text:
What are the psychedelic effects of (star) anise and how many people are affected?
Backstory:
My girlfriend reacts heavily to chocolate and drinks containing stellar anise, in a way that seems comparable to psychedelic drugs.
After consuming it, it takes approximately five minutes for the reaction to become apparent.
Observed Effects:
Due to the heavy reaction, she tends to avoid these foods, however, we could observe the following effects:

Heavy giggling, occasional outbursts of loud laughter;
Much less frequent: Crying (just kind of starts from the giggling and subsequently fades back into giggling);
Minor hallucinations (Sparkling hair, glowing faces);
Loss of motor skills, especially balance;
Feeling time pass much faster (to her, a 15 minute episode felt like 1-2 minutes, an hour like 5-10 minutes);
Some memory loss (probably related to the time perception?);
Unfocused mind;

Her speech remains clear and articulate.
Observations are anecdotal, as I only observed two episodes, and we realized what happened only after the first.
Googling Results:
Apparently, around 1-3% of humans react in some way. However I couldn't find any detailed explanations of the hows and whys, nor any actual research.
I am very curious about this. Is it dangerous? Are there any related effects (genetic disorders, maybe?). All explanations, and hints how to google better, are welcome.

This is interesting, but terrifying. Have you considered the possibility that there may be Japanese Star Anise (Illicium anisatum) adulterating what your girlfriend thinks is edible star anise (Illicium verum)? [Note, using the latin names may help your google searches as well, pointing them towards scientific literature]

No, the episodes we observed didn't happen with any homemade food. The first one happened with regular store brand chocolate (after that, she realized that she always behaved odd after eating this particular chocolate) and with Sambuca, of which we all drank some.
But thank you for the hint!

This is the correct SE site. PS: what is stellar anice? Don't you simply mean star anice?

Interesting question! As this post has been sitting around for a while I am going for some speculations. First you talk chocolate, which essentially contains the alkaloid theobromine. Anise contains the propenylbenzene (E)-anethole (Idle, 2005). Theobromine is a caffeine-derivative and basically produces alertness, but also restlessness and perhaps anxiety when administered in large amounts (wiki). In extremely high doses there can be LSD-like effects (anecdotal report). Perhaps (speculative) your girlfriend is especially sensitive. Then (E)-anethole: the late Alexander Shulgin, Godfather of MDMA, has made the etheric oils (in)famous as precursors for amphetamine synthesis. In themselves the propenylbenzenes like (E)-anethole are quite harmless, as they do not contain an amine group (a prerequisite for being called an alkaloid). However, heating (E)-anethole in the presence of ammonia may lead to the production of PMA, a compound structurally and neuropsychopharmacologically related to MDMA (Idle, 2005). Although a bit of chocolate and a sip of Sambuca do not meet any of these conditions, both chocolate and Sambuca do contain certain psychoactive compounds, or their immediate precursors.


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Does drinking spoiled milk that has been boiled upset the GI tract?
With water, boiling will kill harmful pathogens. Does this also hold true for milk ? If it does not, what in the milk will continue to cause gatrointestinal distress ? Shouldn't boiling kill the harmful bacteria ?
I'd rather not get into a discussion whether animal milk should be consumed by humans. I am asking about a typical person who is not lactose intolerant and does not have any milk allergies.

Toxins could be produced by the bacteria that spoiled the milk that wouldn't be destroyed by boiling. Similarly, spores could be formed that are impervious to boiling as well.

@MattDMo If you would like to create an answer out of this I will mark this thread as answered. BTW out of curiosity, which toxins are they and how do spores upset the GI tract ?

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Ebola: cleaning of protective suit
As far as I know, in developed countries protection suits used by people who treat patients with Ebola are disposed of after a shift.
From a rather ambitious costume last year, I still have a hazmat suit like this one and this full-face gas mask.
More out of curiosity than out of real concern, I was wondering whether it would be possible to use this equipment in a potential outbreak of the virus. My greatest concern would be reusing the suit, as it might not be safe after the first use.
Is there a way to disinfect the suit and mask with publicly available chemicals? For example, I could imagine a friend spraying me with a solution of chlorine. Would that be feasible and make wearing the suit reduce the risk of an infection?

You cannot disinfect the filter of a gas mask. If these get wet, they will become more or less impassable for air.

Then the question would be extended to whether wiping the mask with some disinfectant would be enough, instead of pouring something over it.

Disinfection is not so much a matter of the amount of disinfectant used but of the time it has to be active and of the active concentration.

And please remember that the likelihood of a real ebola outbreak in a developed country with modern healthcare system is extremely low. And in the rare event that an ebola outbreak does occur, you're probably better off avoiding physical contact with people than trying to wear a hazmat suit all day.

Notice: the only select agent I've worked with is VSV which was a USDA select pathogen (not as big of a concern for humans).
TLDR:  It would provide some protection, but I would be most worried about a false sense of security.  It would unlikely be up to rated standards, but it would likely be better than a t-shirt.
First let's start with ebolaviruses.
Ebola, like HIV and many other viruses, doesn't do well outside a host.  This might be because the protein structures beneficial in the host are not the same as needed for stability in exposed air and room temperature.  A counter example of a very stable virus would be something like human rhino virus (HRV).  If HRV was compared to be like a rock, ebola would be over cooked spaghetti.
Certainly the virus has to maintain some stability in the environment, otherwise it wouldn't succeed evolutionary.  As I'm sure you've heard on the news, ebola is spread by contact with contaminated fluids.  I would like to point out a wonderful info-graphic that was made for public consumption, especially the image on viral life cycle:

Assuming that you're not going splunking in bat inhabited caves in West Africa, it's safe to assume that what we are worried about is human to human transmission through infectious fluids.  Ebola actual isn't that stable in water, so just soaking a surface in water and a little oil might help you out (if you don't have bleach handy).  I want to be clear that I'm not recommending this, in reality you should just avoid contaminated objects.  I think that we have clearly established that what we're really concerned about is infectious bodily fluid.
This leads me to the wonderful note by Jose Martin-Moreno titled "Is respiratory protection appropriate in the Ebola response?"  I don't think I can express the problem better than he can, so hopefully I will be allowed a substantial quote:

This transmission [of ebola] occurs via close family contact or in
  health-care settings, particularly when placing orotracheal intubation
  or when caring for a patient who is vomiting or bleeding. Ebola is
  rarely transmitted via an airborne route. Although these routes of
  transmission are well known, most agencies, including governmental
  agencies responsible for repatriating western patients, apply
  infection-control measures appropriate for airborne diseases.
  Excessive precautions could offer reassurance to those responding to
  Ebola, yet complete respiratory protection is expensive,
  uncomfortable, and unaffordable for countries that are the most
  affected. Worse, such an approach suggests that the only defence is
  individual protective equipment, which is inaccessible to the general
  population. Moreover, the image of workers with spectacular protective
  clothing might contribute to the panic in some communities. If this
  leads people to flee affected areas it could increase the spread of
  infection.

With that said, all your full face gas mask is going to help with is prevention of fluids from hitting your head.  You could probably take the actual filters out to breath more easily (I find breathing in them a giant pain).  And as @Chris pointed out, they are easily clogged which could necessitate the need to take off the whole mask (which might be doing some good) to prevent suffocation.
Moving to hazmat suit.
It's actually good news that you don't need the air containment of the suit, as that's the hardest element to maintain.  To state the obvious, the main purpose of the suit is to prevent your body from coming in contact with infectious fluids (in this case).  To do that you don't need to be in positive pressure personnel suit (PPPE), or follow BSL4 considerations.  The respiratory concerns from in an BSL4 environment come from other select agents, and the personal working in such a facility are going to be doing very different activities from what you should be doing as person trying to avoid an outbreak (they could be purposefully growing up purified high-titer virus stocks and running around with pointy things as an example).
Here I'm going to run into citation problems because no one (that I could find) has tested the kind of scenario I'm about to discuss, so it should be seen as informed conjecture.  Assuming yous suit is actually an analog of a Tychem QC suit, it's probably not a rated OSHA unit (A-D), but that doesn't necessarily matter.
On it's first use it would likely be sufficient to protect against incidental exposure.  Let's assume for the sake of argument that you didn't run into any Ebola when you used it as a costume, and don't the next time you put it on.  At this point decontamination (decon) isn't the concern, failure of the material is.  In other words, are you sure you don't have any holes, tears or cracks in the material?  I think this is going to be the real limiting factor in the life of the suit.  Using good old fashioned duct tape will be give you a few more uses, but the suits are just not designed to last through prolonged use.
Now let's assume the worst and that you get substantial blood splatter on you (while wearing your suit) from an ebola patient.  And not a little that could easily be wiped of with a spray bottle of 10% bleach and a paper towel (how most decon could be done).  Instead let's assume you're standing next to someone who suffers a traumatic injury on top of having ebola virus disease (EVD).  I'm imagining something like a point-blank shotgun wound or, given the probability of this scenario, a falling grand piano. In this case, you're going to want to decontaminate the suit before you take it off, which is the same thing professionals are going to do.
If you're friends with your local fire department, and you live in an area with a large enough population to have a HAZMAT team, you can probably get them to at least give you a run through of how it's done in ideal conditions.  YouTube videos are also not hard to find, just search JESTC and decontamination.
Presumably you would have a hard time going through several rinse and wash steps, but you would want emulate this as much as possible.  With ebola, you would be fine to decontaminate with a 10% bleach solution (or if you use bargain/cheap bleach 15%).  The trick is that you would want to do it a few times, and with a friend (also hopefully in a suit).  Thus if you got two generic soap sprayers, filled one with 10% bleach, and the other with water, and then alternated spraying your partner with bleach and water, wiping down as you went, you should be able to decon the suit pretty well.  If possible you're going to want to collect all the run off an rinsate.  Again professionals tend to use actual kiddie pools for this.
But just the act of using so much bleach on the suit is going to weaken the fabric, again leading to the principle problem of failure of the fabric. Thus I would be worried that such a suit would provide a false sense of security, leading one to go into dangerous infectious environments when one shouldn't.  Just avoiding and going away from contaminated individuals is going to be the best solution, regardless of a suit.
I considered going into why I think it's highly unlikely that any of the ebolaviruses would evolve to be airborne, but I consider that outside the scope of the question.

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How do you visualize RNA on a gel?
I have run an in vitro transcription reaction and produced some RNA of a single species and definite size. I would like to visualize it to check if the reaction worked.
Can I do this on an agarose gel? Is it sufficient to simply make a 1% TAE-agarose gel with EtBR that you would use for routine DNA electrophoresis, and run this? Is it necessary to take special measures against possible RNAses in the gel or the running buffer?

Include in your agarose gel 4% household bleach to inhibit rnases. It's a much easier alternative to PFA and just as effective.

You have two possibilities: When you only need a quick check if your RNA is ok and you indeed only get one band, you can try a "quick and dirty" method. Heat the sample for 5 minutes at 65°C and then immediately cool it down in an icebath and keep it there until loading. By doing so, you melt up the secondary structure of the RNA and keep it in this state. You will most likely then see only one band.
If this doesn't work or if you want to use a RNA size marker, there is no way around denaturating gel electrophoresis. Here you denature your sample in the loading buffer and then run a denaturating gel in which prevents the secondary structures. There is a good paper about this:

Denaturing RNA electrophoresis in TAE agarose gels

The classical method using formaldehyde (which is more dangerous in handling) is described in the following paper and also in the "Molecular Cloning: A Laboratory Manual" book by Maniatis and colleagues:

RNA molecular weight determinations by gel electrophoresis under
denaturing conditions, a critical reexamination

RNA is amenable to folding, which produces secondary structure and alters its mobility (compare to supercoiled DNA). Therefore, if you don't denature your RNA appropriately, even a single species will produce a smear.
A common strategy is to incorporate denaturing chemicals such as formaldehyde into the procedure. See this Life Technologies protocol.
Apparently, you can also just make a standard DNA gel with some added bleach. I haven't used this technique, but they have some samle results.

I use a 1% nondenaturing agarose gel with ethidium bromide. I use Better Faster Media LB buffer so I can run a high voltage and get my gels done faster. I usually see 2 bands on the gel due to RNA secondary structure, but that can be fixed by heating it to 65C for 5 minutes, followed by chilling on ice for 5 minutes. My RNA may be different from yours, so you might not be able to get a single band with this trick. What I haven't been able to do is run an RNA ladder on nondenaturing gel, but I haven't really tried that hard.


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All or nothing phenomena
We know that an action potential is produced by an active cell membrane when the stimulus reaches a certain threshold. When it does, an action potential fires, and when it doesn't, nothing happens.
There are dozens of videos online painstakingly illustrating this point, using examples going from plumbing to pebbles falling down a paper towel.
But this is such a simple idea. There doesn't need to be analogies. When I push a button, something moves, when I don't push it, nothing moves.
But what is the fundamental principle behind this? What biochemical device causes this all or nothing phenomena?

The fundamental principle behind this is a "sensor" or the excitation-contraction coupling, regardless where you are.
Let's consider the striated muscle and the cardiac muscle.
The function of excitation-contraction coupling in skeletal muscle is as voltage sensor to tell the SR, "We have got an action potential; release Ca2+ for contraction".
This is a contrast to a heart muscle which works like a Ca2+ channel (i.e. Ca2+ is flowing in cardiac muscle continuously).
Similarly, xcitation-contraction coupling in cardiac muscle translates the action potential into the production of tension.
There are individual steps in this process of cardiac muscle:

The cardiac action potential is initiated in the myocardial cell membrane, and the depolarization spreads to the interior of the cell via the T tubules.
Recall that a unique feature of the cardiac action potential is its plateau (phase 2), which results from an increase in Ca and an inward Ca2+ current in which Ca2+ flows through L-type Ca2+ channels (dihydropyridine receptors) from extracellular fluid (ECF) to intracellular fluid (ICF).

Entry of Ca2+ into the myocardial cell produces an increase in intracellular Ca2+ concentration.
This increase in intracellular Ca2+ concentration is not sufficient alone to initiate contraction, but it triggers the release of more Ca2+ from stores in the sarcoplasmic reticulum through Ca2+ release channels (ryanodine receptors).
This process is called Ca2+- induced Ca2+ release, and the Ca2+ that enters during the plateau of the action potential is called the trigger Ca2+.
Two factors determine how much Ca2+ is released from the sarcoplasmic reticulum in this step: the amount of Ca2+ previously stored and the size of the inward Ca2+ current during the plateau of the action potential.

and 4. Ca2+ release from the sarcoplasmic reticulum causes the intracellular Ca2+ concentration to increase even further.
Ca2+ now binds to troponin C, tropomyosin is moved out of the way, and the interaction of actin and myosin can occur.
Actin and myosin bind, cross-bridges form and then break, the thin and thick filaments move past each other, and tension is produced.
Cross-bridge cycling continues as long as intracellular Ca2+ concentration is high enough to occupy the Ca2+-binding sites on troponin C.

A critically important concept is that the magnitude of the tension developed by myocardial cells is proportional to the intracellular Ca2+ concentration.
Therefore, it is reasonable that hormones, neurotransmitters, and drugs that alter the inward Ca2+ current during the action potential plateau or that alter sarcoplasmic reticulum Ca2+ stores would be expected to change the amount of tension produced by myocardial cells.

I like this figure about the topic in summarising stimuli in the smooth muscle:

In heart

In the gastrointestinal tract, we have then again special cells, Cajal cells, that work as "pacemakers" of the GI tract.
Myenteric Interstitial cells of Cajal [ICC-MY] serve as a pacemaker which creates the bioelectrical slow wave potential that leads to contraction of the smooth muscle.
This activity differs along the length of the system

3 per minute in the stomach
11-12 per minute in the duodenum
9-10 per minute in the ileum
3-4 per minute in the colon

You can see them as to work analogously through the "all-or-none" principle.
Sources

Costanzo, Physiology
Pocock, Physiology
My notes during during years 2011-2014 (in three Physiology courses and research)


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Can the sensory neuron network and the motor neuron network be considered separate networks?
I am reading up on the nervous system using Wikipedia and trying to interpret one infographic on this page:

I've always thought of the human nervous system as a singular network of neurons. This diagram however makes a distinction between 'Motor neurons' and 'Sensory neurons'.
Can the sensory neuron network and the motor neuron network be considered separate networks?
Indirectly they will definitely be interconnected (because of impulse-response relations), but physically, are they connected or disconnected?
Or are there more?
It is very well possible that I am missing some knowledge to make this question make sense.

The sensory and motor pathways can indeed be considered separately both in concept and physically. Of course the nervous systems is a single network of neurons, but that doesn't stop it from having separate components.
One can indeed often simplify neural pathways as "IN (sensory) ===> (black box with decision-making magic) ===> OUT (motor)"
Reflexes
Reflex arcs are a great way of demonstrating this separation because they do not involve the more complicated integration of the brain. Let's take the knee-bend (patellar) reflex as an example: https://en.wikipedia.org/wiki/Patellar_reflex

The diagram is correct in concept but let me add the anatomical detail to illustrate how sensory and motor pathways are separate, yet connected: When the reflex is triggered, the signal travels up from the sensory neuron ends located under the knee cap (these are dendrites) to the sensory neuron's body in the spinal chord. The sensory cell relays the signal via its axon, which then synapses with a motor neuron's body also in the spinal chord. The motor neuron then sends a motor impulse via its axon back down to the leg, where it triggers muscle contraction.
Physically, in this case there will be a separation also in nerves (at least if I may trust Wikipedia for now), where the sensory reflex neurons' dendrites travel from the leg to the spinal chord through an afferent nerve and the motor neurons' axons travel in the reverse direction through an efferent nerve. The only physical and conceptual connection between the sensory pathway and the motor pathway is the synapse between the sensory and the motor neurons in the spinal chord.
More complex sensorimotor pathways might include interneurons or integration with various circuits in the brain, but it is usually possible to define discreet separate parts of the pathway, one sensory and one motor, with the only connection being those interneurons.
Sensory and motor separation in the CNS
The central nervous system (CNS, which includes the brain and the spinal chord) is actually surprisingly organised in this regard, with quite strict separation of motor and sensory pathway components. For example, the cortex of the brain has distinct regions which contain sensory neurons for evaluation of various types of peripheral skin sensation. Separate from these are regions which contain motor neurons for movement of skeletal (voluntary-control) muscle. The interaction of these is of course more complex given that it involves skin sensation and conscious decision making in regards to movement.

Likewise, the spinal chord is structured into sensory and motor regions. In summary, the spinal chord consists of: 1) cell bodies (motor, sensory, inter; grey in the picture), 2) ascending axons (blue), 3) descending axons (red). Similar to nerves, axons going up or down the spinal chord are bundled into "tracts". Sensory axons are never bundled with motor axons, making it possible to create a map of the spinal chord in cross-section.
The tracts' names might be a bit confusing at first, but on second look are actually pretty self-explanatory. They usually contain where the axons come from and where they are going in order to synapse with other neurons. E.g. the spinocerebellar tract is formed of axons coming from the spine and going to the cerebellum. Given that the cerebellum is near the brain and the spine is further down, this is obviously an ascending tract - and ascending tracts are always sensory (because sensory information never needs to be carried downwards due to the brain being at the top).

Where it gets blurry
The sensory/motor separation isn't always as clear as I've described above. In fact, nerves (bundles of axons anywhere in the body outside of the CNS) will usually contain both sensory and motor pipelines. In particular, the cranial nerves (12 of the most important nerves) all include sensory and motor components for the respective part of the body that they manage. E.g. the facial nerve contains both the sensory connections for parts of the tongue and the motor connections that control facial muscles.
Another more complex example is pain sensation, where interneurons in the spinal chord can feed back onto sensory neurons and inhibit their signals, or axons can inhibit those packed in the same nerve bundle simply due to electrical effects.

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Fe(II) and Fe(III) transport from rhizosphere across plasma membrane
Does the graminaceous plants have passive uptake of Fe(II) via a passive Fe(II)-transporter enzyme? Or it it only dicots and non-graminaceous plants that have the Fe(II)-transporter enzyme? Also, can Fe(III)-reductase reduce Fe-EDDHA (Ethylenediamine-N,N'-bis(2-hydroxyphenylacetic acid)) and Fe-DPTA (diethylene triamine pentaacetic acid) without the cost of energy?
Best regards,
Mathias


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iodine: how did they manage without it in old ages? (People who were living far from the sea)
Knowing that today iodine comes either from fish products or (artificially) enriched table salt, how did people who lived far from the sea survive before (especially during the the Middle Ages)?
Edit 1: nowadays we could find some iodine in cow milk, cheese and eggs but those sources are artificial

(Increased iodine content in food due to greater use in: food
  processing, animal rations, antimicrobial agents...)

source
Edit 2

A small amount of iodine enters the atmosphere and, through rain,
  enters ground water and soil near the sea

source
Summarized of the comments: thanks to  ddiez this question has been partially answered. But as vsz pointed out the the mystery remains:

areas with iodine deficiency didn't get completely depopulated during the Middle Ages
  seems to suggest that it does not affect all people that severely.

So the question remains: could humans survive and reproduce without any iodine source?
Edit 3:

“If all women in the UK took iodine supplements while pregnant, IQ
  would rise by 1.2 points per child” but some says "Some observational studies suggest supplements could even lower IQ, perhaps because excess iodine might harm the thyroid gland." (Newscientist, August 2015)

They had problems - strumae were pretty common in old ages.

@Chris, I would like to suggest tagging this question with "iodine" and/or maybe "thyroid hormones". None currently exist. No experience so far with tagging and its rules.

@ddiez I think iodine is a bit too specific to warrant a tag and thyroid hormones as a tag only indirectly describes this question; I think it's prefectly appropriately tagged

@Armatus I understand, and agree, with your arguments. Thanks for the explanation.

@GuillaumeCombot, I am afraid you have misunderstood my answer/comments. Iodine appears naturally in food (although certainly can be added). Iodine deficiency has not been an issue at all in the Middle Ages in places where the water or soil was iodine-rich. Iodine deficiency is still an issue today in many parts of the world. I have updated my answer to make things more clear.

Iodine is naturally found in sea water and soil but it is not evenly distributed, with many areas in the world with low levels of iodine. Iodine accumulates naturally in fish, and plants growing in iodine-rich soil. Mammals that eat these plants get iodine from them, which then accumulates in the milk, making dairy and its products (e.g. cheese) another natural source of iodine. Table 1 from the Iodine deficiency section at the American Thyroid Association web page contains a brief list of iodine-rich food.
Quoting the web site:

What are the sources of iodine?
Iodine is present naturally in soil and seawater. The availability of iodine in foods differs in various regions of the world. Individuals in the United States can maintain adequate iodine in their diet by using iodized table salt (unless they have to restrict the amount of salt in their diet), by eating foods high in iodine, particularly dairy products, seafood, meat, some breads, and eggs, and by taking a multivitamin containing iodine (see below). However, the amount of iodine in foods is not listed on food packaging in the U.S., and it can be difficult to identify sources of iodine in foods.

As mentioned, the amount of iodine in some food depends on how much iodine is present in the water or soil. For example, in the International Council for the Control of Iodine Deficiency Disorders (ICCIDD) there is some mention about the natural sources of iodine and its limitations:

Most of the iodine we consume comes from what we eat and drink. Seafood is usually a good source because the ocean contains considerable iodine. Freshwater fish reflect the iodine content of the water where they swim, which may be deficient. Other foods vary tremendously in iodine content, depending on their source and what may have been added. Plants grown in iodine-deficient soil do not have much iodine, nor do meat or other products from animals fed on iodine-deficient plants. Because the breast concentrates iodine, dairy products are usually a good source, but only if the cows get enough iodine.

Iodine deficiency causes important health problems. Iodine is necessary to produce thyroid hormones. Lack of thyroid hormones causes hypothyroidism, cretinism and goiter. However, iodine deficiency is not mortal per se.
Conclusion
As a consequence, in the Middle Ages iodine deficiency was not an issue in places where water and/or soil was rich in iodine. In other places they would suffer of iodine deficiency, leading to a higher impact of the related diseases.
Nowadays, iodine is added artificially to food in order to prevent iodine deficiency. This practice has diminished the impact of iodine deficiency-related diseases. However, iodine deficiency is still an important issue today, as reported by the World Health Organization in its map describing the Degree of Public Health Significance of Iodine Nutrition. As shown in the map, in many places in the world there is still risk of severe iodine deficiency.

Sources:

Iodine deficiency - Wikipedia
American Thyroid Association
World Health Organization
International Council for the Control of Iodine Deficiency Disorders (ICCIDD)

thank for your detailed response! I added more details in my question, it's more tricky that it sound.

@GuillaumeCombot I am sorry but cannot see how your edits change my answer. Is your question different? Basically in the Middle Ages people got iodine from food, wether it be sea food or other food (e.g. vegetables and dairy) from places with iodine rich soil. Iodine deficiency does not typically cause death - but some (very serious though) diseases. During the Middle Ages those diseases were more prevalent.

I suppose they could have eaten thyroids, that's where the most iodine would have been. But most people at that time probably couldn't get much meat anyway, and they probably wouldn't know enough to associate thyroid consumption with preventing iodine deficiency, or even knew about iodine deficiency. And I have no evidence to say whether or not anyone actually ever ate thyroid.

@user137 certainly in the Middle Ages they did not know about iodine deficiency and eating thyroids would, very likely, not be extended. Iodine deficiency appeared in places with iodine deficiency in soil or water, or (and that is a fair comment) in places where people didn't have access to food or water. However in those places starvation and malnutrition would probably be a much more serious issue than iodine deficiency.

@ddiez the things is that unless they were living near and not too far from the sea they could not get it from food (iodine can only be fund in the soil near the sea since it comes from the sea so for instance around Paris or Berlin or Moscow you would logically not have fund anything is the soil, and thus the food).

@@user137 eating  thyroids (even by chance) makes sense but the problem remains the same: where would this animal iodine would come from at 500 km from the sea? Asteroids, who knows!  Yes could people did die before by starvation, but can human reproduce without iodine? Still looking for an answer...

The fact that those areas with iodine deficiency didn't got completely depopulated during the Middle Ages seems to suggest that it does not affect all people that severely. Are there people who can have good health with much less iodine that can cause others to suffer severe symptoms?

That was behind my question! Could humans survive and reproduce without any iodine source. Updated my question with vsz comment!


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Why do small organisms make faster movements than big organisms?
I hesitated to ask this question because it seems so obvious and intuitive. However, I am not able to explain this tendency.
Background
It seems to me that small organisms make faster movements than big organisms. I don't mean that they are able to travel at higher speed (the cheetah is a big animal and is the fastest terrestrial species) but I mean that their movement are fast, quick and their members undergo high acceleration.
Examples
I would guess for example that the legs of a tiger beetle (clade of fast sprinter beetles) (see movie) undergo much higher acceleration than the legs of a cheetah (fastest terrestrial organism on earth) (see movie). To avoid taking the extreme, I would think that the legs of a Drosophila (see movie) undergo higher acceleration than the legs of a dog (see movie). The organism that is able to create the fastest acceleration is the mantis shrimp. Wikipedia says:

Both types (smashers and spearers) strike by rapidly unfolding and swinging their raptorial claws at the prey, and are capable of inflicting serious damage on victims significantly greater in size than themselves. In smashers, these two weapons are employed with blinding quickness, with an acceleration of 10,400 g (102,000 m/s2 or 335,000 ft/s2) and speeds of 23 m/s from a standing start. Because they strike so rapidly, they generate cavitation bubbles between the appendage and the striking surface. The collapse of these cavitation bubbles produces measurable forces on their prey in addition to the instantaneous forces of 1,500 newtons that are caused by the impact of the appendage against the striking surface, which means that the prey is hit twice by a single strike; first by the claw and then by the collapsing cavitation bubbles that immediately follow. Even if the initial strike misses the prey, the resulting shock wave can be enough to stun or kill the prey.

Finally, note that Gabel and Berg (2003) show that the flagella can rotates up to 270 Hz.
Questions

Am I right to think that small organisms tend to make faster movements than big organisms?
If yes: Why do small creatures make faster movements?

Does it has to do with time for chemical diffusion?
Does it has to do with mechanics? ($F=ma$... But muscles are smaller as well).
Does it has to do with the resistence of biological tissues?
...

This might be explainable with physics, force = mass * acceleration, so acceleration = force divided by mass. If the mass is small enough, then it won't take much force to get large accelerations. While smaller muscles won't generate as much force as the larger muscles, their reduced mass may still allow greater acceleration.

Muscles are much smaller as well so that it is not totally intuitive to me why acceleration is higher in small organisms.

Right, but I'm not sure how mass and force scale with muscle size. Mass should scale linearly with muscle volume, assuming constant density, but force generation might not scale the same way. If smaller muscles can produce more newtons/gram, they could produce higher accelerations.

Yes, indeed! I'd be curious to get some more info to see if this is a plausible explanation.

I think this might have something to do with Kleiber's law which is approximately true. It basically states that larger animals have slower metabolisms than smaller animals. http://equation-of-the-month.blogspot.co.uk/2012/06/kleiber-law.html
If Kleiber's law is true then smaller animals would have more disposable energy per unit mass compared to larger animals which would allow them to have relatively large kinetic energies.

It's a general phenomenon that the time scale correlates with the size scale of complex systems.
Energy consumption is the main concern dealing with the speed for biological organizations.
In the absolute sense, a turtle has a higher speed than a small bug. But based on their sizes, the bug seems much quicker and faster. So we need to normalize the speed with the size scale which we can temporarily call 'fastness".
Here is the relationship between the fastness and the mass:

Where u is speed of the organism, M is mass, alpha is a constant which we assume that the metabolic energy is related to the body mass of the organism with a power law.
The final equation says that if alpha > 1.67 then the larger would be faster. But our observation tells us that the smaller the faster. Therefore, we know alpha < 1.67.
In fact Kleiber's law tells us that the alpha is about 0.75.
You can check some numbers related to some animals here

An increase in linear dimension by $x$ causes an increase of $x^3$ in volume and mass.  The force that a muscle can generate roughly scales with the cross-sectional area of the muscle, an increase of $x^2$ for a muscle scaled by a factor of $x$.
This means that larger animals need proportionally larger muscles (by a factor of $\sqrt {x}$) to achieve the force required to generate any given acceleration.  This becomes impractical fairly quickly, so we just make do with less acceleration.
If you consider a 1 cm ant scaled to human size with no other modifications (a 200-fold increase), it would be 8,000,000 times more massive but its muscles would only be 40,000 times stronger.  It may have started out about 50 times stronger than a human, mass-for-mass, but at human scale, it's only 1/4th as strong; it would barely be able to move at all.
There are other biomechanical factors that can influence speed that favor smaller creatures as well.  One example is the ability of mantis shrimp to store amounts of mechanical energy that are quite large on their scale in the curvature of their exoskeleton (like storing energy in a car's leaf spring.)  Similar energy storage on a human scale is just not practical.


text:
Help me understand how the thyroid secretes
Please have a look at this close up light microscopic image of a thyroid gland:

So I'm guessing the cubic epithelial cells surrounding this big red pulp are the secreting cells...? If so, is the red pulp a blood vessel that they are secreting into?
Am I misunderstanding?

Please do open any physiology/histology text and find the answer better explained than any of us could do it here. When you have read and have further specific questions, you are welcome to ask them here. BTW, no these are not blood vessels.

Do not believe that this is a HW question and if it is, he has made an attempt to answer it so I am fine with it.

That "red pulp" spaces you're referring are not blood vessels but, in fact, thyroid follicles that selectively absorb iodine from the blood for production of thyroid hormones and storage of thyroglobuline. So, they act as a reservoir of the materials used by the thyroid's epithelial cells, also called follicular cells, to produce thyroid hormones (T3 and T4).


text:
What limits our healing speed?
Our bodies can repair quite a number of injuries very well. However, it takes time. For larger wounds, complete recovery can last many weeks. Why is this time so long, what is the most important limiting factor? The speed of cell division? I thought cell division was faster, and if necessary, cells could also be transported in the blood stream. Thrombocytes, as far as I know, are transported to the location of the emergency by the blood, and are not produced locally.
If the pure physics and chemistry allowed, for example, a 2x faster healing rate, wouldn't there be any evolutionary pressure for it?

The limiting problem is the formation of new tissue. New cells could indeed be produced faster, but forming tissue requires much more than just cells. It requires extracellular matrix to provide attachment for new cells, collagen and various other intercellular fluid components (which are secreted by fibroblasts), migration of cells. And bear in mind all of this isn't done on an open end, it needs to be done without actually at any point breaking the blood circulation system or other boundaries between tissue compartments.

One reason is simply "scale". The healing recovery is taking place on a molecular scale, and it involves a huge number of very, very tiny things. How long does it take to place all of the bricks in a brick wall (for a trivial analogy)?

Do you want speed, or accuracy. Uncontrolled cell growth is CANCER. We do not want cells growing extra fast or it is cancer. Also, it takes time to correctly sequence dna strands. Do you want fast healing with lots of scars, extra skin, some new limbs and extra tumors. It takes time to form correct cells.

The process of wound healing is pretty complicated and is much more than only cell division. The woundhealing process starts almost immediately in the moment of the injury and depending on the injury can take quite a long time. Have a look at the figure below (from the second reference), which shows the phases:

Basically this can roughly be diveded into four phases:

Hemostasis/Coagulation:

vascular constriction (blood vessel contraction)
platelet aggregation, degranulation, and fibrinformation (formation of a thrombus and closure of the wound)

Inflammation:

neutrophil infiltration
monocyte infiltration and differentiation into different kinds of macrophages
lymphocyte infiltration

Proliferation:

re-epithelialization
angiogenesis (formation of new blood vessels)
collagen synthesis (formation of new connective tissue)
formation of the extracellular matrix

Remodeling:

collagen remodeling
vascular maturation and regression

This process takes some time and can be prolonged when a wound is infected.  So I don't think there is much room to speed this up, as you need to go through all these phases. This process is also the result of extensive evolutionary processes; otherwise, such complex cooperation between different cells is not possible. For more details on the process itself, have a look at the references.

References

Factors affecting wound healing.
Cellular aspects of wound healing.

+1 just for HIPR.  You imply it, but it might be worth stating out right that remodeling is most likely to be the rate limiting step (to answer directly)

Thats possible. If there is no additional infection. Although this is not really "rate limiting" but takes time to clear.

The time needed for a wound to heal is related to the type of tissue injured and the amount of tissue that needs to be 'reconstructed.' Cell division rates are also a factor.
Healing is a complex process that involves multiple stages.

The body has to limit the damage that can result from an injury. So, first it tries to stop the bleeding and then a local inflammatory process is triggered. This inflammation will:

stop pathogens from entering the systemic circulation
'clean' the injured tissue by removing dead cells

In order to recreate the tissue, there is the need for blood which will deliver nutrients and other factors. So, fibroblasts and endothelial cells migrate in the wounded area and form temporary tissue and new blood vessels; the new tissue is called granulation tissue.
The granulation tissue allows for the formation of definitive tissue. This is the remodelling phase. Depending on the wound, the tissue that grows can either be the same as the original one or be fibrous scar tissue.

Looking at the time required by each of these steps:

should be the fastest as it relies on blood cells and factors that are already present in blood. Also, the wound itself will stimulate the local production of some cells/factors involved (inflammatory factors, vasodilator, vasoconstrictor factors.)
and 3. depend on the duration of cell-division processes, extracellular matrix formation, and vascularization. Cell division time can be slowed down by a lack of required nutrients and/or substances.  While the granulation tissue forms in almost constant time no matter the injury, the final tissue depends on what type it will be. One simple example is bone tissue versus skin.

References & Links:

Wound healing on Wikipedia
John Miller: http://physioworks.com.au/treatments-1/what-are-the-phases-of-a-soft-tissue-injury

While it's a good answer in describing how the healing of wounds works, most of this I already found on Wikipedia and other sources. I'm still curious about what actually causes it to have this speed? What physical or chemical processes are most responsible that a certain step takes 8 days instead of 8 hours?

I claim that one great limitation in our understanding of the healing process is that biologists have no understanding of the progression of disease or infection, that not enough time may be given for the body to recover, and that doctors might not understand how to help their patients recover from disease or infection.
Each patient is different, and personalised recovering plan is often important.
So, too few resources — e. g.:  the time of a doctor and/or a nurse — are offered to patients, so doctors have little time to build their understanding of the disease or injury with which their patients are dealing.
It is the patient who makes himself or herself able to recover.
But, without understanding, the recovery process is not optimal.
Healing from upper respiratory infection:
I will give one example in LOR Medicine.
Upper respiratory infections are one of the most common infections and most expensive diseases in society.
One reason is that people do not understand:

how to recover from disease
how long the common cold or flu lasts (doctors underestimate the time that it will take for their patients to heal very often.)

In nursing school, they teach students how to, among other things:

prevent reinfection
prevent acute hyaline membrane formation by elevated sleeping position (in LOR, for instance.)

There is no way to measure what the correct course of treatment is for any given patient during the course of, for example, an upper respiratory infection.
Nurses ask the patient when he or she feels their best and adjusts treatment accordingly.
So, good communication is essential in nursing.
Wound healing:
Chris and Cornelius cover some of the basic cellular processes of wound healing.
However, some big steps are still missing in regards to healing.
The primary healing of wounds is aided by:

adequate wound-edge coaptation
healing without complications
minimal scar tissue

through the cellular processes of wound healing described by Cornelius and Chris.
Secondary healing of wounds is characterized by:

wound tissue left exposed (open)
defect filled with granulation tissue
surface covering the epithelium
less functionality
possible thermal and mechanical injuries

Embryological and biochemical aspects of tissue healing
I cover here some growth factors.
If they are not present, then their absence will surely be a limitation to the healing process.

TGF - transforming growth factor
MDGF - macrophage-derived growth factor
HB-ECG - heparin-binding epidermal growth factor

Here are some other factors:

bFGF - basic fibroblast growth factor
KAF - keratinocyte-derived growth factor

Special cytokines for inflammation may later come into play.
Sources

Human skin wounds: a major and snowballing threat to public health and the economy. Sen C.K., Gordillo G.M., Roy S., Kirsner R., Lambert L., Hunt T.K., Gottrup F., Gurtner G.C., Longaker M/T. Wound Repair Regen. 2009 NovDec;17(6):763-71.
My notes during 4 years of nursing
My notes during classes of Surgery
My notes of Embryology and Surgery about the growth factors

Once again: Why the downvotes without explanation? Answers can only get better with some explanation what can/should be done.

@Chris : While I didn't vote on this answer yet, I guess it's because it is about why medics cannot treat wounds faster. The question was about the biological process itself, and not why we don't have the technology to speed it up.

@vsz: That would be a perfect comment on this topic.

I think the challenge of the case is that the main question is open and asks much more than some processes. Your body then again explains much more narrower thing about biological level. The answer should be adequate to the question in title - not only textbook answer and/or simplification what can be found in books and/or review articles. Simplification is NOT enough for practical purposes. The body is user's attempt to answer it so well as possible. Biology is not only about one process. It is a multidisciplinary field with limitations.


text:
Why do our epiphyseal plates close up in our late teens or early twenties?
What causes our epiphyseal plates close up in our late teens or early twenties?
I realize that one's genetics plays the main role in this. I assume there is a gene that controls the epiphyseal plates in our long bones. I guess there would be genes dedicated to every single epiphyseal plate found in our body too. So to rephrase the question:
Why does the gene for our epiphyseal plates turn off in our lates teens or early twenties?

During Endochondral ossification  chondrocytes in the plate are rapidly dividing, newer daughter cells stack facing the epiphysis while the older cells are pushed towards the diaphysis. As the older chondrocytes degenerate, osteoblasts ossify the remains to form new bone.
In puberty increasing levels of estrogen, in both females and males, leads to increased apoptosis of chondrocytes in the epiphyseal plate. Depletion of chondrocytes due to apoptosis leads to less ossification and growth slows down and later stops when the entire cartilage have become replaced by bone, leaving only a thin epiphyseal scar which later disappears. Once the adult stage is reached, maximum height is reached.
Your question addresses the genetics of this process however it is more so regulated by the endocrine system. There has not been a single gene assigned to growth plates, or its regulation, and I find it unlikely that there ever will be.
Rather, endochondrial ossification takes place because of hundreds of genes interacting with each other. If you start to look at genes involved in apoptosis and the estrogen receptor pathway, you will begin to appreciate more the complexity behind the physiology.
I have a hunch you were looking for a gene, that with age just shuts off, or turns on. Recent evidence has show this does in fact happen as methylation may be a candidate mechanism of mediating not only environmental, but also genetic effects on age-related phenotypes.
http://journals.plos.org/plosgenetics/article?id=10.1371/journal.pgen.1002629

Interesting. So maybe this should be another posted question but, what else besides life style choices (food quality, air quality, stress level, exercise) constitutes environmental effects on age-related phenotypes?


text:
If DNA is the input, what is the output?
How does cells use the DNA inside them? I am looking on DNA as a strip of tape of Turing machine, but with machines its easy. I can read the tape and calculate the behavior of that machine. With cells its different we don't really understand the language of DNA.
So instead of trying to understand the language I was wandering if there are any particular behaviors of cells that we can associate to different "outputs" of the DNA tape.

DNA changes to RNA, which can either effect the behaviour of DNA itself through non-coding RNA or changes into proteins, which can also affect the DNA.

We actually really do understand DNA...

the analogy with the turing machine is correct I think, but there is still much and more research to do in biology order to make ideal cell-computing models

@canadianer really? That's news to me. We understand a lot about it but not everything. Not even close to everything.

You might find this article interesting: http://www.ncbi.nlm.nih.gov/pubmed/11504843.

@terdon Who said everything?

@canadianer well, you claimed "we actually do understand DNA" and I'd argue that we understand very, very little. Especially when it comes to complex questions like how "different outputs" are chosen (think alt. splicing/choice of splice site/cis+trans regulatory elements/% of genome transcribed/methylome and epigenetics in general etc, etc). We understand the basic mechanics but are still very very far from understanding the regulation.

@terdon Well, you make a good point.

but with machines its easy.

It's not that easy...the Turing machine can't interpret the tape without knowing something about what the 1s and 0's mean.  A complied C++ program is gibberish if read through a Perl interpreter.
DNA isn't as abstract as that, anyway.  A DNA molecule interacts with other molecules based on its shape, which the sequence of letters defines.  There are thousands of molecules in a cell which the DNA strand can interact with, and those molecules are affected by other molecules.  Think about it...for the most part, all the DNA in your cells is the same, but obviously the cells in your liver are doing different things than the cells in your skin.

With cells its different we don't really understand the language of
  DNA.

That's not the problem.  We just don't understand ALL the relevant interactions, because there are so many of them.  There is not one thing reading through the string of DNA once.

I was wandering if there are any particular behaviors of cells that we
  can associate to different "outputs" of the DNA tape.

The outputs would be proteins, but you can't just look at the DNA sequence and know what proteins will be made when and in what quantities, not without having empirically learned a lot about those proteins.
Look, there are lots of people who know a lot about computers and a lot about biology.  If thinking about DNA as a simple string of information was fruitful, people would be doing that.  We don't, because biology is more complicated than that.

The central dogma of molecular biology states that DNA encodes the information for building proteins, the information is copied to messenger RNA through transcription, and messenger RNA is used to build proteins through translation. DNA is also copied through replication.
So while it's true that DNA contains the information needed to build a living organism, I don't think it can described as "turing tape" If I understand turing machines correctly, you have a string of 1s or 0s, and a machine reads this string. Based on rules provided by an instruction set the machine can set positions on the tape to 1 or 0. The analogy with DNA fails because DNA does not have a separate instruction set and cannot be written to. DNA produces RNA and DNA with the help of many many proteins and other molecules, all tightly regulated to coordinate replication of the genome and to produce the right amounts of RNA and protein at the right times. DNA can mutate when replication makes an error, but this is accidental, not comparable to turing machines.
If you're interested in how DNA might be used like a computer, there are several articles on DNA Computing, though you'll have to sort through those papers because many look like they just used a computer to analyze DNA.


text:
Does the Jungian notion of collective unconsciousness have any legitimacy in the light of modern neurobiology and epigenetics?
Carl Jung has long ago proposed a rather controversial notion of collective unconsciousness [1, 2, 3],

a form of the unconscious (that part of the mind containing memories
  and impulses of which the individual is not aware) common to mankind
  as a whole and originating in the inherited structure of the brain. It
  is distinct from the personal unconscious, which arises from the
  experience of the individual.

While the complete original formulation of the idea may be interpreted as unfalsifiable and hence unscientific, suppose that we try to redefine it to some more modest idea, e.g. a set of inheritable subconscious memories, impulses and reactions present in populations/groups, with some expected degree of variation.
Now, it has been shown that memories reside in specific brain cells [4]. What is also known is the direct impact of environment (which - as far as I understand it - also includes our thoughts, feelings and expectations) on gene expression and epigenetic inheritance. In the light of these insights, could the notion of collective unconsciousness be revitalized and interpreted in some non-trivial way that could be used to better understand the way we dream, feel, identify with characters in stories etc.?
In other words, do new discoveries in neurobiology, evolutionary biology and epigenetics shed any new light on Jung's writings (e.g. timescale for such structures to adapt between generations etc.) and perhaps confirm some of his ideas? If not, could experiments be performed that would provide some new insights? Or is the idea so trivial at its core that basic evolution is enough to explain it in its entirety?

Perhaps this question is more suited for Cognitive Science.

@Superbest I would agree to an extent, but I think that the epigenetic/evolutionary aspect is better handled here.

Peripherally related: http://cogsci.stackexchange.com/questions/1116/what-form-might-jungian-archetypes-take-in-the-brain

Jung's premise is rather plausible: consciousness evolved rather than appeared suddenly, and therefore carries "pre-conscious" elements common to humans as a species. However, Jung goes very far in his interpretation of what may be hidden in subconscious, bordering on open mysticism - predicting accidents, wars, etc. I doubt there may be any evidence for that.
Among the more plausible of Jung's arguments are his comparative studies of the similarities between fairy-tales, legends and other folcloric features between cultures. This however does not necessarily prove that these existed in subconscious - they could evolve as a part of different human cultures encountering similar problems, e.g., dealing with incest (Edip), reaching sexual maturity (Beauty and the beast), etc. - which was already Freud's view. Essentially, Jung attributes to collective subconscious many of the things that Freud attributes to superego, that is to the cultural influences.
Less far reaching claims are made by modern theoretical linguistics, since all the existing languages are shown to obey similar generative grammar, see my post about the subject. While I am not aware of any conclusive results for this view from neuroscience, the evidence collected by linguists is rather strong.
References

K. Jung, Man and his symbols
S. Freud Totem and taboo
S. Freud The psychopathology of everyday life
S. Freud New introductory lectures on psychoanalysis
D. Isac and Ch. Reiss, I-Language: An Introduction to Linguistics as Cognitive Science

I believe it does. From looking at collective unconscious as a whole it states to say it’s “inherited beliefs and behaviors of ancient ancestors. As it’s been proven the collective unconscious is related to the subconscious. When you think about epigenetics it’s connected to the junk dna, which is 90% of gene regulation they thought to be unuseful, years down the have been proven wrong. Junk dna can be the subconscious of genes so now to put these understandings together, you have inherited (genes) beliefs and behaviors (subconscious mind) collective (genes) unconscious (mind)
A perfect example of this manifestation: imagine an individual in a ancient culture that experience pagan sexual rituals then down the ancestral line in our disposition you have certain events like pride or even home events like house parties this experience causes certain genes to be turn on and off leading to mental activity similar-to those involved in a archaic world.

Most of this answer reads as nonsense opinion to me that's unrelated to the question asked, but at least it shares that with Jung and Freud. In any event, we expect answers here to be cited and referenced when going beyond basic textbook knowledge. What can you cite to support what you write here?

@BryanKrause I think the swipe at Jung and Freud is totally unnecessary.

@RogerVadim I disagree and I think they remain a bit of an embarrassment to psychology, whatever influence on therapy they've had.

@BryanKrause First, let us not confuse psychology with neuroscience. Secondly, apart from their most controversial claims (controversial mainly to laymen) Freud, Jung and their followers are pretty much the basis of modern psychology, to the extent that their most revolutionary claims are considered so obvious, tha they are not even credited to them.

@RogerVadim Guessing we'll have to agree to disagree then. I think Freud and Jung belong with Aristotle and Plato - we can respect their insight and historical role while recognizing that their approaches are extremely flawed. The difference is that Freud and Jung came far far later, once scientific philosophy had advanced quite a bit further, and that their flawed ideas are so embedded in the way the lay audience talks about psychology that it's hard to convince students and the lay public to think another way.

@BryanKrause again, I see no problem witj Aristotle, Plato or other ancient Greeks, who are at the source of modern philosophy, math and scientific method. Neither do I see problem with Darwin, whose theories were mere conjectures and are no less different from modern views than the psychology from Freudian views. Important thing to keep in mind is the limitations and applicability of the scientific method.

@RogerVadim The difference is that when people reference Aristotle and Plato they use them as historical references.

@BryanKrause the point is that psychology, macroeconomics, and many other domains are not sciences - because their subject is not amenable to the scientific events - they are interested in what is unique about their objects of interest, rather than what is in common between them.

Let us continue this discussion in chat.

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


text:
Are neural connections one-way?
I'm trying to think about how two neurons communicate, typically shown in pictures as an electric pulse traveling along a long, thin connective tissue.
Is this depiction somewhat accurate, and if so, what happens if both neurons fire at the same time on that connection?
Perhaps the connections are one-way, or they can facilitate pulses going in opposite directions at the same time, or perhaps it's something different all-together. It'd be interesting to have this explained, at least vaguely.

Are neural connections one-way?

Yes. Action potentials travel only from dendrites towards axon.

typically shown in pictures as an electric pulse traveling along a long, thin connective tissue.

What connective tissue? That thin "wire" which carries the action potential is a part of the neural cell body called axon.
Depending on what the axon connects to, there are 6 types of synapses:
"Blausen 0843 SynapseTypes" by BruceBlaus. When using this image in external sources it can be cited as:
Blausen.com staff. "Blausen gallery 2014". Wikiversity Journal of Medicine. DOI:10.15347/wjm/2014.010. ISSN 20018762. - Own work. Licensed under CC BY 3.0 via Wikimedia Commons.
A synapse is the connection between two structures: the axon of a neuron which "outputs" a signal (chemical or electrical) and the other structure ("input") that can be:

a dendrite or any other specific receptor from a cell
a neural body (can receive both electrical and chemical stimuli)

what happens if both neurons fire at the same time on that connection?

In the situation of an axoaxonic synapse (example 2 and even 5 and 6 from the above illustration), the presynaptic neuron can have inhibitory action (nicely explained on michaeldmann.net at Presynaptic inhibition) from where I quote:

Activity at the axoaxonic synapse partially hypopolarizes the terminal so that, when an action potential comes down the [...] afferent fiber into that terminal, its amplitude is reduced. Because the amount of transmitter substance released by a bouton is proportional to the amplitude of the action potential in it, less transmitter substance is released, resulting in a smaller EPSP and less excitation of the postsynaptic cell [...]

Links:

http://en.wikipedia.org/wiki/Synapse
http://www.getbodysmart.com/ap/nervoussystem/neurophysiology/synapses/introduction/synaptic_contacts/tutorial.html
http://michaeldmann.net/mann13.html

Dendrites don't transduce action potentials. They convert various inputs into membrane potential changes which propagate along them by diffusion towards the cell body. All incoming signals ultimately influence the potential gradient across the membrane of the axon hillock, where an action potential will begin if the depolarisation is large enough. https://en.wikipedia.org/wiki/Neuron#Anatomy_and_histology

First of all, let me clear up a small confusion: a connective tissue is a histological term and isn't relevant to this question :) Check https://en.wikipedia.org/wiki/Connective_tissue on that
That already suggests that the depiction you describe isn't accurate. I would hope that you have seen something like this, which shows a neuron's structure in a very simplified version:

Summarised and simplified, various kinds of impulses (chemical, mechanical or electrical for example) are received at the dendrites, where they generate electrical potential changes. These spread by diffusion across the cell body. At the axon hillock, the point where the axon starts, all of these changes collect and sum up to a net change. If this crosses a certain threshold, the axon hillock generates a so-called action potential, i.e. an electrical impulse. This impulse then travels down the axon until it reaches the terminals. Terminals attach to other neurons (or e.g. muscle cells) via synapses. When an action potential reaches a terminal, the impulse will be carried across the synapse and cause a specific effect on the next cell.
As you can see, there is a clear single-direction signal transfer here: Input -> Cell body -> Axon -> Output. The cell that receives the output can't "fire back" in any way because it receives that signal as an input itself.
A diagram of a pathway including several neurons might thus look like this (neurons are drawn as yellow cell bodies and arrows to indicate where their axons reach):

(Taken from Hubel, D: Eye, Brain and Vision, http://hubel.med.harvard.edu/book/b6.htm)
This does get a bit more complicated when you consider nerves rather than individual neurons. Nerves are bundles of several axons and contain no cell bodies. This means that in effect, nerves are a lot like electrical cables, and like cables it is actually possible to force electrical current running either way along the cable, or to override a signal running in one direction by sending a signal in the opposite direction. This is relevant for example in pain perception where some theories suggest that pain signals might actually be interrupted on their way up a nerve by direct inhibition on the axon bundle (caused by other neurons), see the first diagram here under 8.2: http://neuroscience.uth.tmc.edu/s2/chapter08.html

Neural axonal connections are physiologically one-way, in that an action potential would never back propagate. Since the signal is physiologically initiated near the cell body (dendritic input region) the normal flow of information therefore is dendritic-to-axonal. However, when axons are electrically activated (through neural implants such as auditory or sensory prosthetics etc), the signal will propagate both ways, i.e., to the axon terminal, but also to the cell body. It is by means of the ion channel opening-and-closing kinetics that action potentials travel only one way, namely away from the point of initiation. The axon itself is not gated in any way- it has no sense of directionality and sustains both directions.

The connection is one way, the input comes in the dendrites, while the output goes on the single axon in the neuron.

Figure 1 - wikipedia - neuron

The axon of the presynaptic neuron can connect e.g. to the dendrite of a postsynaptic neuron, and so they can form synapses in which they use neurotransmitters to transmit the signal.

Figure 2 - synapse between two neurons

Figure 3 - neurotransmission

There can be different targets to an axon, not just dendrites, e.g. another axon, muscle cells, etc...


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Additive genetic variance components from LMER in R
I've set up some dummy data in R which makes 40 genetically related lines, they are all siblings within a line so are genetically related by a factor of ½ thus additive genetic variance should be twice the variance explained by line. For the lines there are 200 individuals being measured, for three characters/traits. The first trait has low phenotypic variance, the second has high environmental variance, and the third has high genetic variance.
rm(list=ls())
re = 200 # replicate individuals per line
li = 40  # lines

# setup
set.seed(5)
data = data.frame(rep(1:li, each = re))
colnames(data)="Line"
library(nlme)
library(lme4)
par(mfrow=c(1,3))

# trait 1: little variance (Va or Ve)
data$Trait = rnorm(li*re,10,1)
boxplot(data$Trait~data$Line, ylim=c(0,20), main = expression("Low V"[A]*"& Low V"[E]))
var1 = var(data$Trait); mean1 = mean(data$Trait); m1 = lmer(data$Trait ~ (1|data$Line))

# trait 2: high enivronmental variance, little Va
data$Trait = rnorm(li*re,10,1); data$Trait = data$Trait + rnorm(re*li,0,3)
boxplot(data$Trait~data$Line, ylim=c(0,20),main = expression("Low V"[A]*"& High V"[E]))
var2 = var(data$Trait); mean2 = mean(data$Trait); m2 = lmer(data$Trait ~ (1|data$Line))

# trait 3: high additive genetic variance, little Ve
data$Trait = rnorm(li*re,10,1); data$Trait = data$Trait+rep(rnorm(li,0,3),each=re)
boxplot(data$Trait~data$Line, ylim=c(0,20), main = expression("High V"[A]*"& Low V"[E]))
var3 = var(data$Trait); mean3 = mean(data$Trait); m3 = lmer(data$Trait ~ (1|data$Line))

Plots of the three traits,

Then to estimate additive variance ($V_A$) I extract the line variance ($V_L$) from the lmer model and double it,
# line variances (variance in additive effect of each haploid genome)
m1_line = unlist(VarCorr(m1))[[1]];
m2_line = unlist(VarCorr(m2))[[1]];
m3_line = unlist(VarCorr(m3))[[1]]

# additive variance (double the line variance because it is a hemiclone)
m1_add = 2*m1_line;
m2_add = 2*m2_line;
m3_add = 2*m3_line

Residual variances should be (assuming perfect experimental design, no measurement error etc.) the estimate of environmental variance ($V_E$) and phenotypic variance ($V_P$) should be the sum of $V_L$ and $V_E$,
# residual variance
m1_res = attr(VarCorr(m1), "sc")^2
m2_res = attr(VarCorr(m2), "sc")^2
m3_res = attr(VarCorr(m3), "sc")^2

# phenotypic variance
m1_phe = m1_line + m1_res
m2_phe = m2_line + m2_res
m3_phe = m3_line + m3_res

Heritability is additive variance divided by the phenotypic variance
$h^2 = V_A / V_P$
But I think it is correct in this case to use line variance rather than additive variance (if someone could explain in an answer that would be useful), so I've done,
# heritability (line/ (line+ residual))
m1_h2 = m1_line/ m1_phe
m2_h2 = m2_line/ m2_phe
m3_h2 = m3_line/ m3_phe
m1_h2; m2_h2; m3_h2

My question(s):
Is it appropriate to use the lmer function in R to extract variance components in this manner?
Have I calculated $V_A$, $V_E$, $V_P$, $h^2$ correctly? I think $V_A$ and $V_E$ are correct, $V_P$ could perhaps be the sum of $V_A$ and $V_E$ rather than $V_L$, and subsequently $h^2$ may be $V_A/V_P$.

Can you add a flowchart or just methodology instead of/in addition to the code.

I deleted my answer. I am too unsure of what I was saying! Sorry. I might give another try thinking about that later when I'll have the opportunity to use R.

From what I understood of your code and what you are asking I am guessing that you do the following:
Generating a virtual set of 40 individuals (lines) of which you have 200 measurements (repetitions). You say that they are full siblings, so they share both parents. Then you use the lmer function (which I am not familiar with) to give you the total variance, within-group variance and between-group variance, ($V_{T}, V_W, V_B$ respectively). What you call $V_L$ would be the $V_W$.
We know that $V_P=V_A+V_D+V_E$
In full siblings we also know that $V(A,A')=\frac{1}2V_A+\frac{1}4V_D$ where $A$ is the additive value and $D$ is the dominance value because they share a quarter of their gene combinations.
If you are treating with full siblings the $V_W$ should be then the $V_E$ and the $V_B$ would be the $\frac{1}2V_A+\frac{1}4V_D$ as you are seeing the variance between siblings.
So no, you are not calculating correctly the $V_A$ because you are missing your $V_D$ on your counting. The code itself looks fine for what I understood, but maybe you should take that to corssvalidated with the R tag

Thanks - I actually use Hemiclone lines, which are like full sibs (related by a half) but have no dominance effect, I just wrote siblings rather than having to explain hemiclones. If then half sibs were used, the code I use would correct except for $V_A = 4V_L$ right? And likewise if there was no dominance then for full sibs $V_A = 2V_L$

I could check it thoroughly but my gut says that $V_A=2V_L$ in this case as there would be no dominance effect then, but in the rest of the effects it would be full sibs.


text:
Will an 11W UVC lamp kill bacteria?
If I shone a UVC lamp (11W) on something (say for example a plastic phone case) for an hour, would that kill off a noticeable amount of bacteria? That is, if I were to go over the case with a cotton swab before the hour and swipe the cotton swab over a petri dish with nutrients and if I were to do the same after the hour with a different cotton swab and a different petri dish. Do you think that after a week there would be a noticeable difference in bacterial growth between the dishes? I think it should, since some filters for ponds work the same way, but I'm not sure, since in my case, the light needs to penetrate about 10 inches of air first and the environment isn't as closed off. What are your ideas on this?

I think you should add distance parameter to it because it has inverse relation with any rays that use for such uses

Some physical methods of sterilisation are in hospitals

Steam autoclaving
Dry heat – thermostat
White light / UV light sterilization

where continuous UV light has poor penetration.
UV radiation heat is absorbed by proteins and nucleic acid.
All micro-organisms contain tehm.
They inactivate the DNA.
There will be electronic and photochemical reactions by

photolysis
loss of colony-forming ability
enzyme inactivation
destruction of nucleic acid.

If I shone a UVC lamp (11W) on something (say for example a plastic
  phone case) for an hour, would that kill off a noticeable amount of
  bacteria?

Direct answer: Not all bacteria, but some.
UV light has poor penetration so it will not expose all bacteria.
Most prevalent bacteria there

streptococci,
staphylococci and
some others.

I estimate that the majority of the bacteria will remain because the light cannot reach each corner of the object.
In clinics, many hours and high temperatures are used to kill bacteria.
UV light is not efficient there.
I think the problem is that you cannot reach each corner of the object.
The high temperature and disinfectants can then again reach the clinical instruments throughly.
Manual work is however still needed.
You can then take examples of bacteria.
Search their corresponding temperature ranges.
The survival can also be dependent on the nature of the light of the bulb.
Each bacteria has an individual structure.
We can manipulate the environment to make bacteria more vulnerable to the heating i.e. to change the structure of the bacteria.
We can increase the duration of the heat exposure to make kill of the bacteria more effective.


text:
Book-recommendation: Ethology
I am looking for a book that covers the following topics in ethology:

Behaviour

Sensory filtering, reponsive-ness, sign stimuli, learning and memory, instinct, habituation, conditioning, imprinting.

Role of hormones in drive

role of pheromones in alarm spreading; crypsis, predator detection, predator tactics, social hierarchies in primates, social organization in insects.

Navigation and Biological Rythms

Orientation, navigation, homing, biological rhythms, biological clock, tidal, seasonal and circadian rhythms.

Methodology

Methods for studying animal behaviour including sexual conflict, selfishness, kinship and altruism.

Do you have any suggestions?

Hope you don't mind that I edited your question. I think it looks better like this and will attract more attention and better answers. Good design is essential for a good communication. There is probably still room for improving your question if you want to give a try.

Thanks a lot I will take care in the future for he same.

I can suggest three books, none of them cover all those aspects, though:
1) The Foundations of Ethology, Konrad Lorenz. The best introduction I know for the field of ethology. Lorenz is called by some "the father of ethology".
2) Sociobiology: The New Synthesis, Edward Wilson. The deepest study of animal societies I know of.
3) Evolutionary Ecology, Eric Pianka. If my memory is right, it says something about the Navigation and Biological Rythms part.


text:
Evolution, What would the first plants have been like?
I am curious what the first plants are thought to have been like, what they may have evolved from, and how much earlier (or later) than animals they are thought to have moved to land, if they even started in water like animal-life?

You can have a look on tolweb.org to see what the most basal branches in plants look like and what the sister branch of plants look like. You will find the plants (archeoplastidae) here on this website

You can have a look to the most basal branches and you may get a pretty good idea of what those early plants looked like.
What we call plants is what we call plantae or Archaeplastida in Latin. This clade contains the red algae and the green algae. Within the green algae are the land plants. In the land plants are the embryophyta which contain all what you think of when talking about plants. Below are a bunch of pictures so that you can get an idea of what the basal branches look like.
(Basal Plantae) Red algae

(Basal Green Algae) Green Algae

(Basal embryophyta) Green Algae > Embryophyta > Hornworts

(Basal embryophyta) Green Algae > Embryophyta > Mosses

You can explore the tree of life by yourself by going on tolweb.org. You can try to find the apple tree, the ladybug of the human by clicking on the links. It is fun and it is good to learn a bit how the tree of life looks like.

A pair of comments: 1. fossil record must much more illustrative for multicellular forms. 2. simplest and basalmost red algae are unicellular.


text:
Why does some skin hold perfume longer than others
I was wondering my girlfriend and I used the same perfume for a while and we sprayed the same place. And after a day her skin still smells nice while mine smells normal.
Will different types of perfume hold longer on different skin types?


text:
How does electrolarynx work?
I have heard that this is an effective replacement for patients who have a dysfunctional larynx, partly due to cancer.
I am curious to know the inner working of this device and why such a robotic voice comes out?
What is the basic principle of this device. Does it simply captures vibrations and converts it to sound? Just like how a mic does?
Thank you.

Your vocal chords vibrate to produce a tone, but your mouth shapes that tone into the sounds that make up voice. If your vocal chords fail or are removed, the electrolarynx can be used to vibrate the throat for you, but your mouth still needs to shape that sound into words. Because the electrolarynx produces a mechanical buzzing vibration, you get mechanical buzzing words. This is similar to how the talkbox works with electric guitars, the guitar sound is piped through a tube into the musicians mouth, they have to shape that sound into words with their mouth. Go listen to Peter Frampton for a good example.


text:
Can anyone identify this caterpillar?
Can anyone identify this caterpillar we found on a cauliflower? This was the only photo we could get of it.
Location : Ceres, Fife, Scotland

Can you tell us where you found this caterpillar?

Hi Chris it was found in Ceres, Fife, Scotland. I thought it could perhaps be a Green-veined White caterpillar?

It might be an imported cabbageworm:

or a green-veined white:

Both exist where you are, and the former is more common than the latter. I can't tell them apart, but consulting the pages might help.


text:
What is refractory proteinuria?
I've stumbled upon the article "Telmisartan Treatment of Refractory Proteinuria in a Dog."* What is refractory proteinuria?

*Bugbee AC1, Coleman AE, Wang A, Woolcock AD, Brown SA. J Vet Intern Med. 2014 Sep 30. doi: 10.1111/jvim.12471. [Epub ahead of print]

The article itself1  defines what the authors mean by both proteinuria and refractory:

...progressive proteinuria, with [urine protein-to-creatinine] values ranging from 0.6 at initial evaluation to 5.16 at highest (reference interval, <0.2), despite medical intervention with increasing doses of benazepril HCl (0.5-1.02 mg/kg PO q12h) and control of systemic hypertension.

Background note
Proteinuria is normally quantified as a ratio of urinary protein to urinary creatinine to account for the wide fluctuations in urine concentration according to hydration status. Normally, in humans and (apparently) in dogs, there is little to no detectable protein in the urine. In certain disease conditions (most commonly: hypertension and diabetes), proteinuria tends to increase with poorly controlled blood pressure/glycemia. Proteinuria2 may represent a novel risk factor for coronary disease in humans. Angiotensin converting enzyme inhibitors (ACEI, e.g. benazepril) and angiotensin receptor blockers (ARB, e.g. telmisartan) are commonly used to mitigate proteinuria (citing a dog article this time - this benefit is widely accepted in humans).
The point of this article seems to be that an ARB was superior to an ACEI to decrease proteinuria in this dog.

1. Sorry, I was able to access it through a library but free text is not available without such access to my knowledge. If it is, OP please post it!

2. Also sometimes measured (as in the cited article) as albuminuria - ratio of albumin to creatinine - rather than total protein. There are subtle differences is these approaches, but they are highly correlated.

Proteinuria is the presence of proteins in urine. Refractory means "persistent" or "stubborn", but in medical terms it means resistant to treatment or cure.


text:
What studies are there showing the effectiveness of any substance on canine hypertension?
Searching on http://www.ncbi.nlm.nih.gov I could only find the article titled as "Telmisartan Treatment of Refractory Proteinuria in a Dog".

Check out this consensus statement (PMID 17552466):
J Vet Intern Med. 2007 May-Jun;21(3):542-58.
Guidelines for the identification, evaluation, and management of systemic hypertension in dogs and cats.
Brown S1, Atkins C, Bagley R, Carr A, Cowgill L, Davidson M, Egner B, Elliott J, Henik R, Labato M, Littman M, Polzin D, Ross L, Snyder P, Stepien R; American College of Veterinary Internal Medicine.
It includes 185 references, at least a dozen of which are related to your question. Also, if you look to the right of the article on PubMed, there are links to other relevant articles.
FYI: I located this article using search string
(canine hypertension) NOT pulmonary Filters: Review

There are quite a few others. (Canine pulmonary hypertension is apparently a popular research topic, so I found it useful to exclude those.)


text:
Simplest Biological Organism?
What is the simplest biological organism from which a DNA sample has been or could be obtained?  Could the resulting DNA be processed and examined in such a way that the resulting information would give biologists a rudimentary understanding of life's minimal requirements?

I think scientists already have an good understanding of "life's minimal requirements". What you need to do is define life for yourself.

You should also look at Synthetic biology and Mycoplasma laboratorium, which deals with minimum requirements of life.

Could not fit in a comment...
This post (and the excellent answer from Richard Smith-Unna) lists the species that have the smallest genome that we are aware of in different clades.
Yes we can/could sequence these tiny genomes and try to understand what each sequence does. I think that to understand the minimum requirements for life you will mostly be interested in theoretical cytology and synthetic biology than in sequencing simple genomes.
Note that the basic requirement really depends on how you define life. Is a virus alive although it has no metabolism? Would a self-replicating RNA be a living thing? Because we were able to artificially synthesize self-replicating RNA. While the subject is interesting, the main issue is a purely philosophical one: How do you define life?

Consider prions...

Yes, prions is another example of limit case


text:
Neurons with thousands of connections: where are the extra connections coming from?
If every neuron has only one Axon but can can have thousands of (or let's say, even just ten) incoming Axon connections via its dendrites, where are the extra connections coming from?

It seems to me that since neurons dont act as initiators (that is, decide to initiate signals) but rather act more as repeaters (that is, sending incoming signals forward to the neuron that their axon is connect to), then for every neuron, there must be at least one neuron whose axon is connected to it, and at least one neuron that its axon connects to (because without those two things, the neuron does basically nothing, right?), but since each neuron can only have one axon, I'm confused about where all of these extra axons are coming from.
Based on that understanding: 1 billion neurons means exactly 1 billion axons and one billion required inputs (axon -> dendrite connections), eliminating the possibility of any one neuron having more than one dendrite connection, since there can only be one billion axons to connect to those dendrites (and each neuron would require at least one input to function, right?).
But regardless, I've been hearing people talk about neurons having thousands of connections. And based on my understood model, the brain would have to be just one long linear chain of neurons, which makes no sense at all.
So clearly I've got something wrong in my understanding of neural structure. What is it?

As you say, a neuron can have thousands of inputs via its thousands of dendrites.  Each of those dendrites can have a synaptic connection to the (axonic) output of a different neuron.  So the neuron can take inputs from thousands of different neurons, not just from one other neuron.
At the other end of the neuron, the output of the axon can form synaptic connections with many distinct neurons; that's what the branching at the end of the axon is for.
Also, it's misleading to say neurons don't "decide to initiate signals".  Neurons in the brain do "decide" when to initiate an output.  The decision is a complicated function of the arrival of pulses at dendrites from different neurons.  Only some combinations of incoming pulses will cause the neuron to fire a pulse on its output axon while other combinations will not.  The specific combinations can change over time; this forms the basis of learning.
So a brain neuron is in the middle of a very complicated network of synaptic connections from many neurons to many other neurons.

I guess the figure included in the question can be misleading in the sense that it seems to imply that an axon can connect to one neuron only. Therefore the OP's confusion.

The figure is an oversimplification in many ways. Some neurons project their axon trough different brain regions making synapses with many other neurons along the way. In other hand, the idea that neurons without inputs do nothing is wrong too. For example pacemaker neurons fires action potentials regularly even in the absence of any input.


text:
Mechanisms of extracellular stimulation of neurons
When stimulating a group of neurons with an electrode, let's say we put it in a region that contains axons, what is the mechanism by which the axons are stimulated?
I've been told electrodes (usually silver or gold) must be coated with ions, usually chloride, to allow the passing of the stimulus. So I'm not sure if the stimulus is based on changing the extracellular concentration of ions by injecting chloride, therefore changing the membrane potential with a depolarization (elevating the potential, possibly generating an action potential). Let's call this idea A.
The other idea, B, that seems possible would be having the ions in the extracellular fluid conduct the current to the nearby axons, thus changing the potential but not the intra or extracellular concentration of ions.

The electrodes just produce an electric field that will change the membrane potential. They need not be coated with anything. Electrodes are not for conducting current

I get that they change the membrane potential. The question is how. Do they generate an ion flow, or a an electron flow? Obviously, the can and do generate an ion flow if the depolarization of the membrane leads to an opening of Na channels, for example, but that'd be the response mechanism, not the stimulation.

Electric field is created between two electrodes separated by a dielectric (non-conductor). It is a fundamental nature of a charge. When the charge moves it creates current but your charged plate of electrode is static and no current can flow between the electrodes- therefore a potential is generated.

Great, sorry if I seem a bit thick around basic stuff but i've had no formal training in either physics, chemistry or biology. So there is no current, the electrode just polarizes the extracellular solution? So if the membrane potential is -65mV, by introducing extracellularly a negative electrode, the potential of the membrane is depolarized?

@WYSIWYG I think you should write a longer answer if you have time. :)

Good question. Just to set some stuff straight: In contrast to a comment placed earlier, there is definitely a current flow between electrodes in neural tissue, as long as the impedance is not too high. The potential difference between the electrodes and impedance determines how much current flows, basically following Ohm's law: I = U/R.
As to your hypothesis (A) - I confirm  WYSIWYG's answer - electrodes indeed do not have to be coated, as long as they are conductive. For instance, Ag/AgCl coatings are used to electrically stabilize the electrode, mainly for sensitive reference electrodes used for recording purposes (see a commercial link here). For stimulation purposes chloride salts are a big no no, as AgCl or comparable chloride salts will be converted into metal (e.g. silver) + Cl2, obviously a toxic gas.
As to your hypothesis (B) - It is the electrical field that activates neurons (Basser & Roth 2000) by means of inducing current flow. For example, imagine a cathode (negative electrode) placed close to a neuron. Normally in rest, a neuron's membrane is hyperpolarized (more negative ions inside the cell, the extracellular fluid can be considered to be neutral). The negative electrode will now cause the extracellular fluid to be negatively charged. Subsequently, positive current will flow out from the cell close to the electrode and into the electrode. According to Ohm's law, the membrane voltage is thus positive (note Ohm's law: U = IxR, with I being positive and R being always positive, means U is positive). Hence, the membrane is depolarized, as the resting state is a negatively charged state (hyperpolarized). With an anodic electrode neurons can also be depolarized but due to a slightly different mechanism. Basically, the flanking regions of the now negative current flow to the positive electrode become subject to positive current, as it counterbalances the negative flow to the electrode.  The chapter of two veterans in electrical stimulation, Abbas and Miller, in (Cochlear implants) is particularly helpful, as is (Basser & Roth 2000). I can't link a pdf to Abbas and Miller, excuse me for that. I bet your university library will have access to it. Hope this helps.


text:
How do we determine a disease's incubation period?
There was a suspected case of Ebola in France, which was later dismissed, since the suspect lastly came into contact with a potentially contaminated person more than 21 days before, which is the maximum of Ebola's incubation period.
So, more generally speaking, how does one determine the period of incubation ? How do we know the day a person was contaminated ?

You need to know the growth dynamics (develop a mathematical infection model) of the concerned pathogen.

It could be determined empirically, by tracing how much time passed between the sick person coming into contact with another sick person and developing symptoms of their own.


text:
Incomplete Dominance and Probability
I have a follow-up question about an in-lecture question (this is not a homework question). As you can see I have already answered the question and the question is closed to further submissions.

In any case, this is my reasoning.
The male has the genotype Gg and BB. Fur color is incompletely dominant so to have black fur this implies the male has the genotype BB not Bb (which would likely be gray).
The female has genotype Gg and Bb because as the question states, the female is doubly heterozygotic.
The two have a FEMALE offspring - this is critical. This means that the male "donates" a copy of his X chromosome to the offspring. Now if the question had asked about a male offspring, then that would mean the male had donated a copy of his Y chromosome instead, and the male would have no "say" in the male progeny's eye color.
So the probability of green eyes between a cross of Gg with Gg is 3/4.
The probability of black fur between a cross of BB and Bb is 1/2 given that there is incomplete dominance.
So the probability of both events occurring simultaneously is 3/4 * 1/2 = 3/8 = 0.375.
Is this correct? Or should I account for the "female" offspring part and half the answer?

The male has a phenotype XGY BB, and the female, XGXg Bb. Thus the probability is 0.25.

Eye color is sex-linked. So a green-eyed male has genotype G- (only one X chromosome) for eye color and BB for fur color. The female has genotype GgBb. For the offspring to be female, 1/2 probability, to have green eyes 1/1 probability (G is dominant and it will receive the G from the father), and for gray fur 1/2 (1/2 chance it will receive b from the mother). So 1/2 * 1/1 * 1/2 = 1/4