the fact that other lizards in the same family, Anguidae (and therefore, more closely related to them than snakes) possess legs (see Gerrohonotus and Abronia).
Things are complicated a bit because work by Fry et al. (2006) shows that the Anguimorpha (slow worms), along with Varanids (monitor lizards), Iguanids (iguanas), Helodermatids (gila monsters and beaded lizards) and snakes form an evolutionarily related clade, since all of these possess some or all of the components of snake venom.
However, for anatomical and phylogenetic reasons, it is clear that the slow worm is more closely related to other lizards than it is to snakes.

The argument in the first paragraph is circular because you justify something based on an artificial categorization. Animals have often been re-categorized later into another family etc. Also some snakes do have remnants of legs (pythons), so what now?

Yes, pythons and some boas have remnants of legs. All this proves is that the common ancestor of anguimorphs and snakes was likely to have had legs. So what? The argument is not circular at all. I'm using established phylogenetic relationships to make an  argument about evolutionary relationships between taxa.


text:
What are some examples of scaling laws in biology?
I've seen that metabolic rate scales logarithmically as function of mass for many animals over an extremely large span of parameters. What other scaling laws exist at the individual level?

Obviously, one has surface-area to volume issues (e.g., it is speculated that huge dragonflies were possible in the past due to increase O2 despite lack of lungs) and cross-sectional area to volume/mass issues (e.g., bigger animals tend to require disproportionately thicker legs).

Here are some off the top of my head.

The height an animal can jump depends on the muscle cross-sectional area ($l^2$) and its mass ($l^3$). Mass grows faster with body size ($l$) so small animals can therefore jump higher relative to their body size ($l$) than large  animals. Very similar scaling exists for strength of limbs vs. mass, ability to fly vs. mass, etc.
In pinhole eyes (as found in clams and nautilus) sensitivity to light depends on the size of the pupil ($l^2$), the bigger the hole the more light gets in. However the ability to focus depends on the reciprocal of the size of the hole (but I don't know the scaling, so $l^{-n}$). Therefore there is a trade off between sensitivity and  ability to focus.
There are some recent models about foraging behaviour in a 2D terrestrial environment (with the front of the animal being a length  $l$) vs. foraging in a 3D marine environment (with the front of the animal being a surface $l^2$). The model predicts different behaviours for the size of prey animals should aim for.
The rate at which sound attenuates scales with the frequency of the sound as $1/f^2$. The frequency of a resonator scales with the reciprocal of volume $1/l^3$. So small animals make high pitched sounds which attenuate quickly and don't travel very far.
Finally, the properties of fluids change with size. The Reynolds number describes viscosity and is dependent on linear scale $l$. Therefore small animals experience fluids as viscous and can "crawl" through water whereas large animals have to "swim" through water.

However, any directly physical or chemical-physical property of biology will experience scaling laws.

This is great! Do you have any references for some of these so I can read more, especially the first three?

Are you looking for academic paper style references or something a bit softer? Here's a few papers anyway. Hope you don't get stuck with paywalls.
http://www.sciencedirect.com/science/article/pii/S0003347271801343 <- Bats calls
http://www.damtp.cam.ac.uk/user/gold/pdfs/purcell.pdf <- 70's paper about Reynolds
http://jeb.biologists.org/content/208/18/3581.full <- allometry of flight

Just for the record, jumping height depends also on the distance ($l$) along which a muscle's force delivers energy. The net result is independence ($l^0$) between jumping height and body size, but smaller animals still jump higher relative to size (by a factor of $1/l$).


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Why is the blood pressure in the superior vena cava during inhalation less than during the exhalation?
For further investigation into the progress of the blood pressure, we will measure a patient's blood pressure in the superior vena cava measured during inhalation and during an exhalation. His heart function remains the same during the measurements
Why is this subject's blood pressure in the superior vena cava during inhalation less than during the exhalation?

The diaphragm moves down during inspiration. This leads to air being sucked in, due to the pressure difference created. The converse is true during expiration. As the thoracic space is where the SVC sits, it's pressure decreases during inspiration as it is subjected to the surrounding decrease in pressure.