text:
Why is saltatory conduction in myelinated axons faster than continuous conduction in unmyelinated axons?
How does spacing apart sodium and potassium channels allow the action potential to travel faster down the axon? This is the reason always cited for saltatory conduction and myelination, but my mental model of conduction tells me that the density of ion gates along the axon should not affect the speed of the AP.
To illustrate, consider a myelinated axon. A wave of Na$^+$ from action potential site 1, a node of Ranvier, rushes into and quickly diffuses down the axon. (It travels in both directions, but backwards is still in the refractory period.) It diffuses through the myelinated region, its concentration always diminishing. Before it attenuates too much, however, it happens upon node of Ranvier 2, where it triggers another action potential. A new wave of Na$^+$ rushes in and the cycle repeats. This should be plain so far.
Now imagine that there is actually a node of Ranvier halfway between node 1 and 2, called node 1.5. The wave of Na$^+$, on its way to node 2, happens to trigger an action potential at node 1.5, from which a wave of Na$^+$ pours in and either boosts the original wave or replaces it by taking its momentum. Now the reinforced wave proceeds to node 2 and triggers it just as soon as, perhaps even sooner than, if node 1.5 had not existed. Repeatedly insert nodes at higher densities until the situation is simply lack of myelination, and we conclude that unmyelinated axons can transmit an action-potential-triggering wave of Na+ as fast as or faster than a myelinated one.
In short, my point of confusion is this: I cannot see how a higher density of gated channels can possibly slow down the wavefront of Na+ that triggers action potentials. If anything, the additional influxes of Na+ should speed up the all-important wavefront, assuming that new waves really "either boost the original wave or replace it by taking its momentum", and also assuming that the wavefront of Na$^+$ is really all-important for signal transmission, and also assuming that the mere presence of (voltage?) gated ion channels in the membrane does not significantly retard the wavefront.
But the usual explanation for why saltatory conduction is faster than continuous conduction (a fact I hope is empirically and unambiguously established) relies on the putative slowing effect of ion channels on the signal fore. Please explain this effect in more detail, if it is not a misconception.

This is similar to, but I think slightly different than http://biology.stackexchange.com/questions/8026/what-is-the-function-of-nodes-of-ranvier-in-axons

@kmm Actually, my question is in some sense the polar opposite of that question. That one asks why the whole axon is not completely covered in myelin, whereas mine asks why myelin is useful at all. I can understand that without regularly replenishing the Na+ inside the axon, the signal attenuates. Its wavefront is not a 'block'; like the Romans (pardon the analogy), it diffuses its previous territory as well as advancing its border, weakening itself.

My best guess is that people actually don't know. I'm usually quite good at comprehending science when it is there. In the absence of true models or explanations though it is impossible to comprehend. Take a simple thing like how hydronium ions drive osmosis, without knowing that and people just saying "water evens out its concentration", you cannot possibly wrap your head around it.. http://citeseerx.ist.psu.edu/viewdoc/download?doi=10.1.1.618.291&rep=rep1&type=pdf

 Short Answer
Myelination acts as an electrical insulator and allows saltatory propagation.

By reducing membrane capacitance and increasing membrane resistance, myelination increases the velocity of signal (i.e., Action Potential) propagation.

If you want to see a really wonderfully simplified explanation, see this Quora post by Edward Claro Mader. Four great figures that Edward created show this phenomenon simply:
Decreased Membrane Capacitance:

Increased Membrane Resistance:

 Long Answer
So you're right: myelination speeds up electrical conduction. Unmyelinated axon conduction velocities range from about 0.5 - 10 m/s, while myelinated axons can conduct at velocities up to 150 m/s -- that's 10-30x faster!!
But why? ...
 Let's Look at Action Potentials & Signal Propagation:

You can get a background of this process in numerous places (e.g., here), so I will just mention this briefly:

When the neuron is at rest, ions are distributed so that the inside of the neuron cell is more negatively charged than the outside. This creates an electrical potential, called the resting membrane potential, across the cell membrane.

Sodium and potassium channels in the cell membrane control the flow of positively charged sodium (NA$^+$) and potassium (K$^+$) ions in/out of the cell to maintain this negative charge.

During depolarization, the cell membrane essentially becomes more permeable allowing NA$^+$ to enter the cell. This causes that section of axon to have a positive charge relative to the outside.

When this positive voltage is great enough (i.e., when an action potential is created), the influx triggers the same behavior in the neighboring section of the axon. Gradually, this positive charge on the inside of the cell moves down the length of the axon to the axon terminals.

 The Main Takeaway:
In this process, action potential generation occurs repeatedly along the length of the axon.
It's important to note two things about action potential propagation:

Each action potential takes time to occur.
The charge (i.e., voltage) that is created dissipates with $ \uparrow $ distance.

 Time for some Math & Physics:
In fact, we have equations to calculate both the time a voltage change takes to occur and how current flow decreases with distance.

You can read more about the mathematics behind this and passive membrane properties in general here and here.

Importantly, these equations rely on two constants: length and time.
The time constant, $\tau$, characterizes how rapidly current flow changes the membrane potential. $\tau$ is calculated as:
$$\tau = r_mc_m$$
where r$_m$ and c$_m$ are the resistance and capacitance, respectively, of the plasma membrane.

Resistance? Capacitance? Huh?...

Resistance = the measure of the difficulty to pass an electric current through a conductor.

Capacitance = the ability of a structure to store electrical charge.

A capacitor consists of two conducting regions separated by an insulator. A capacitor works by accumulating a charge on one of the conducting surfaces, which ultimately results in an accumulation of oppositely charged ions on the other side of the surface. In a cellular sense, increased capacitance requires a greater ion concentration difference across the membrane.

The values of r$_m$ and c$_m$ depend, in part, on the size of the neuron:

Larger cells have lower resistances and larger capacitances.

Importantly, however, is that these variables also rely on membrane structure.

c$_m$ (the capacitance of the membrane) decreases as you separate the positive and negative charges. This could be the result of additional cellular structures (e.g., sheaths of fat) separating intracellular and extracellular charges.

r$_m$ (the resistance of the membrane potential) is the inverse of the permeability of the membrane.

The higher the permeability, the lower the resistance.

Lower membrane resistance means you lose ions quicker and therefore signals travel less far

But why? This is where that length constant becomes important. The length constant, $\lambda$, can be simplified to:
$$ \lambda = \sqrt {\frac {r_m}{r_e + r_i} } $$
where, again r$_m$ represents the resistance of the membrane and r$_e$ and r$_i$ are the extracellular and intracellular resistances, respectively. (Note: r$_e$ and r$_i$ are typically very small).
Basically, if the membrane resistance r$_m$ is increased (perhaps due to lower  average "leakage" of current across the membrane) $\lambda$ becomes larger (i.e., the distance ions travel before "leaking" out of the cell increases), and the distance a voltage travels gets longer.
 Why am I telling you all of this??
How are the time constant and the space constant related to propagation velocity of action potentials?
The propagation velocity is directly proportional to the space constant and inversely proportional to the time constant. In summary:

The smaller the time constant, the more rapidly a depolarization will affect the adjacent region. If a depolarization more rapidly affects an adjacent region, it will bring the adjacent region to threshold sooner.

Therefore, the smaller the time constant, the more rapid will be the propagation velocity.

If the space constant is large, a potential change at one point would spread a greater distance along the axon and bring distance regions to threshold sooner.

Therefore, the greater the space constant, the more rapidly distant regions will be brought to threshold and the more rapid will be the propagation velocity.

Sooo....

If you increase the layer of cells around the membrane, you decrease the electric field imparted by extracellular ions, which allows intracellular ions to move more freely in the axon. In other words, you decrease the capacitance.

As a result, you have more cations available to depolarize other parts of the membrane.

If you decrease the permeability of the membrane (i.e., if you prevent ion channels from moving ions in/out of the axon), you increase the resistance of the axon membrane, which allows for the voltage created in the action potential to travel farther before dissipating.

By allowing the voltage to spread farther before necessitating the generation of another action potential, you reduce the time it takes for signal propagation.

In other words, if you "block" ion channels and decrease the concentration of anions near the axon membrane, you increase  membrane resistance (r$_m$) and decrease membrane capacitance (c$_m$), respectively. Together, this decreases the time of electronic conductance through the axon (and thus increase conduction velocity).
 Finally, to Myelin!
Myelin greatly speeds up action potential conduction because of exactly that reason: myelin acts as an electrical insulator!

Myelin sheath reduces membrane capacitance and increases membrane resistance in the inter-node intervals, thus allowing a fast, saltatory movement of action potentials from node to node.

Essentially, myelination of axons reduces the ability for electrical current to leak out of the axon. More specifically, myelin prevents ions from entering or leaving the axon along myelinated segments. As a result, a local current can flow passively along a greater distance of axon.

So instead of having to contantly generate new action potentials along each  segment of the axon, the ionic current from an action potential at one node of Ranvier provokes another action potential at the next node. This apparent "hopping" of the action potential from node to node is known as saltatory conduction.

 So Why not Just Myelinate the Entire Axon??
The length of axons' myelinated segments is important to the success of saltatory conduction. They should be as long as possible to maximize the speed of conduction, but not so long that the arriving signal is too weak to provoke an action potential at the next node of Ranvier. The nodes also can't be too frequent because, although adding a new node to the axon would increase its ability to generate sodium current, it would also increase the capacitance and thus diminish the effectiveness of other nearby nodes.

Sources:

Purves D, Augustine GJ, Fitzpatrick D, et al., eds. (2001). Neuroscience. 2nd edition. Sinauer Associates, Sunderland, MA.

The Brain: Understanding Neurobiology

Byrne, J.H. Chapter 3: Propagation of the Action Potential. Neuroscience Online. Univ. Texas.

Understanding the Passive Properties of a Simple Neuron

Quora

Wikipedia

This question is also relevant on the topic of how myelin actually influences membrane capacitance.

So in brief, myelin makes the axon less "leaky" and less "sticky" for ions, by increasing membrane resistance and reducing membrane capacitance, respectively. Thank you for this simple and fairly complete answer!

I realize that I originally assumed the cell could just try to avoid placing non-gated ion channels along the membrane, to keep the conductance low, but it must be much more practicable to myelinate the whole thing than to attempt uneven distribution of proteins. In my model, the axon could "spam" action potentials, and the super high concentration of ions would speed up diffusion and offset any slowing effects of R-C. LOL but that would be metabolically backbreaking, and extremely salty.

see Graded Potentials, Action Potentials, Electrotonic Conduction, Myelin on YouTube  [harrywitchel, 14.5 min]

There are two factors that need to be taken into account here:
1. Myelination decreases membrance capacitance.
The rate at which sodium influx through a node can depolarize the axon at the next node is related to both the current and capacitance across the membrane (in addition to a few other factors). So while adding a new node to the axon would indeed increase its ability to generate sodium current, it would also increase the capacitance and thus diminish the effectiveness of other nearby nodes. So it doesn't help to move the nodes closer together. What if instead we increase the distance between nodes? In that case, the trade-off is reversed and conduction velocity is again decreased. So there is some optimal internodal distance at which conduction velocity is maximized, and it turns out most axons happen to have just that geometry. [See: Waxman, SG. 1980]
2. Action potentials are metabolically expensive.
The brain uses a lot of energy (about 20% of the body's metabolism at rest)! Maintaining the proper balance of ions inside the neuron is the major reason for this energy usage. Every action potential incurs metabolic cost and if we double the number of nodes along an axon, we (nearly) double the metabolic cost of propagating spikes down that axon. So although conduction velocity appears to be the primary determinant in the choice of internodal distance, it is important to remember that it is not the only factor the organism must take into account.

Hi Luke! Thanks for the answer. StackExchange notified me about it only a couple of days ago, which is why I've taken a week to respond. I would like to add another important factor, which I had overlooked when I first posted: ion leakage (specifically, outgoing ion pumps). Myelination prevents leakage, which may slow down the wavefront IF we assume that an attenuated (less concentrated) wave travels slower down the axon.

Certainly minimizing membrane conductance is another potential benefit of myelination. To maximize conduction velocity, we would ideally want the inter-nodal membrane to have very high resistance. I did not include that as part of the answer because the cell could (and in some cases does) achieve the same effect by simply localizing channels to the nodes. This could be done without myelin at all, so I'm not sure it should be considered one of the primary actions of myelin.

Wow! It is fascinating that the cell can localize channels to small points along the axon without myelin. Thanks a BUNDLE for taking the time to post. Although I give this answer the check mark, I certainly hope others are not discouraged from contributing their knowledge.

I'd just like to add that, if your information is accurate, this discussion should be pretty interesting, since usually people seem to take it for granted that myelination simply allows the action potential to somehow "hop" from node to node, and therefore the signal is faster. That may be a useful abstraction somewhere, somewhen, but it has no physical meaning, I think.

Regarding 1. You write: "... while adding a new node to the axon would indeed increase its ability to generate sodium current, it would also increase the capacitance ...". Why or how would it increase capacitance? Regarding 2. How does that (help to) answer the question at all?

While Luke's answer is perfectly correct, the answer can be given in a more intuitive manner.
First, the main point is that it is increased positive voltage (inside the axon) that opens the sodium ion channels to propagate the action potential. The question is: how fast can this voltage get to the sodium channels?
In an unmyelinated axon, the movement of voltage across the membrane is due to ion flux (i.e the flow of ions through the channels, the current), and this movement is limited by the time it takes for the sodium ions to diffuse into the axon.
On the other hand, in a myelinated axon, the first bolus of sodium enters at the axon hillock.  Because the capacitance is low, this means that the voltage can propagate down the axon, not by ion diffusion, but as an electrical field.  The electrical field carries the voltage force much much faster than ion diffusion. Therefore, when the ions first enter, the voltage force moves, basically at the speed of light to the next node, where the voltage force opens the sodium ion channels there.
So, by allowing the voltage to be carried by the electrical field, the effect is that the distance between the nodes is effectively eliminated.  Myelinated axons conduct faster because they are >>effectively<< much shorter than unmyelinated axons.
Finally, the optimized distance between nodes mentioned by Luke is exactly that distance in a given type of neuron's axon where the voltage force decays to the bare minimum needed to activate the sodium ion channels at the next node.

Hello Don! Again, StackExchange emails are sluggish.... That's a really dam good explanation, and if it had been given early I might have checkmarked it. I like how it truly explains 'hopping'. However, my understanding of capacitance is not as good as it should be, so I cannot totally grasp the mechanism here. Therefore I am a little skeptical. Could you point me to a resource confirming and developing your answer, so I can study it more closely?

What stops the voltage from propagating down the axon as an electrical field in an unmyelinated axon?

"this means that the voltage can propagate down the axon, not by ion diffusion, but as an electrical field." This is a main point for me. Would you have a reference discussing this?


text:
Did human hairs actually evolve from scales?
What is the evolution of hairs? Did they evolve from scales?

From a little research I have been able to find some of the hypotheses and speculations but no papers expressly confirming or denying the matter.
One theory displayed in "The evolution of mammalian keratinized structures" (abstract only) is that mammalian hair developed along the following pathway:

Hair follicles develop between reptilian like scales.
A granular layer formed in the pilosebaceous canal (see diagram of modern human skin)
The granular layer extended into the epidermis.  I read this as the point where scales started to more resemble mammalian skin.  It is suggested that this was as a result of a need for increased flexibility and agility.
Hairs began to protrude through the follicles (as seen in rat tails today).  Adaptations to organisms living in cold conditions led to the production of wool to help conserve heat.

So this paper would suggest that hair production evolved separately from but parallel to the movement away from reptilian scales.
"Some Speculations on the Evolution of the Vertebrate Integument" (Paul F. A. Maderson) suggests an entirely different origin of hairs.  He proposes that hairs ultimately evolved from sensory appendages that were involved in the detection of temperature in early synapsids.  The extension of these micro-limbs into hairs was selected towards as a result of their thermally insulating effect by-product rather than for their sensory role, however.

As to the early evolution of mammalian hair, Rowe et al. (2011) hypothesized that the primitive function for hair was not thermoregulatory, but rather for tactile sensation (contra the hypotheses of Spearman and Maderson). Rowe et al. say:

Body hair develops as migrating neural crest cells induce patterns of
  tiny placodes that mature into hair follicles equipped with
  mechanoreceptors. These include lanceolate endings (velocity detectors
  excited by hair deflection), Ruffini receptors (tension receptors
  activated as hair is bent), and Merkel cells (slowly adapting
  sensors). In ontogeny, hair is first sensory, and only later does it
  insulate, as underfur thickens and thermoregulation matures.

So the developmental argument is in favor of tactile sensation.

source: Stack Exchange

license: Creative Commons - Attribution Share-Alike - https://creativecommons.org/licenses/by-sa/3.0/

sort: votes


text:
What is this black shelled insect found in Western Arkansas?
This bug was running around my driveway last night. It was very fast and wouldn't hold still - this is about the clearest shot that I got of it. As far as I could tell, there were no legs behind that 3rd segment - it was just dragging those.
I've never seen this, or anything like this in Arkansas. What is it?

Approximate size?

Looks like the larvae of a carrion or burrowing beetle (i.e. some beetle species of the family Silphidae). Not sure on the species yet.
Wikipedia provides a good introduction to this family of insects.
Here's a picture:

And another:
Silphidae larvae
Did you see (or more likely smell) any dead carcasses around your property?

That's surely it. We actually have a cat that kills moles, a variety of rodents, and (sadly) birds. I suspect it was after one of those. It's odd, though, because it looks like the adult beetles are fairly large, and I haven't noticed any of them yet.

all_licenses: Creative Commons - Attribution Share-Alike - https://creativecommons.org/licenses/by-sa/3.0/


text:
Is it possible to identify this chrysalis?
At least I believe it's a chrysalis. I found it hanging from my gate the other day.
I'm in Western Arkansas:

More photos here

Could you provide approximate size? (or is it too late? :p). Also, if you have nay additional photos they would be helpful.

it's about 1.5". I actually posted this elsewhere, I forget the exact species but it's the kind that glues sticks and bark to itself as camouflage.

My guess is a bagworm (Thyridopteryx ephemeraeformis). University of Arkasnsas has a page about these "pests"

@theforestecologist yes, that was it

Wayne or @theforestecologist why don't you write an answer and mark it as resolved?

Based on the image and location, I'd say you've got the chrysalis of a bagworm moth (family Psychidae) or some related species of case-building moth.
There are over 1350 species of Psychidae, and I am not certain of the exact species.
Caterpillars of this family are known to create protective cases out of local debris. Because this debris can vary, so too will the appearance of the case. Different species likewise prefer to use different materials. Sticks, leaves, tree scales, etc. have all been known to be used in their chrysalii. As a result, Googling for images should produce a wide variety of chrysalis structures. Here is one example using Eastern Redcedar scales in NC:

The University of Arkasnsas has a locally-relevant page about Thyridopteryx ephemeraeformis, one species that is often considered a "pest".


text:
Why do blue jays eat my cat food?
We buy some run of the mill big-box store cat food. Over the last several weeks, I've observed a blue jay landing on the cat food dish, taking a piece or two, and flying off with it. I assumed it was eating it then, and this morning I just saw it actually eat a piece.
Why would a blue jay eat cat food?
Edit:
I just looked at the ingredient list and apparently corn is the first ingredient. But there's also "poultry by-product" and a variety of other "meats." Would the jay just smell a lot of corn or something?

It's food. It's easy to "catch". Blue jays eat insects; why not cat food?

@anongoodnurse But he says it has corn too

@TalhaIrfan - Blue Jays are omnivorous. Easy food is easy food.

Like other Corvids (Jays, Crows, and Ravens), Blue Jays are omnivorous and can eat and digest both animal and plant matter. Animal matter can include insects, carrion, small birds and mammals, and the eggs of other birds. Then there is plant matter including corn, seeds, etc. Your catfood was not only convenient but contains a good source of both animal and plant matter and the opportunistic tendencies of Blue Jays allowed them to take advantage.


text:
Where does all the food go?
Food goes in, excrement come out. This seems obvious.
But it seems like the mass of the excrement is less than the one of the food.
Most people I asked answered: "There's a difference because it's transformed into energy, like heat...". I think that's bull-excrement.
There's still the law of conservation of mass: our body does no nuclear reactions, or does it?
Example:
Someone's on a "high protein / low carb" diet, he may ingest like 1kg of food, he isn't really productive on the toilet (it's difficult to find any fibers in those diets), he loses 500g in a day... My question is: where does the 1.5kg of matter go?

Whatever the diet, the food intake contains macronutrients: carbohydrate, fat and protein. When they are metabolised all of these molecules will end up, for the most part, as carbon dioxide, water, and ammonia, unless they are incorporated into components of the body.
These waste products are, of course, lost via breathing, and via the urine. That's where the "missing mass" goes.
A related question is here.

Thank you, the fact that we aren't carrying around a nuclear reactor is reassuring for me.

Yup, faeces is only the matter that wasn't taken up by the digestive system - plus some stuff excreted via bile by the liver.

If the total mass of everything released (as carbon dioxide, urine, faeces, etc.) was equal to the mass of the intake then animals wouldn't function. Your friend is wrong, Roman, in that the conversion of mass to energy does not account for the energy difference but it does occur albeit it at very low levels. It is this conversion of mass to energy that provides the energy needed for the body to function with the energy eventually being lost as heat.

Metabolic heat comes ultimately from thermodynamically favorable chemical reactions---breaking chemical bonds whose energy of formation is high, creating chemical bonds whose energy of formation is lower. Technically, yes, the mass of one glucose molecule is ever so slightly more than the mass of six carbon dioxide molecules and six water molecules, the difference corresponding exactly to the energy released when the glucose is catabolized, but we usually don't think of this as mass-energy conversion; we think of it as releasing energy stored in chemical bonds.

(ugh, months later I notice that I should have said "the mass of one glucose molecule and six oxygen molecules...")


text:
Is it possible to simulate the effects of high altitudes for plants?
Note- I considered asking this on gardening.stackexchange.com but i believe it is better suited for this site since it deals with more complicated material.
As I understand it, certain plants (Camellia sinensis, Coffea, etc.) grow best at higher altitudes. What factor, biologically speaking, is responsible for this?
I know that the oxygen concentration at higher altitudes is lower, is this the reason?
If so, is it possible to use machinery to alter the gas concentrations in a grow room and simulate the effects of high altitudes? Are there any other factors such as pressure or anything that can also be altered? Would simulating this environment be practical for large scale applications?

The higher altitude means lower atmospheric pressure which in turn means lower oxygen concentration. Just pumping the air out of a sealed chamber would simulate this. Temperature, humidity and sunlight intensity/composition should also be taken into account.

I'm not sure that it's known which factor is responsible for this. Altitude changes the air pressure, but it can also drastically change the temperature, rainfall, drainage, soil type(no silt on mountaintops), etc. You can simulate almost anything with varying degrees of difficulty, but most would be impractical for fields on fields of crops.


text:
What sort of seed pod is this?
My son found this floating in a stream in Massachusetts, in the northeastern US. It was intact when he found it, but he cracked it open to see what was inside. I did some Google image searching, but couldn't find anything. Any idea what it is, and where it came from?

Are there any trace of a hole through which a bug could have entered? The content looks messy. Can you isolate seed ?

@bli no, there weren't any holes in it. I haven't dug around in it, but I can take a look for seeds when I get home from work.

Looks like a gall such as an oak gall.

Looks like a gall. was it delicate and lightweight? If so I'd guess it belongs to the oak apple gall wasp

It's actually not a seed pod, but rather a gall (see here or here for more info about galls). Specifically, it most likely is a gall belonging to the Oak Apple Gall Wasp (Amphibolips confluenta). You can read about this species and its gall here.

Yes, it was quite light for its size, and I suppose "delicate" could be used, but it was certainly difficult to cut open :)


text:
Why is the human body able to repair a broken bone and not a heart muscle?
The human body can repair skin/organ laceration, fractures, even repair nerves - albeit the duration and rate of recovery differ.
Why can the heart muscles not repair themselves?

I think you may need to specify to what degree of damage... increased muscle strength is (in part) achieved by damage to the old tissue, which is then repaired by immune and stem cells. At least, that's how skeletal muscle works. This differs massively from the kind of damage that impairs the function of that muscle/bone/whatever (e.g. a break/fracture). You can rest and recover from a broken bone. You die from a 'broken' heart (excuse the expression). I will be very interested to see an in depth answer.

Erm. I don't have an answer )+: just lots of inane questions

Heart muscles aren't the only exception: think of neurons. Once they're dead, they're gone for good.

@LanceLafontaine: Wasn't there an article online that said neurons regenerate - albeit at an extremely slow rate. The magnitude of regeneration was something like 1mm , but i forget the unit of time over which this growth was determined.

Part of the answer may be(*) that in bone, you have still stem cells everywhere (blood capillaries that grow until checked and osteoblasts), i.e., also in the vicinity of the wound. The same applies to skin, by the way, where the epidermis continues to produce skin layers until eternity. This facilitates repair enormously, as new cells won't have to move far to take their place.
Contrast this with heart or spinal cord, where the placement of the cells took place in early development when distances were small and most cells were undifferentiated. Also, no tissue like epidermis was left in the vicinity that could act as a near source of new cells.
(*) I said "may be" because 1. I have no ref for this, and 2. I have no idea to what extent other factors are involved. I would be thankful for counterexamples.

+1 for the suggestion. At the same time I must beg to differ to the extent that some repair happens in the eye - an organ which develops early; why should the heart then be different?

The heart does have stem cells in it, and there is cell turnover in the heart, of about 1% per year. Which is much slower than your skin, but not nothing. This allows your heart to grow during your life, and remodel itself slightly to become stronger/more efficient when you get in shape.
The heart can repair itself, when damaged it doesn't simply stay damaged. Unfortunately, the 'repair' leaves particularly useless scar tissue. After a heart attack, the dead muscle does repair itself, but very poorly. This 'scar' barely contracts, and isn't as strong as the heart wall around it.
This is mostly a function of the very specialized heart myocytes, and the evolutionary (relative) uselessness of being able to regenerate your heart after injury. In the wild, if your heart was injured, you were probably dead.

Part of the answer is in fact extremely simple: coronary arteries (irrigating the heart muscle) are terminal vessels. This means that when a coronary artery sustains damage, the area it was irrigating becomes biologically dead with a very limited potential for recovery. The affected area turns to fibrous tissue produced by cells with much lower oxygen requirements than cardiomyocytes.
A fractured bone is not dead at all, in most cases. Put a fracture under a microscope, and you will see plenty of cells performing heavy duty. That is because the area, although damaged, still receives nutrients and at least some blood.
However, there are special cases:

bone that is terminally vascularized: such bone regions will die when fractured, since they receive no more nutrients and oxygen. The classic example is fracture of the scaphoid bone in the wrist. Some types of fracture in this bone shear the nourishing artery, and the bone dies off instead of healing.
slowly progressive ischemia due to atherosclerosis: when a coronary artery progressively gets clogged instead of this being a sudden event, the cells inside the danger territory secrete messengers that will activate new vessel growth. This phenomenon is called collateralization, and will allow a subset of the cells at risk to survive when the coronary artery gets completely clogged.

Now about the stem cell issue: I seem to remember that stem cells do exist in the heart, but this is less pertinent in this case, since even stem cells need oxygen and nutrients to survive.

Ignoring the actual physiological mechanism(s) for why, consider that from a natural selection point of view, there probably isn't as much incentive for a body to heal itself of a condition that largely affects post-reproduction age individuals. While healing a broken bone would likely allow a young person to further reproduce, healing a heart ailment would have a disproportionately lower chance of doing so.

It would be great if you add some references for your response!

In simple terms, heart injury, most likely to be myocardial infarction (heart attack) involves death of the vascular heart tissue. Thus the word infarction. Death of a tissue just simply leads to the production of a fibrous scar. Therefore the heart muscle cannot repair that area of injury to 100% as before.

It would be great if you could add references to your response! From what I can tell here (http://en.wikipedia.org/wiki/Chest_injury), cardiac injury can be caused by several events, which are not all heart attacks, such as Pericardial tamponade.


text:
Identification of this humpbacked, brown, clawed insect climbing up my wall?
I noticed several of these guys outside, all in a vertical position clinging to a wall. I didn't come to them too closely, but my immediate reaction was that they are scorpions.

I thought that maybe it's a curled-up scorpion, or maybe there's some kind of particular scorpion that is this circular in shape? These are probably silly conclusions, but I'm not an expert in this field. I would really appreciate the insight of a professional!
thanks very much.

Could you add some additional information like where you are located and the size of the organism in question?

That's the exoskeleton (shed outer shell) of a young cicada, left behind when it emerged as an adult and (we can imagine) flew off somewhere to sing, and find a mate.
This article on EarthSky has a nice description of the big cicada hatch this summer (2013), and also a great picture of an adult cicada emerging from the exoskeleton. However, this article and other recent news about cicadas mostly deals with the Eastern US genus Magicicada, and it's likely that in Arizona you're seeing a different genus (that is, a different type of cicada).
You'd probably have to find an adult in order to identify exactly what genus and species of cicada you've got. Alternatively, you could listen for their songs – this site has examples of calls from many Western US species, including the Apache Cicada Diceroprocta apache, which seems to be a common cicada in your area.

I wanted to add a more thorough answer to this post (with some pictures) since they are bound to get a lot of press (and questions) this summer (2021) -- more on that later....
Short answer
This is the abandoned exoskeleton (called an "exuviae") of a molted cicada nymph.

 Credit: Valeriy Kirsanov/Fotolia, Britannica.com
Here is a time-lapse of one molting:

 Credit: T. Nathan Mundhenk (July 2007 in Centerville, Ohio USA)
Long answer
Cicadas are a superfamily of insects of the true bug (Hemiptera) order; most species are in the family  Cicadidae.

Cicada Mania provides a nice list of North American species with photos, audio, characteristics, and ranges. (It's really an excellent resource for cicadas!)

They list Cacama valvata (common cactus dodger), Diceroprocta apache (Citrus cicada), Okanagana bella (mountain cicada), and Pacarina puella as common Arizona species. However, Sanborn & Phillips (2013)1 makes clear there are more than 50 species found in Arizona, so I will not try IDing the OP's specimen to species.

Life cycle
Cicadas actually live most of their lives underground as immature nymphs. They feed by sucking out xylem from plant roots. Their enlarged claw-like forelimbs are used for digging in the soil in which they live and for excavating chambers near food sources [source]. After 2-17 years (see below) underground, the nymphs emerge, crawl up a vertical structure, and molt for the 5th time into their final adult stage. Their exuviae are often left clinging to the plant (or wall) after molting due to the relatively sharp tarsal claws they use for anchoring and climbing. Adults often live for multiple weeks: sucking on xylem from aboveground plant structures, mating, and depositing eggs in branches. After eggs hatch, nymphs drop to the soil below, and begin their multi-year subterranean life.

 Life cycle of periodic cicada; Credit: Roy Troutman and Elias Bonaros, cicadamania

 Nymph crawling up tree; Source: Peggy Notebart Nature Museum
Annual vs 13- and 17-Year Cicadas:
In North America, there is a need to distinguish between "annual" and "periodic" species of cicadas. Annual cicada species can be found essentially every single summer (although their life cycle is 2-5 years, there are enough overlapping broods that one can see them annually).
Periodic cicadas (genus Magicada), on the other hand, spend most of their lives living underground and synchronously arise only every 13 or 17 years depending on species and brood (13-year species more common in SE US and 17-year species more common in NE and midwestern US). They survive by sucking on xylem from deciduous tree roots.2. These periodic cicadas are unique to the Eastern US, and such long life cycles aren't found in insects anywhere else in the world.
These two subgroups of cicadas are easy to tell apart as a number of species of annual cicadas tend to be larger and green-hued whereas the periodic species are smaller, black-bodied, and have very conspicuous red eyes and tinted wings. Even the few darker annual species (e.g., Diceroprocta apache and various Okanagana species) lack the bright red eyes and red/orange-tinted wings seen in the periodic species.

 Image sources: (L): Purdue Extension; (R): Carol Toman on whatsthatbug.com
The swarm is coming back!!
Periodic cicadas have the longest life-cycles of any insect, and their almost magical synchronous emergence every 13 or 17 years always captures the attention of many media sources and social circles/media. However, some of you may wonder: "wait, has it really been 17 years since we last saw these insects?..."
Well, the answer could be yes if you live in the right place, haven't moved, and haven't turned on your TV/computer lately. However, in certain areas, it's possible to see these insects more frequently! You see, there are actually multiple broods of these insects -- essentially separate populations -- that arise at different times.

The brood that is making all the media hype for emerging in 2021 is Brood X:

[The various species of North American cicadas] form mixed-species cohorts called broods whose members arise like clockwork on the same schedule. The broods are identified by Roman numerals. Brood X is the largest of the 12 broods of 17-year cicadas, which emerge in different years. Scientific American

 Brood map for periodic cicadas. Source: Liebhold et al (2013)3 US Forest Service
As you can see, Brood X can be found in 10-11 states ranging from New Jersey to Illinois.
You can read more about periodic cicada broods on Wikipedia, and you can see range maps of both 13- and 17-year species here (from here).

Citations:
 1. Sanborn, A.F. and Phillips, P.K., 2013. Biogeography of the cicadas (Hemiptera: Cicadidae) of North America, north of Mexico. Diversity, 5(2), pp.166-239.
 2. Lloyd, M. and Dybas, H.S., 1966. The periodical cicada problem. I. Population ecology. Evolution, 20(2), pp.133-149.
 3. Liebhold, A. M., Bohne, M. J., and R. L. Lilja. 2013. Active Periodical Cicada Broods of the United States. USDA Forest Service
Northern Research Station, Northeastern Area State and Private Forestry.

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


text:
Do repeated freeze-thaw strip nutrition from vegetables/food?
Some of my family and friends seem to believe that vegetables/food should be subjected to as few freeze/thaw cycles as possible. The rationale put forward is that each such cycle reduces nutrition (sp. nutritive?) value, and accelerates rot.
I'm skeptical; Do repeated (sp. repetitive?) freeze/thaw cycles strip nutrition from vegetables/food?

Not as far as I know, they do however open the frozen foodstuffs to infection. It is not a good idea to thaw and refreeze for that reason.

Repeated freeze-thaw has virtually no effect on macronutrients, such as proteins, lipids, and sugars, because these are broken down to their basic building blocks (such as amino acids and simple sugars) upon food digestion anyway.
According to this paper freeze-thaw has no effect on micronutrients, such as vitamins, as well.
What affects nutritious quality is the length of time the food remains frozen. Most household freezers maintain a temperature of -20°C. At this temperature, the food doesn't get spoiled by bacteria, but degradation of vitamins still occurs, albeit at a slower rate. This is critical for some unstable vitamins, such as vitamin A and C. But elements such as iron, calcium, zinc, and phosphorus are not affected at all.
If you want to prevent vitamin degradation for a very long time, you need a freezer that maintains food at -80°C. This is only if you want to keep the food frozen for many months though.


text:
Why is the opposite of plantar flexion called "dorsiflexion"?
Why is the action of flexing the foot so that the toes move anteriorly/superiorly (i.e. in the direction opposite that which they move during plantar flexion) described as "dorsiflexion?" In the same vein, why is the top surface of the foot called the "dorsal surface?"
If anything, the action opposite to plantar flexion moves the foot in the ventral direction, doesn't it? And surely if you've ever seen a human in the anatomical position, you can see that there's nothing dorsal about the top surface of the foot - it's superior, perhaps, but by no means dorsal.

It comes by logical extension of the hand... which side of the hand is the front side? In many languages, the back of the hand is called the back, dos in french for example means the back.

Anatomical terms must be able to fit a wide variety of organisms, from insects to fish, dogs, horses, chimpanzees to humans. That's why the terms are sometimes confusing to people who are thinking only of bipedal humans.
In anatomy, the dorsum is the upper side of animals that typically run fly, swim or crawl in a horizontal position. In vertebrates the dorsum contains the backbone. In such an animal the "ground side" is the ventrum.
Due to varied orientation on quadrupedal mammals (where the term is more appropriately used) the "back"-side of the hand, the "top"-side of the foot and the upper surface of the tongue are referred to by the term dorsum.

Does this picture help? Note the dorsal surfaces of the body, muzzle, feet.
In anatomy, the sole of the foot is called the plantar surface. The top of the foot is called the dorsum of the foot. (Imagine us walking on all fours like apes.) Therefore when you extend your foot, it's called plantar flexion; when you flex your foot upwards towards your head, it's called dorsiflexion.
Similarly, the arteries feeding the bottom of your foot form the plantar arch. Those feeding the top are the dorsal artery (or the dorsalis pedis).
Because anatomy must describe other animals than ourselves with other orientations, it must be consistent. In a quadruped, the dorsum of the tongue and the feet do actually point to it's "back" surface. See the picture below:

Lynxes have big paws, so it's more obvious that the surface facing the backbone is appropriately called the dorsum of the paw/foot. This picture is particularly interesting because it shows three degrees of dorsiflexion and one paw in full plantar flexion.
In humans, the "back" is actually the posterior surface, because we are not primarily in a horizontal orientation. The ventral surface is called "anterior". Thus we speak of the anterior chest wall and the posterior chest wall, not the dorsal and ventral surfaces, although those designations would still be entirely correct.

I mean, I get that all of that is true. The question remains - why would you call the top of the foot the "dorsum"? Some anatomist at some point in time must have figured that there was a good reason to call the top of the foot the "dorsum", and what I'm hoping to find out is what that reason was.

It is because anatomy must describe other animals than ourselves with other orientations. In a quadruped, the dorsum of the feet do actually point to the back.

Minor nitpick: The dorsum of gorillas' hands do not point to their backs

@March Ho - They do if the hands were splayed out. As I said, it's meant for quadrupeds: think cats and dogs, etc. Obviously, it has to be able to fit kangaroos and gorillas as well. The bigger problem comes with elephants and hoofed animals, I should think.

@anongoodnurse Ah, that's what it is - I wasn't thinking about how the feet would be positioned on a quadruped.

Anterior and posterior is described in the upper limb based on anatomical position. In human anatomical position the palms face forward, so it becomes anterior. I think this would translate to ventral.

Enlightening explanation, But being philosophical,  the surface at the top of the foot is a surface, not a stick with a point, so it doesn't point. And if you did look at the the surfaces as pointing in some way, then both surfaces of the foot are nearer the front/belly of the animal than the back/vertibrae. .  You could say the foot is parallel with the front and back, and  the surfaces correspond, and in that sense the top of the foot corresponds to the back and the bottom of the foot to the front.

@barlop - you can philosophize till the cows come home; that won't change the nomenclature, which I thing is based on clarity, consistency (an iguana's foot really does stick out like a stick) and function, not personal views; those are too variable.

@anongoodnurse all feet are stick like, n an iguana or any four legged animal's feet don't point towards its belly or back.And if u wanted to talk of where the dorsal surface points to,well,if u put a little spaceship on the dorsal surface of the foot and travelled up,you'd hit the front of the animal,not the back.So if the surface points anywhere, it points to both the front and the back of the animal,and the front first.So I don't think it makes much sense to talk of where feet point if you're talking about a surface and ignoring the surface it points to first when saying what it points to.

I suppose what one could say is the foot and back (in that diagram / the default position for a quadruped) is parallel and if you were to write in a top and bottom, and have 2 planes for the foot and 2 planes for the torso all parallel, then the planes can be said to correspond in that 2 planes, one on the foot and one on the back, could be said to be nearest the top(the so-called dorsal/posterior), and 2 nearer the bottom(the chest and what in humans would be the fleshy part of the foot), would be the ventral/anterior planes of that body part..

Although the other 2 answers are accurate and well thought out, I just wanted to answer this with a bit different focused response.
Two things to note:

In general, one should think of flexion as decreasing the angle of a joint (see here, here, here, here, here, here or here for reference). From Saladin's 2015 Anatomy textbook$^1$:

Flexion = a joint movement that , in most cases, decreases the angle between two bones.

Put differently,

Flexion refers to a movement that decreases the angle between two body parts.

As the other linked answers have aptly described, the superior surface of the foot is referred to as the dorsal surface (dorsum meaning "back"), and the inferior surface is referred to as the plantar surface (from Latin plantaris, from planta meaning "sole").

Given these two pieces of information, we can understand why the terms dorsiflexion and plantarflexion are used:

Dorsiflexion = decreasing angle between dorsal surface of foot & anterior side of of the leg.
Plantarflexion = decreasing angle between plantar surface of foot & the posterior side of the leg (or, more realistically, between the plantar surface and coronal plane of the leg).

From University of Michigan:

A transverse axis through the ankle joint allows a pair of actions similar to flexion and extension at the wrist joint.
The analogous action to wrist flexion is one that would tip the sole of the foot downward, increasing the angle between foot and leg. The usual term for the increase in such an angle would be extension, but in order to emphasize the relation between foot and hand, this action is instead termed plantar flexion .
The action similar to extension at the wrist would be a tipping of the upper surface (dorsum) of the foot toward the anterior surface of the leg. However, this would decrease the angle between the body segments, and action usually termed flexion. Since the term, plantar flexion, has been used for the opposite action, this is now referred to as dorsiflexion.

$^1$ Saladin, K. S. 2015. Anatomy & Physiology: The Unity of Form and Function. Seventh ed., McGraw-Hill, New York, NY. 1248pp.

While this makes sense superficially, it doesn't hold up universally, because there is more than one relationship to body parts. If in one position one angle is decreased, the corresponding angle(s) will be increased. It makes more sense (to me) if flexion (etc.) is described by position rather than by angles. We don't describe abduction as increasing the angle of the arm to the ribcage. (At least I never heard of this either in anatomy class or surgery or neurology of any other study in which anatomy is used.)

Ah, but it does hold up universally. Flexion/extension are very often defined as "increasing/decreasing the angle of a joint" (e.g., see references above or see often used Saladin 2015 textbook). Adduction/abduction are different because they refer to movement of a body part away/toward the midline of the body. They are not in reference to angles, per se. However, since flexion/extension are relevant to all different parts of the body, it is better to define them generally as increasing/decreasing angles of joints in general.  (cont.)...

(cont)...And yes if you increase/decrease any angle, you have to do the opposite (decrease/increase) its adjacent complementary (or supplementary) angle. But even though that adjacent angle is always present,  it  is more relevant  for the given muscle's  antagonistic  partner and not relevant to the muscle moving. That does not disqualify these valid definitions of these movement terms.

I think the angles thing is throwing you off. But remember, we're talking about angles of individual joints. That's why flexion/extension differ from abduction/adduction, which refer to movement relative only to the midline of the body.  Regardless, I'm addressing the definitions and origins of these terms -- I'm not making this stuff up :p. I'm surprised you've not heard of extension/flexion being defined or used in this way, but I would think my answer doesn't deserve a downvote because this is the way these terms are often defined.

I do understand all that you're saying. But, I have never - and I've been a doctor for decades - seen it defined in this way (therefore "...this is the way these terms are often defined" is not true to my knowledge.) You obviously have. It's just less clear cut to me.

Huh, weird. Yeah,  I've been teaching  human A&P at  the University level for over half a decade and this is what we're  teaching  up and coming doctors / health professionals. This  was the way I was taught a  decade ago myself.  It's as general of a  set of definitions/explanations as I've seen.

I don't know how to explain it either. I asked my son (finishing med school in May) if he was ever taught the way you identified, and he said no, never. Maybe it's a geographical thing?

Well, I found a number of universities and textbooks using a quick search (see the 7 new sources cited in my answer) that support the "decrease joint angle" definition. So it's a fairly common way to define flexion (though, I'll admit I only found US examples). I also provided a directly quoted explanation about dorsiflexion/plantarflexion to my answer to provide additional support. Although defining these terms this way was not true to your knowledge previously, I hope this overwhelming evidence can convince you that it's very common and valid and true.

I can't argue with evidence.

I just realized you thought I downvoted you. I didn't; I upvoted you. If I could share this bounty with you, I would be very happy to. Your answer is excellent.

@anongoodnurse Ha no worries. I actually didn't think so. Our extended chat convo was simply me kicking into teacher mode. Thanks for the compliment :). glad we were both able to provide informative answers to this Q -- always great when a Q gets multiple good answers :D. [woww neat bounty, where'd that come from??. I could put in a feature request ;p]

Only fair to give you the larger part of the bounty since your answer is better than mine. :) I had forgotten about this until recently.

@anongoodnurse whoa! What a surprise. Thanks a lot :) ! Glad to share that bounty with you -- our answers compliment each other well

Dors/dorsum in Latin simply means "back", and it is rather normal and reasonable to use the equivalent term in English with regard to the extremities (hands and feet), see "back of my hand".
It is medical convention to refer to the non-gripping surfaces of the feet and hands, as well as the upper (towards the brain) surface of the tongue as "dorsal".
My best guess for the etymology sequence is that all the terms were borrowed from Latin anatomical books written by Roman and Greek doctors (Dioscorides, Galen) which named the anatomical structures in normal language (back/dorsum, stomach/venter, sole/plantarum) and these terms were then fixed into modern medical terminology as jargon.
Caveat: I could not find any citation for the etymological sequence, but it seems a rather reasonable explanation to me.

Yes, I am aware that "dors" or something like it is Latin for "back". For the hands, this makes sense, since the non-palmar surface of the hands faces dorsally in the anatomical position. The same is not true of the feet. Are you saying that calling the top of the foot "dorsal" is because it is homologous with the dorsal part of the hands?

@senshin Saying that it is due to homology would be at best a speculation. What I am saying is that in many languages, the non-gripping surface of the extremities are referred to as "back" (eg English as above, and Chinese "手背，脚背"). Therefore, I believe the Latin name is just an extension of this naming convention.

I suspect that the etymology might derive from the fact that much of the scholarship of medieval and renaissance Europe was written in Latin.

In the same vein, why is the top surface of the foot called the "dorsal surface?"

I don't think the above answers are correct -- they do not really address the question of why the top of the foot is the dorsal surface, and why the surface of the hand opposite to the palmar surface is dorsal.
The reason why the top of the foot is dorsal is due to how the body develops embryologically. See the below figure:

Figure taken from Dr. Ann-Judith Silverman's human development notes, Columbia U. See: Human Dev Notes
The dorsal side of the upper and lower extremity begin on the dorsal/posterior surface of the body. However, during the 6-8th weeks of development, both the upper and lower extremity will turn medially, so that the originally dorsal surface is now anterior/ventral.

The position of the human foot by human anatomical convention dictates that the human foot is perpendicular to the human body in a standing position, such that the rest of the human body (including the hands with the palmar surface facing forward) , but except the foot, will conform to the anterior or ventral plane versus the posterior or dorsal plane. The foot, at conventional anatomical position will have its own plane, consistent with the same reasoning such that the top of the foot is the dorsum, while the underside is the plantar surface (more correct), or the ventral surface (less acceptable due its confusing orientation).
The plane of reasoning for the entire human body at anatomical position above ends at the distal junction of the tibio-fibula with the tarsal bones, such that the human feet will have its own surface plane directly perpendicular at 90 degrees to have its own 'dorsal' and 'ventral' surface.
The feet as such is in a special position compared to the rest of the human body's plane surfaces to warrant its own. Thus by convention, one may acceptably hear 'antero-flexion' or 'dorsi-flexion' of the foot, but not 'supero-flexion of the foot' which sounds sort of disagreeable.
The same way, oppositely, it is customarily said the 'plantar-flexion of the foot' which is more accurate (rather than infero-flexion or ventro-flexion or postero-flexion of the foot which sounds quite confusing)

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


text:
Cheapest way to measure S. aureus and Rhinoviruses density at home
I would like to measure the surface density of Staphylococcus bacteria and Rhinoviruses (only those two, to be specific) within my home.  What's the cheapest way?
The textbook procedure is to:

rub a clean wet cotton swab on the surface in a controlled way
dip the swab into a clean agar (or some living media to detect viruses?) dish
incubate the dish
"look for genetic patterns from special enzyme reactions".

Is it possible to do the last step at home?  Or, is there some easier way if I only care about Staphylococcus bacteria or Rhinoviruses?

What sort of budget do you have in mind? A quick Google using the search terms "Staphylococcus home test kit" returns many kits, the top hit costs $64. There are bound to be other kits that can detect other pathogens.

Maybe $500 for 100 samples.  That $64 basically gets you a swab and envelope for one sample, so it sounds expensive (and doesn't include Rhinovirus).

Use care if you incubate at home - some bacteria in small quantity are low risk however, if you happen to incubate a contagin to colony size it could be dangerous indeed.  I saw this first hand with a fellow student who had recently recovered from a pneumonia bout - we had MASSIVE quantities of those and went straight to the lab steralization phase upon discovery.

For anyone getting ideas
S. aureus and Rhinovirus are risk class 2 infectious substances that should only be handled in a BSL or containment level 2 environment. Your only feasible step here is swab, seal, and send to a lab that can handle it.

There are some kits available to detect the presence of S. aureus on surfaces using agglutination factors like This one. These kits tends to be worth 70$+ though and they do not in any way quantify, only detect.
To have quantity results you would need to respect a protocol for swabbing a specific area and then have a lab do the testing for isolation and quantification of Staph.
Rhinoviruses on the other hand need more advanced techniques to detect and quantify, like PCR, and for this you need lab equipement which are costly.
There is always ways to send samples to labs for them to test but this is a costly solution.


text:
Where can I find historical data on world-wide ecology parameters?
I hope this is the right StackExchange forum for such a question.
I'm looking for large data sets on world-wide ecology parameters, such as annual temperatures by latitude, annual rainfall, CO₂ and O₂ concentration in the atmosphere and in the oceans, data about the insect population, plants, algae, and so on.
Is there any research institute or NGO collecting such data and making it available to the public?

What time interval are you interested in? NASA collects a whole lot of information about abiotic parameters with their satellites on a global scale. They can be explored here: http://earthdata.nasa.gov/ and here http://oceancolor.gsfc.nasa.gov/ (for the oceans).

That's a great resource, I didn't even know NASA did that.

These examples are good

Adding some additional database sources:
-- Climate --
Prism
The PRISM Climate Group gathers climate observations from a wide range of monitoring networks, applies sophisticated quality control measures, and develops spatial climate datasets to reveal short- and long-term climate patterns.
WorldClim
WorldClim is a set of global climate layers (climate grids) with a spatial resolution of about 1 square kilometer. The data can be used for mapping and spatial modeling in a GIS or with other computer programs.
NOAA's NCEI
NOAA's National Centers for Environmental Information (NCEI) are responsible for hosting and providing public access to one of the most significant archives for environmental data on Earth with over 20 petabytes of comprehensive atmospheric, coastal, oceanic, and geophysical data. See NCDC (climate), NODC (Oceans), NGDC (Geophysics), and NCDDC (Coasts).

NCEI has a HUGE repository of datasets. Sometimes you have to dig (e.g., here).

TROPICAL STORM TRACKS DATABASE
The storm tracks database is derived from the storm data published by the National Hurricane Center (NHC). This web page provides a convenient user interface for casually browsing storm information, including location, category, and wind speed.
-- Traits --
TRY
TRY is a Plant Trait Database. More formally, it's a network of vegetation scientists headed by DIVERSITAS/IGBP, and the Max Planck Institute for Biogeochemistry, providing a global archive of curated plant traits.
BioTraits
This is an online resource for empirical data on how biological traits respond to environmental drivers such as temperature, light, and salinity.
-- Species --
GPDD
The CPB / NCEAS Global Population Dynamics Database largest collection of animal and plant population data in the world, and brings together nearly five thousand time series in one databa
Global Invasive Species Database
The GISD is a free, online searchable source of information about species that negatively impact biodiversity. It focuses on invasive alien species that threaten native biodiversity and covers all taxonomic groups from micro-organisms to animals and plants.
Movebank
Movebank is a free, online database of animal tracking data hosted by the Max Planck Institute for Ornithology. They help animal tracking researchers to manage, share, protect, analyze, and archive their data.
Global Plants
Global Plants is the world’s largest database of digitized plant specimens and a locus for international scientific research and collaboration.
COPEPOD
The Coastal & Oceanic Plankton Ecology, Production & Observation Database (COPEPOD) is an online database of plankton abundance, biomass, and composition data. COPEPOD's online zooplankton and phytoplankton data content ranges from long term ecosystem monitoring surveys to detailed process studies
COMPADRE & COMADRE
COMPADRE Plant Matrix Database and COMADRE Animal Matrix Database site. Contain matrix population models of hundreds of plant and animal species
Catalogue of Life
One of the most comprehensive and authoritative global index of species currently available. It consists of a single integrated species checklist and taxonomic hierarchy. The Catalogue holds essential information on the names, relationships and distributions of over 1.6 million species.
-- Forests --
FAO Forestry Database
The FAO Forestry Department maintains an array of online databases where information covering various aspects of forestry is stored for analysis and further dissemination.
FIA
U.S. forest Service's Forest Inventory and Analysis database contains continuous forest census data for the United States.
European Forest Institute Database
EFI is running a number of online databases with data and information on different aspects of European forests, forestry and forest research.
CTFS-ForestGEO
The Center for Tropical Forest Science - Forest Global Earth Observatory (CTFS-ForestGEO) is a global network of forest research plots and scientists dedicated to the study of tropical and temperate forest function and diversity
-- Other --
NutNet
The Nutrient Network (NutNet) is a grassroots research effort to address pervasive human impacts on ecosystems (via alteration of global nutrient budgets and changes in the abundance and identity of consumers) within a coordinated research network comprised of more than 40 grassland sites worldwide.

...Also see the Ecological Databases page on INNGE Wiki for more resources!!

Ex: Ecological Data Wiki:
The site is a source for finding ecological datasets and quickly figuring out the best ways to use them. Just think of it as the Wikipedia of ecology data.

You're quite welcome. Feel free to add more in the comments if you find any!

Wow, thanks! Wish I could upvote you three times. For Europe, the LEDA traitbase is used often: http://www.uni-oldenburg.de/en/biology/landeco/research/projects/leda/

For species occurance data the Global Biodiversity Information Facility (http://www.gbif.org/) database should be an obvious choice. It contains both historical records from museums etc and information from more recent surveys and inventories. Note that the occurrence data can both come from standardized inventories and observational records from specialists and amateurs (Citizen science data).

For climate related data you can start from Realclimate pages on data repository. For ecological data I always found less global data, but a good starting point may be the Ecological Society of America Data Registry page. An overview of repositories can be found the the Simmons University Open Access Directory.


text:
Identification of an Insect (Hemiptera)
I found a a few of these guys on my composter, so they could have easily been eating bugs or decaying organics (or both):

To me it looks like a stink bug with oversized legs, not like the ones I'm used to seeing. His body measures just under 3cm, and I haven't pulled on his legs to get a measurement (I haven't pulled on it at all).  The legs seem to be at least 1.5 times the body length as do the antenna.  The body is grayish brown and the antenna and parts of the leg seem reddish brown.
I'm a microbiologist, so things big enough to see in a jar are not really my specialty.  That said, here's info that I've been trying to use ID it:
Wingless Normal compound forelimbs (don't seem to have any kind of   prey modification)
Segments filiform antenna (I think)
2 Tarsomeres (I think)
In the middle of South East US
Have had (unusually) heavy rains
Underside of the limbs and antenna seem red, but to seems gray
I've never seen it before! (and I usually notice such things).
Update: Despite my 4 year old putting other bugs and some leaves in with it, the bug died.  I took the opportunity to get some much better photos, and low and behold when I started manipulating it I was able to pull out a substantial rostrum that I missed!  These guys are good at hiding those.  So going back to assassin bugs, can anyone id which assassin bug it is?
More photos: [I would add more but I think this should be plenty]

I at least think it's quite a pretty specimen (to betray my mammalian aversion to bugs).

Also if anyone could rule this out as a potential threat to vertebrates, ie Triatominae, that would also be appreciated (even if not a complete answer).

Thanks for the new pictures; see ID edit in my answer below

species ID
I feel reasonably confident this is a late-instar Acanthocephala declivis nymph (that is, almost-but-not-quite-adult).
Compare your pictures with those on bugguide of a similarly-aged individual, or the bugguide ID page. Also see the key here; which gives three characters for declivis

Humeral angles of pronotum broadly expanded, extending laterally well beyond maximum lateral abdominal margin. Distal dilation of hind tibia broad until apex, then curving in at right angles to tibial shaft. Anterior pronotal lobe with 2 small shining blunt tubercles along midline

If you look at your pictures, you'll see that you're three for three here: the broad 'shoulders' (pronotum), the right-angle in the leg flange (dilated tibia) just above the the 'ankle', and the two rounded bumps on the pronotum (visible in photos 1 and 3).
original answer / working towards the ID
You're right on track, it definitely looks like a true bug (Hemiptera/Heteroptera). Possibly immature if it looks wingless. Maybe some kind of Assassin Bug (Reduviidae)? They don't all have burly forelimbs. You might also want to consider Coreidae, for instance the genus Leptoglossus (pdf on Leptoglossus in Georgia).
You could try this key to Florida bug families, it looks pretty user-friendly.

Thanks for the link, I looked at that and didn't see it.  I'm also not in Florida, but it's more fuel for the search.  I agree it looks kind of like the assassin bug, but it seems to missing some of their features.  I'd vote you up but I don't have the rep here.  I'd accept any definite answered on the species/genus with a reference to a good description on the bug.  Happy for someone with editing power to bring in the images if possible.

Added in images for you (waiting on peer review)

Lacking a rostrum: interesting. Do you have a picture? I thought most bugs had piercing mouthparts of some kind. Often they're tucked away in a special groove underneath.

Thanks! Regarding the bug-beak, I'm not saying it's necessarily a vital diagnostic character, but if you're interested it should be there see e.g. http://bugguide.net/node/view/63015

let us continue this discussion in chat

I was completely wrong, it has quite a rostrum!

Nailed it. That bug guide photo looked like it exactly!

Maybe this is a late answer, but the difference between an assasing bug (Reduviidae) and a squash bug (or leaf-footed bug, Coreidae) is the structure of the beak.  Reduviidae, being predaceous, have relative short, bended beaks, made of three segments and do not go beyond the first pair of legs.  Coreidae, herbivores, have a long beak made of four segments.  This can be see it clearly in the third and fifth picture, it is a Coreidae.

It looks very much like a squash bug, which look close too assassin bugs but don't eat insects, probably explaining what it was doing in your mulch. I have the same thing.


text:
What is allele-specific gene expression?
I read somewhere that the two different alleles which we (and other species) inherit from our parents are not expressed equally in our cells. Which genes show allele-specific expression? How and why?

There are a few well known examples of allelic exclusion (which is what you've described):
In females (human and probably other mammals too) one of the two X-chromosomes is silenced (shut down) during embryo development. This means that some cells have one allele (from maternal X) active, while other cells have the other one (from paternal X) active. The actual mechanism behind this is quite complex, but ultimately results in the complete epigenetically-controlled prevention of gene expression from one X-chromosome. This is necessary because otherwise females would produce twice the amount of all proteins on the X-chromosome compared to males.
Another well known example relates to the genes that lead to the building of the B-cell receptors and antibodies. During maturation of the B-cells different segments of these genes are rearranged in a process call VDJ recombination. In order to make sure that the cells produce only one kind of B-cell receptor/antibody one of the two alleles for these genes is silenced after a certain rearrangement step has taken place.


text:
Are human beings evolved to eat meat?
I know humans can cook and prepare almost anything, but are humans specifically adapted to eat meat?
One of my doubts humans are not particularly well adapted to eat meat because they lack canine teeth. I read more reasons for this here.
What does an evolutionary biologist have to say on this matter? Perhaps evolutionary biology is the field related to this?
Some links supporting my doubt:

http://www.peta2.com/blog/humans-supposed-eat-meat/
http://mindfullybliss.com/humans-are-designed-to-eat-meat/

Please correct my question edit it for something wrong and put related tags

Human beings, or any living creatures, are not designed to do anything. There is no "design" in evolution, merely the accumulation of changes in gene frequencies.

And of course humans have canines - just look in a mirror. I'm not likely to trust anything published on "celestialhealing.net"...

what about the lost tail bone that we have, i think i used the design as the wrong word . but if you say the accumulation of changes in gene frequencies what accumulation of changes in gene frequencies so far we have been got up to from thousand of years back to us humans.are we vegetarins or carnivores or both.I know we can cook and eat anything

have you googled any of that questions?

yes i did, http://www.rense.com/general20/meant.htm and http://www.celestialhealing.net/physicalveg3.htm

@MattDMo we have canines but why they are so under developed and not like a tiger

that is another secondary benifit from large canines i guess but primarily i think it is for ripping out flesh, holding a prey with claws and large  canines, and puttting those canines on the neck of the prey kiiling them perhaps by stopping airflow

If you really think humans were "designed", you should move this question to your religion-of-choice site.

@jamesqf design was a wrong word i should have used evolved instead i guess.I think comment from kelt here is good explanation for this.It seems like an answer that should be here in biology.stackexchange.com for my question.OK, I changed it to evolved

@Munish: I will rebut that page, even if Mr. Blomstrom has begun to do so.

Carnivores don't swallow food whole.  That's why they have other teeth rather than just four large fangs.
Birds have no teeth.  There are many birds of prey that eat other animals, and there are birds that are nut/seed/fruit eaters.
Stomach acid: we have an extremely strong acid in our stomach, that if it weren't for a mucous layer protecting us, we would have a dissolved stomach.  Average pH of stomach acid is about 1 to 3.5 - that's very acidic.
Our intestinal tract is intermediate.  Well suited for both, not just one.  More importantly we lack the enzymes that can break down cellulose in plants.  If we were strict herbivores, wouldn't it make sense to have the enzymes necessary?
We are probably the best hunters on earth.  We have been able to hunt and kill almost any animal wanted and allowed.  We have highly developed brains that allowed us to invent firearms and send men to the moon.  People around the world rely on fishing for their dinner, and hunt deer legally for food.  Hunting is just not that economical for most people.
To say that were weren't designed to process flesh is absurd.  I ate beef the last two evenings.  Safe food handling is the contributing factor in "meat illness", unless the person eating has a GI disorder.
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1262767/ : This is one journal that concluded there was no evident relationship between excess protein intake and renal function.

That is a vegan website, and should stimulate skepticism considering they have a bias.  The point I'm trying to show isn't that we are made to eat meat, but rather choose for yourself.  Gain the information you need and make the choice based on the lifestyle you would enjoy more.

we can't eat raw meat like other animals do.i don't if our stomach will favour that , it won't taste good either but we can eat raw veggies and it tastes good. though there are some people who eat raw meat on live TV shows it seems favourable to their stomach

@munish: Humans certainly can eat raw meat, as attested by e.g. innumerable sushi bars.  Likewise, there are a good number of vegetables that can't be eaten unless cooked or otherwise processed, and others, like potatos, that are much better cooked.  There are also far more plants than animals that are actively poisonous when eaten.  It is also quite possible to get food poisoning from improperly-processed plant foods.  Indeed, from news accounts this seems more common than meat-related food poisoning.

Humans(aghoris) will do anything even eat discarded dead human bodies raw.Thats survival to save money, or may be religion

@jamesqf Great response, well said.  munish there is also a dish called steak tartare which is raw meat.  We can eat raw meat, but with all of the possible pathogens, it is advised to properly cook it first.  Many wild animals who eat raw flesh also can have a higher chance of parasitism, so it does come with negatives.

@MG_MD you are right that is a vegan website so they are vouching for that,  but i am not sure about this, do you have to say anything or those guys are wrong/manipulative.is this some sort of consipracy theory?the video and arguments seems legitimate.

@munish: If you want an answer, or even a comment, please post a link to readable text.  I do not wish to waste my time trying to extract information from videos.

@jamesqf though its not related to my question heres the link, just scroll down if you dont want to see the video

@munish I know that farming animals is not as ideal environmentally as hunting.  The sheer demand and amount of animals raised for consumption is beyond staggering.

@munish: Thanks for the text link.  However, it seems obvious that they are not addressing whether humans evolved to eat meat (the answer to that seems trivially yes, since basically all human societies do eat meat, when they can get it), but how & whether modern industrial agricultural methods can sustain massive human populations without causing environmental damage.  So one might, with equal justification, ask whether humans evolved to live in large cities, getting their food from supermarkets, instead of hunting & gathering.


text:
Do octopuses have better eyes than humans?
I've read that unlike humans, octopuses have eyes "designed" the "right way", i.e. with the nerve fibers behind the retina, thus getting rid of the blind spot we humans have as well as theoretically improving eyesight.
Have there been tests to compare octopus sight with that of humans, and do they indeed have better vision than us?

I'd suggest adding the tag "cephalopods".

Why would removing the blind spot result in better vision?

the blind spot perhaps not, (although it could come in ahndy if the eyes are on the side of your head and not in front), but mostly one would think that the lack of nerve fibers would somehow improve resolution, vision in dim light, etc.

monkey eyes can move so fast as to examine 10 branches and stems every second while they jump through the trees with awesome focus and positional mapping. chimps eyes have positional mapping for tree climbing that is 10x faster than human eye movement, so eyes have specializations for fine movement, distance, speed, narrow, wide, all very refined. eyes and ears are extremely advanced and perfected for the given environment. animal's primary senses are normally very near to perfection for their actions and needs. probably octopi trade range of eye movement for a more fixed structure.

There are a couple of advantages and disadvantages of possessing the eyes of octopuses.

The first advantage of the octopus eye is that it has no blind spot. This means that octopuses can see everything that is going on in their environment, and are more aware of predators and prey than some vertebrates. Also, they have many more photoreceptors than vertebrates, at roughly 20,000-50,000/mm2 which means that their vision is much better than that of any human.
The disadvantage of the octopus eye is that it can not see in colour. The eyes possess no cones, only the invertebrate equivalent of rods. This means that  octopuses can only distinguish between light and dark.

So if a diver and an octopus where to be threatened by a shark, the octopus would see the shark first?

Of course it depends, As I cleared above both have some advantages and disadvantages. So, It's completely depends. But In some manner of course the Octopus will see the Shark first because they didn't have blind spot so their field of view is more than a common person.

Nice answer, +1. Do you have a reference for the photoreceptor claim?

"Like other cephalopods, they can distinguish the polarization of light. Color vision appears to vary from species to species, being present in O. aegina but absent in O. vulgaris." - http://en.wikipedia.org/wiki/Octopus#Sensation

Would the blind spot matter? The respective blind spots of the two eyes don't overlap, so unless you are a pirate (I suppose a frequent victim of sharks), you will still see all the things in either of your blind spots, there will just be two small spots in your FOV where you don't have depth perception.

In terms of the number of photoreceptors; that may only benefit light sensitivity and not visual acuity dependent on the connections with the secondary neurons. The blind spot in humans is mitigated by binocular vision.

Adding to the answer above, another advantage of cephalopod eyes is the lower risk of retina detachment. (HumanEvolution)
Also, cephalopod eye focus image by moving the lense (like a camera or telescope), not by changing the lense's curvature, as in vertebrate eye (Wiki). Hence, I speculate that cephalopod would not experience either myopia or hyperopia. Cephalopod may still have problem with presbyopia at old age, affecting both near and far vision, however.
Furthermore, this article comparing human and cephalopod eyes might be of interest: QuarkPhysics

I thought presbyopia would not affect cephalopods. In vertebrates it's due to the lense becoming stiffer with age so it can't change shape, but as you say this is not how cephalopod eyes focus.

Ah, I mean if the muscles that move the eyes are not working properly when the animal ages, cephalopod would suffer presbyopia as vertebrates do.

Thanks, that's a good point (although I have no idea if old octopusses suffer a similar kind of muscle stiffness as humans, there's probably a lot more here that we don't know!).


text:
What does "delineate" mean in this context?
I was reading a Scientific American story, “Controversial Spewed Iron Experiment Succeeds as Carbon Sink” (by David Biello), when I came across this sentence:

“The problem for scientists is that oceanic waters tend to mix, which
  makes monitoring and delineating an experiment in the ocean
  challenging.”

I'm wondering what “delineate” means in this context. I think I grasp the general idea of this sentence, but it is the exact meaning of the word that has been troubling me.
Could someone kindly enlighten me on this?
Thanks!

I think this would me more on topic at English.SE, but (from Merriam-Webster):

Delineate:
1 a : to indicate or represent by drawn or painted lines
                b : to mark the outline of
2 : to describe, portray, or set forth with accuracy or in detail   — de·lin·ea·tor  noun

In this case, it could be either meaning that is used. Either 2, as Richard Smith said in his answer, to define the experiment's parameters in general, or 1b, to mark, limit a specific area of the ocean in which the experiment will be done. Obviously, delimiting an area in a body of liquid is not very easy.

Didn't think of that!

Thanks for your help, terdon. Your explanation has given me a clearer understanding about the implication. I like 1b myself.

To delineate an experiment is to describe precisely the conditions and the states of all the parameters.
So in your sentence it probably means a scientist might struggle to keep track of all the confounding factors (changing salinity, composition, dissolved gases, particulates, pH, temp, etc.) which might affect an experiment in such a dynamic system as the ocean.

Preamble
This is a very old question, the relevance of which to biology is not immediately apparent. The source is not cited, and the extract is so short that it is impossible to deduce the intention of the author from the context. However because the question relates to clarity and precision in written communication in science I am providing an answer.
Answer

The word ‘delineate’ has no special meaning in science that differs from that in everyday use.
Its everyday use in the sense of defining the boundaries of something makes it clearly inappropriate to apply to the word experiment. Thus, the confusion of the original poster was quite justified.
One possibility is that in using the word ‘delineate’ the author was thinking of the lack of a clear boundary between two oceans because of the mixing. In this case he should have written something like
“The problem is that ocean waters tend to mix, so it is difficult to devise experiments that distinguish between them.”
A second possibility is that having this idea in his mind, the author used ‘delineate’ when he meant ‘devise’, ‘design’, ‘construct’ etc.

Observations

Just as in designing software interfaces, if the user is confused it is the designer — not the user — who is at fault. (And there is no indication here that the OP was confused because of not being a native English speaker.)
Nobody is perfect, and writing articles where there is a word limit can often mean sacrificing clarity for brevity. However that does not justify pretending that the emperor is fully clothed when he is quite clearly naked.

I disagree that it's meaningless, the context of the sentence is quite clear; ocean water mixes, so it's difficult to do an experiment there, but not just any sort of difficult, it's particularly difficult because the boundaries/delineation of the experiment cannot be drawn clearly. If only the first part of the sentence was present the writer would be entirely leaving it up to the reader to draw the conclusion on their own; possibly they'd come to the same realization, but if you're the author why not just state it explicitly so that they know what you mean? That's not padding out.

"Distinguish the two" what? What two? To delineate an experiment would be to delineate (the boundaries of) an experiment, but it's not necessary to state (the boundaries of) part.

@BryanKrause — I have deleted my previous comments to present my argument in a revised and extended answer.


text:
Why does the apex of the human heart usually point to the left?
In the majority of human beings, the apex of the heart (left ventricle) points towards the left side of the body.  Sometimes however (approx. 1/12000 births), a person is born with a condition known as "Dextrocardia", in which the apex of the heart points to the right side of the body instead.
Is there an evolutionary reason as to why the human heart usually points to the left side as opposed to the right side of the body?
(Note:  Please don't answer with, "because there is a notch in the left lung", because I will simply reply with, "is there an evolutionary reason for the apex of the heart AND the cardiac notch being on the left as opposed to the right side of the body").

Also note there is a condition known as Situs Inversus with Dextrocardia, which is where the placement of all the organs in a person with this condition is a mirror of that of a normal person.

So I am asking that since people can live normal lives with Situs Inversus Dextrocardia, why is the placement of the heart on the left so much more common than placement of the heart on the right?  What's the evolutionary advantage?  Thanks

Is the orientation of the heart in humans different from other mammals? If not, then there would appear to be nothing special about humans. Heart orientation is just inherited from ancestral mammals.

Good point Kevin.  I'm not sure if mammals hearts also are directed to the left or not.

https://www.sciencemag.org/content/306/5697/828.abstract seems to have the answers you seek. You'll need a subscription to Science though.

From a quick look at the paper @ChinmayKanchi links to (Palmer, 2004) it seems that:

All living vertebrates possess a heart that is conspicuously asymmetrical and normally displaced toward the left (Fishman & Chien, 1997).

So the heart orientation seems to be evolutionary conserved in vertebrates (as are many fundamental traits), and no specific explanation is needed for humans.
This is said with the reservation that human anatomy is not my subject field, and the refered paper also digs deeper into the molecular basis for the orientation/symmetry of organisms. For instance, it also says that:

Second, the molecular pathway directing hearts leftward—the nodal cascade—varies considerably among vertebrates (homology of form does not require homology of development) and was possibly co-opted from a preexisting asymmetrical chordate organ system.

so the molecular mechanisms governing this seems to differ between species. This could indicate that there is a selective pressure molding species into the same heart orientation. This is pure speculation on my part though.
I also want to mention that evolutionary outcomes doesn't have to have a "reason" (i.e. a selective advantage). Much depends on chance events and evolution can only act on what is present at the moment (i.e. is restricted by earlier evolutionary history).

I think it is because of the reason that the left ventricle pumps blood throughout body, thus is bigger than the right ventricle. So, actually, the human heart is along the center septum, but seems just a bit to the right. 1.5 cm to be precise.


text:
What are these caterpillars eating a potato plant?
I saw these caterpillars rapidly consuming a potato plant in Central Texas:

They have thin, dark green-blue bodies with yellow-white longitudinal stripes and a bright rust-red head. Their body seems to be covered in fine hairs which may be difficult to see in the photo. They are about 1 cm long.
On some leaves of the same plant I saw what appear to be eggs - little black balls 1-2 mm in diameter, with a shiny appearance reminiscent of black caviar (well, I suppose they are black caviar). They seem to cover only a handful of leaves, in groups of about 100 or so (rough guess). Some can be seen in the photo.
Curiously enough, nearby there were tomato and strawberry plants, but they were not affected, while the potato was extensively predated (a few dozen leaves consumed).
What are these caterpillars? How do you kill them?

The "eggs" are poop (good for th soil, though I wouldn't call them caviar ;). As the caterpillars grow, their poop increases in size. (I've raised a number of caterpillars in an effort to increase the population of endangered butterflies.)

I think they are eggs. They are round and occur in clusters (can't see easily in this picture). The caterpillars leave what I think is poop as well, it is smaller, cigar shaped, irregularly shaped and fluid.

If they are in dense clusters, you are very likely correct. I don't know what you're describing is... I've never seen it. @theforestecologist will know, though.

@anongoodnurse They might be poop as well, it's hard to tell, but they seem like eggs to me (not in this photo). I'll see if I can get a high quality image of the eggs.

A better photo would help! I'm stumped. I've searched everywhere I know to. I like the rear end of these caterpillars: slightly bulbous with kinda fake eyes?

An Armymoth I think, probably Southern Armymoth(Spodoptera eridania). Id and
Management.

@anongoodnurse Well looks like you were right after all - I was really thrown off because the poops were concentrated in several (~20) clusters of 3-10 on certain leaves, while most leaves had very few of them. But the accepted answer has convinced me.

I believe this is the middle instar of a Southern Armyworm (Spodoptera eridania) larvae. Or some closely related species in the Spodoptera genus (family Noctuidae).

 © 2016 Wings, Worms, & Wonder
The larvae undergo six instars as they grow to attain a length of about 35 mm.

You can see a series of life stage pictures from Mississippi State.

Armyworms are so called because you typically find 100s at a time on a single leaf or plant. According to here:

Armyworms strike in the blink of an eye, and there are so many in their army that you will be finding them for weeks after the primary attack.

Behavior: larvae are mostly active at night and hide on leaf undersides, in curled leaves, or in leaf litter during the day.

This University of Florida site claims

Young larvae feed on under surface of leaflets leaving upper epidermis intact ("windowpaned"). Older larvae consume foliage and eat large holes in fruit.

Range: native to the American tropics (occurs widely in Central and South America and the Caribbean). Also found in US (principally in the Southeast but extends West to Kansas and New Mexico). It also is reported from California.

Here's a map showing some confirmed sightings [source]:

Host Plants:
This species has a very broad host range including important crops (including potatoes).

I would be concerned for your nearby tomatoes, because thy too are a favorite food of these insects.

See here for more information including management suggestions.

Defecation vs. Eggs??
The picture in the question shows S. eridania's feces.

This Mississippi State site includes a great zoomed-in picture of S. eridania's feces:

 © Lee Ruth
Note: caterpillars don't lay eggs. Only adult moths/butterflies lay eggs.
Eggs: large masses of 100-200 eggs covered with moth body scales, found on underside of leaves, hatch in 3 days.

 © 2016 Wings, Worms, & Wonder
Here's a picture of inside the seed casing of closely related S. exigua [source]:

 © 2016 Wings, Worms, & Wonder

Finally, here's a picture of the nocturnal adult:

Enter the cavalry! How did you find this?

haha :D. Well, truth be told, I don't know my lepidoptera as well as I could. So I simply started by googling a general description, then followed some links to seemingly related-looking species and eventually I narrowed it down. Took about 10 minutes :p.

Really nice answer and info!


text:
Does endo- and (or) exocytosis require energy? Do they belong to active / passive transport?
I expect vesicle formation and fusion to require energy input; however, I'm not sure about which of endocytosis and exocytosis require energy and how they use the energy input.
Do they belong to active or passive transport?

Wikipedia is your friend:

Exocytosis... is the durable, energy-consuming process by which a cell directs the contents of secretory vesicles out of the cell membrane and into the extracellular space.

and

Endocytosis is an energy-using process by which cells absorb molecules (such as proteins) by engulfing them.

Emphasis mine.  Here's a nifty paper which gave some evidence a few decades ago for some basic intracellular thresholds for budding and fusion, and this paper shows that endocytosis definitely requires ATP, using a novel assay.  Check the sources, too, some of them are excellent.

What on earth does 'durable' mean in the context of that first quote?

@AlanBoyd Durable=long lasting, survives wear-and-tear.  I interpret it to mean that exocytosis doesn't just pop in and out of existence, quantum mechanics style, it's "intentional" and can last.  That's my guess anyway, it's a weird word choice to be sure.

Just to extend the answer from @Amory slightly, I think that the terms active and passive transport are best kept for describing transmembrane movement of molecules.
In the case of exocytosis the only transmembrane event is when a secreted protein is first inserted (usually cotranslationally) across the endoplasmic reticulum membrane. I'm not aware of any evidence that this uses more energy than that already expended during polpeptide elongation by the ribosome. At that point the secreted protein is topologically extracytoplasmic, and everything else is achieved by rounds of vesicle formation and fusion of vesicles with target membranes.
The same is true in reverse for endocytosis. Any molecule that is internalised in an endocytic vesicle is still extracytoplasmic unless some process specifically moves it across the membrane of the vesicle, or a downstream organelle such as the endosome. At that point whether the transport process was active or passive would depend upon the properties of the carrier system.