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Why heart is on the left side?
I am not a biologist
but I wonder if there is any benefit for the human to have hearts on the left side?
do animals have their hearts on the left too? or on the right?

Well, it's not... it's in the center, pointing to the left side: https://biology.stackexchange.com/questions/60718/why-is-the-heart-not-in-the-middle-of-the-body https://biology.stackexchange.com/questions/5597/why-does-the-apex-of-the-human-heart-usually-point-to-the-left

There are humans with it on the right side. which side does not matter.

Possible duplicate of Why Is Most Life Symmetrical Externally But Not Internally?

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Why do some moles grow longer and darker hair than the rest of the skin?
In different parts of the body I have skin moles or in medical terms, nevus.
In some of them hair grow seemingly either darker/thicker (I'm not sure how much of the two) and notably longer. Here are pictures very similar to what happens. What is the reason behind this?

You could have easily find this answer on the internet (e.g. here: https://www.zocdoc.com/answers/3728/why-do-hairs-grow-on-some-moles

@RickBeeloo I ask this question here because I want this site to improve and to have many interesting biology questions. There was a discussion if easily google questions should be deleted or embraced, my position on that is that there are not stupid question and that this site should become the actual place where the answer is, the place that shows up when a google search is made. That's why I want the question to remain here. I thank you the link and not downvoting me, however!

Before answering the question (about the hairs) I will first go in some detail about what moles actually are:

Moles are growths on the skin that are usually brown or black.  They
  are formed by clusters of melanocytes, the pigmented cells responsible
  for your skin color.  Moles typically appear during the first 30 years
  of life, can be flat or raised, and can darken with sun exposure,
  puberty, or pregnancy.

There are no articles covering this topic in detail (most of them are about the skin cancer, if you are interested in this topic check out this article). However there are some medicial experts talking about the hair growth.

Joshua Zeichner, M.D., Director of Cosmetic & Clinical Research at the
  Mount Sinai Hospital in New York City. "If the mole also contains a
  hair follicle, the hyper-pigmentation can cause the hair that comes
  out of it to be coarser and darker."

Junji Takano, a Japanese health researcher said the following about this topic:

This is due to the fact that capillaries of a mole are growing rapidly
  and excessively, and this includes the hair follicles

Actually moles are benign tumors(wiki), the cells in the body in charge of normal skin color, are being produced at an extremely fast rate. Thus causing the melanocytes to form in clusters instead of spread out, causing abnormal skin pigmentation in some areas of the body(wiki). So based on the above quotes this "fast production" also affects the hairs which are present in this piece of skin. More interesting is that people hate these hairs (which make sense offcourse) but in most of the cases this is a sign that this mole isn't cancerous:

A mole that has a hair growing out of it usually means that is was
  present since birth or at a young age and is typically normal.

references: first quote, second quote, third quote, last quote

source: Stack Exchange

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sort: votes


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Why do eyes feel overwhelmed by light when we wake up?
Many people (I saw a 9gag post 3 days ago and couldn't find it, I'll edit later if I do find it)experience dry/hurting/overwhelmed eyes when they wake up because the light feels too bright. I happen to "suffer" the same. Why this occurs? Is it because the eyes are dry, or because the pupils are contracted, or why else?

When you are asleep, your eyelids are closed and your pupils dilate. When you wake up and open your eyes, you are not used to the light, and it takes some small amount of time for your pupils to contract and your eyes to "get used to" the light. Simple as that.

The reflex responsible for the phenomenon you described is called the Pupillary Light Reflex. According to the Textbook of Medical Physiology, Guyton & Hall, Elsevier, 11th edition, 2005, p. 649 (reworded by me in order to avoid direct copying):
When light reaches the retina of the eye, the optic nerves are stimulated. Most of the generated nerve impulses participate in the creation of an image in the brain etc., but a few reach an area in the brain called the pretectal nuclei. These nuclei then generate secondary impulses to another nucleus called Edinger-Westphal nucleus, which sends a signal through parasympathetic nerves to constrict the sphincter of the iris.
Conversely, in darkness, the reflex is inhibited, which results in dilation of the pupil.

To summarize, in darkness (either when you are in a dark room with your eyes open, or when you are anywhere with your eyes closed) the pupil will be dilated since stimulation by light does not occur. When stepping into the light or when opening your eyes, light immediately stimulates the optic nerve, which causes a signaling cascade that results in constriction of the pupil to a certain size, depending on the amount of light present (primarily to protect it from exposure to too much light).
Naturally, you can see this constriction happening every time you open your eyes in front of the mirror (focus on the pupil). It was also depicted rather accurately in the end of Disney's excellent rendition of the Hunchback of Notre Dame (skip to 1:22).

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What makes us "tired" in the gym that forces us to rest?
If I'm doing push ups or any other of gym exercise, I can do 10 in a row, but each one I do I feel more "tired", but if I rest for 5 minutes, I'm much "full of energy". Please explain me exactly what is different in my muscles chemistry.
I read that lactic acid overproduction is possibly linked.

I think you refer to the Muscle fatigue:

A state of exhaustion or loss of strength and/or muscle endurance following strenuous activity associated with the accumulation of lactic acid in muscles. (Source)

So yeah, you're right about the lactic acid overproduction :)
How Muscle Fatigue Works ?
During short term (anaerobic) exercise, ATP and creatine phosphate (CP) are used up within the first 7 seconds of training. This signals the metabolism of glycogen to produce energy for your body. This process is known as glycolysis.
During glycolysis, glycogen (muscle sugar) is broken down to produce more CP. The breakdown of CP releases energy, which catalyzes a reaction to produce ATP. The production of more ATP allows movement of the muscle to continue.
Lactic acid is a product of glycolysis created by the breaking down of pyruvate.
Lactic acid is then disassociated to produce lactate. When lactic acid (C3H6O3) releases a hydrogen ion (H+), the remaining compound binds to a sodium ion (Na+) or a potassium ion (K+) to form a salt. It is this salt that is lactate.
Now the cell contains a lactate compound and a free H+ for each compound of lactic acid that is produced. It is this increase in cellular H+ that causes the pH to decrease, becoming more acidic. The acid in the muscle causes the fibers' calcium-binding capacity to decrease, thus limiting muscle contraction. This is the cause of muscle fatigue.

So the muscle Fatigue occurs when the muscle experiences a reduction in its ability to produce force and accomplish the desired movement.
Short term fatigue (failure to lift a heavy weight, do more push-ups, etc.) is different than long term fatigue such as as a marathon run, a 100 mile bicycle ride, or a full-day hike through the Rocky Mountains of Colorado.
Muscles become fatigued during high intensity exercise, most notably that the demand for oxygen can be greater than the supply. The blood flow to the muscle can be reduced because of :

muscles intensely contracting can reduce blood flow and thus oxygen availability, or
the muscle is simply working so intensely that there literally is not enough oxygen to meet demand (a sprint at top speed).

The factors that explain fatigue are complex and after more than 100 years of investigation are still a topic of active research, you can check those articles for more informatoins :

Experiment: EMGs during Muscle Fatigue
All About Muscle Fatigue
Skeletal Muscle Fatigue: Cellular Mechanisms


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Do pulled hair from the root grow back?
There is not much to explain, I'm wondering if pulled hair, for example of the head, normally does grow back again or not. In reddit, It says this may depend on the follicle integrity, if the follicle is  not hurt then it will grow back and viceversa. It is the case?

There's no harm in plucing a hair, but it won't do you much good

Plucking the hair will indeed get rid of the hair - but only temporarily

"The follicle (the little tube beneath the skin that produces the
  hair) is still alive and will produce another hair to replace the one
  that was pulled out

So actually if you DON'T damage the follicle (which is really rare, this could be the case if you remove skin) the hair will definitly grow back.
To get into more depth here is a figure that shows the root and the follicle so it's clear what the difference is:

I don't know in how much depth you want this question to be answered but if you are interested in the growth stages (which can influence the hair regrowth) you should take a look at this answer, I won't copy someone else effort here..
source: Randy Schueller (link)


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How much time does HIV live outside the body?
I'm wondering HIV viability outside the body of an infected person, for example in a knife that contains blood of an infected person, with N virus cells. (N could be for example, 1000).
Some virus might live more than others, then I'm asking the half-life of it.

The general response to that question is not long, the HIV is a weak virus and that once exposed to air, it can survive for maybe a few minutes at best.
BUT Under specific conditions, HIV can survive for a far longer period of time, sometimes for hours or even days if the right temperatures, pH balance, light exposure, and humidity are achieved.  It is a very difficult set of conditions but is nevertheless possible.
Source : How Long Can HIV Live Outside of the Body ?

In certain conditions, the virus can survive outside the body for several weeks.
Survival depends on which body fluid it is in, volume of the body fluid, concentration of the virus within it, temperature, acidity, and exposure to sunlight and humidity.
HIV transmission has not been reported as a consequence of contact with spillages of blood, semen or other body fluids.

Source : HIV transmission & testing, Survival outside the body

If you've come into contact with some blood or other body fluid that you think might contain HIV, it's understandable to have some concern about the possibility of HIV transmission. But you can rest assured that there haven't been any cases of HIV transmission through casual contact with blood or semen that has left behind on a surface. There haven't even been any cases after people have come across discarded syringes or needles.
This is partly because it's extremely unusual for this situation to involve any opportunity for an infected body fluid to enter the person's bloodstream -- it does not reach a mucous membrane (such as the vagina or rectum) or an open wound.
So in practical terms, there's little reason to worry about contact with body fluids that have already been outside a person's body for some minutes.
There isn't a simple, straightforward answer to the question of how long HIV survives outside the body. In certain, specific circumstances it may survive more than a few minutes. But it generally does not remain infectious and certainly does not pose a threat to people's health.
The conditions that a body fluid is exposed to greatly affect survival. Air dries out the fluid, which contains the virus, greatly reducing viral amounts. On the other hand, in the enclosed space inside a used syringe (with limited exposure to air) the virus can survive some time -- this explains why re-using needles and syringes is risky.

This question is about virus time survival, not about my concern of contact with virions, and that's reflected in my question. You aren't providing a source of a experiment or any source with a numerical response to how much time does it take. You have used this link  ( or another source with the same text) in for example the last sentence of your answer this explains why re-using needles and syringes is risky.. without citing it, that's wrong.


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At what minimum distance the direction at which eyes point becomes parallel?
This is very similar, but different than this question about focus, let me explain why it's not a duplicate at all.. That other question is about the distance of EACH individual eye FOCUS, this one is about VERGENCE, focus plays no role in this question, here what matters is the angle formed between the direction each eyes points. When objects are close to our noses, eyes get cross-eyed. As objects get further away, the eyes get more parallel, so called wall-eyed. There must a distance just become totally parallel, I deduce this by analogy to what happens to the focus, for which the distance is 6 m as this answer says. What is the corresponding distance for vergence?
I couldn't find the answer in the relevant wikipedia article on vergence.


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How small does a nanobot have to be to "swim through the brain" and access any neuron it wants to?
I read on this question What is in the space between neurons in a brain? that there is actually not much empty space in a brain. But my question is slightly different. Is there a visual demonstration I can see of approximately how "packed full of cells" the brain actually is?
Obviously there wouldn't be a fixed answer as it is likely a continuum where the bigger you get the harder it is to swim through without being blocked by all the neurons/synapses. But what is a good ballpark size to be to swim through with relative ease?

Is there a visual demonstration I can see of approximately
how "packed full of cells" the brain actually is?
Yes. You can inject tracers in the CSF (Cerebrospinal fluid) or in the ventricles and monitor them. In this study, the authors have injected a fluorescent tracer in the CSF and used a direct imaging.

We used in vivo two-photon imaging to compare CSF influx into the
  cortex of awake, anesthetized, and sleeping mice. The fluorescent
  tracers were infused into the subarachnoid CSF via a cannula implanted
  in the cisterna magna for real-time assessment of CSF tracer movement.

You can also inject a radiolabeled tracer. The tracer should be a molecule that is not taken up by the cells. You can then visualize the space using Positron Emission Tomography (PET).
 But what is a good ballpark size to be to swim through with relative ease?
You may find this interesting: the abovementioned study shows that the "space" expands during sleep and CSF percolates deeper into the brain. This allows clearing of toxic metabolites. Having said that, some interior regions would be difficult to reach. Apart from neurons, there are several glia which occupy the space. I am not entirely sure about this but in interior regions there would be very less of extracellular space (I am just guessing it would be less than ~1µm. See the black regions in the figure below). Extracellular space is 20% of total brain tissue but it is not constant throughout. For more details refer to this book.

I wonder if you could repeat that experiment using labeled nanoparticles of known size, as they get larger they'd eventually stop moving throughout the whole space. But if that image is accurate, the space between the membranes doesn't look much thicker than the membranes themselves.

This is a SEM image from the book (that is linked). In the figure captions it is mentioned that "The scale bar is 1µm" but I am not able to find it. The ECS is as you can notice non-uniform (but certainly thicker than membrane in most places) :P
That injection experiment can certainly be repeated with nanoparticles (perhaps some kind of traceable ones like quantum dots).


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Consequence of touching Formaldehyde
I accidently touched formaldehyde some days ago. Skin on my hand got dehydrated as if I had placed it in salt solution. I washed it with water and it returned to normal state after 5 minutes.
But now whenever I wash my hands with water my skin gets dehydrated again, but returns to normal state after some time .
What's the reason behind it getting dehydrated again when exposed to water ? Will it return to normal state when new skin grows back ?
By dehydration, I mean something like this.

Even my hands have bcom like that. I accidentaly was holdin a leaking formalin bottle. Which later lead to dehydration in my hand and also I'm not able to feel anything that I touch.

@biogirl did your fingers ever get back to normal?

cool pics!
Firstly, Formadahyde is a terribly toxic substance.

Skin Contact: CORROSIVE. Contact can cause pain, redness, burns, and blistering. Permanent scarring can result. Can be absorbed through the skin.

Formaldehyde causes organ failure and scarring if ingested.
In this case, since you don't have burning or blistering, it seems like a reasonably low exposure. You should nonetheless call your doctor to check in or drop by the campus infirmary or what you have.
A good experience to remind you to wear gloves when working with chemically active reagents or solvents (DMSO for instance!)
I'm not a doctor, but as a non professional and informal opinion, your finger will probably become normal again, eventually all the cells will do their best to repair themselves.

Those rnt my fingers. The pic is on google :) why do my finger dehydrate after washing with water again ?

You mean your fingers getting wrinkled after washing them (or keeping them in water for a longer time)?

not sure, but the docs do seem to indicate that your fingers would have chemical burns if you had had a more concentrated solution or longer contact, so a reaction that is not seen as often perhaps.

@Chris After washing them.

@biogirl, formaldehyde chemically denatures the proteins and some other biomolecules. The damage is not mainly because of dehydration (in case of $H_2SO_4$ it is the strong dehydrating effect that is one of the the primary reasons for the burn)

@WYSIWYG Thanks! Could you answer my second question - why would it lead to dehydration again after I wash my hands ?

It is not dehydration. The wrinkling is because of damaged skin, perhaps. And the wrinkling is because of hydration

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Activity of glucokinase
From Solomon et al, 2013 ACC Synthetic biology and from this video :

Here, there are 2 competing reactions for glucose - one with glk as enzyme and other with gdh as enzyme.
In the graph, y axis is gluconate yield and x axis is glk activity. Logically, as glk activity increases, gluconate yield should decrease.
This is the case for most of the graph. But why is there an increase in gluconate production initially(when glk activity is somewhere between 0.2 and 0.27 )?

Are you talking about this paper? Can you please either cite journal name, volume and page numbers or give the title? Solomon is not very specific.

See the horizontal standard deviation bars of first and second points: they overlap. The estimation process might be error prone.

This is one point which is questionable. For the others I will have to take a look on the paper first, but this has to wait for the moment. I'll do that later.

@Chris I have confirmed, this is the same paper as what you cite.

First of all lets have a look, what these guys want to accomplish: They want to use bacteria to make certain products. To do so, they want to exploit the bacterial metabolism at steps where no alternative pathways are available. One of these steps is the first step of glycolysis, when Glucose gets phosphorylated to glucose-6-phosphate (G6P). In bacteria the phosphorylation is done during the import of glucose into the cell by the "phosphoenolpyruvate (PEP):carbohydrate phosphotransferase system", which uses Phosphorenolpyruvate as a phosphate source. This has the disadvantage, that there is almost no free glucose inside the cell, but mostly G6P.
To overcome this problem, the group expressed alternative transporters (which transport glucose into the cell) and Glucokinase (Glk) to allow the cells to survive. This steps decoupled import and phosphorylation of the glucose and resulted in free glucose inside the cell. This free glucose can now be used by different proceses. It also allows glycolysis, since the Glk phosphorylates the glucose which then enters the glycolysis pathway. The Glk was put under different promoters to make different mutants in order to test how the different expression of Glk affects the cells viability.
To bring in another enzyme which also metabolizes glucose, they used glucose dehydrogenase (Gdh) which was expressed from a plasmid with a strong, IPTG inducible promoter. They then used different concentrations of IPTG to test the effect on the production of gluconate and cell viability (I am not going into this).

The figure above is figure 5 from the paper and shows the effect of the three different IPTG concentrations used to induce the expression of the Gdh. For 10 and 25uM IPTG the yield of gluconate is getting smaller, the higher the Glk activity gets. Only the smalled activity shows a lower yield. This is complete different for the highest concentration, but here the cells get probably messed up by the high expression of the Gdh (which also consumes a lot of energy).
In the paper they give no explanation or at least discuss the behaviour of the gluconate yield at the smallest Glk activity (I would like to read the reviewers comments on that). From the data I would expect a higher production. It is possible that the lower energy production (low amounts of G6P means little glycolysis) has negative side effects on the cells. It is also possible, that the Gdh is inhibited at lower Glk activities by some other substances in the cell. Gdh activity is for example inhibited by higher concentrations of nucleotidtriphosphates (ATP and so on), see here. Since Glk needs ATP as a cofactor it would be possible that the ATP concentration at lower Glk activities has a negative effect on the Gdh activity (my own speculation).
Or it is simply some artefact from the experiment. This has some points which can be critisized (I would like to see the reviewers comments here as well). First the error bars are pretty big, so this can also be somewhat different. In the text they mention that the data was acquired by

at least 2 parallel cultures in a representative experiment

I would expect some more repetitions (at least three independent experiments), which would make the data more reliable. Then (and this point is much more important) they can not measure the activity of Glk and Gdh in the same culture due to restrictions in the detection system. Glk activity measurements use a coupled system which in the end measure the concentration change in NADH, while Gdh uses NADPH as a co-factor. Both versions can not be differentiated by measuring a spectrum, so activity measurements of Glk can only take place in untransfected cells. Since the expression changes conditions in the cell (and we don't know how), I would expect at least some discussion about it, but it is missing.

You`re welcome. The paper was fun to read.


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Does conjugation support gene selection?
I have already posted this on chat but haven't got any response. A recent question on group selection stimulated me to ask this here.
QUESTIONS: Why should bacteria conjugate? If we consider that a bacterium is another bacterium's rival (in terms of obtaining resources) why should a bacterium "share" it's antibiotic resistance gene, for example, with another bacterium? I can think of 2 reasons. One is group selection, and the other is "Gene Selection". Group selection has been highly criticized in recent years, and individual selection has dominated thinking, but here my support goes for gene selection rather than individual selection.
Gene selection seems to me the easier explanation over individual selection. Even if we consider the fact that a colony is made from divisions of single cells and the cells are extremely similar and also that conjugation is more probable between cells of a colony, we should also consider that conjugation can happen between very different bacterial species.

I would love to discuss this in chat with anyone interested as I think this question is more of a question to be discussed.

Does it make any difference, for the purpose of your question, if we speak of bacterial conjugaison or of any sexual reproduction? Isn't you question rather something like "Why would sex evolve?" Such question would require a very long answer that presents many different models!

@Remi.b The biggest difference between conjugation and sexual reproduction is - that there is no reproduction of an organism in conjugation. I don't understand why you think the questions are same. I don't want to know the advantages of having " recombination " events in life of an organism. Here, I want to know whether this is  an example of selection at individual level or at gene level ?

As I understand it: In order to answer to your question, one should think about the Muller's ratchet, the advantage of recombination for the group, how a selfish gene causing recombination might spread, about the speed of adaptation, effect on genetic variance, resistance to parasites, DNA repair, libertine bubble theory, etc…

It is roughly the same hypotheses than for recombination through sexual reproduction. But it does not mean I find your question uninteresting. I just wanted to say that there are certainly lots of different models to compare and that you might find your answer in the standard discussions about evolution of sexual reproduction. I might be mistaken though!

@Remi.b I have finally found the perfect words to ask this - Do you think antibiotic resistance gene(for example) spreads because the bacteria wants to protect the whole genome of other bacteria(which will often have the same genome) or it happens because that little plasmid likes to spread it's own genes ? I think the 2nd explanation is better because it can explain conjugation between different species

let us continue this discussion in chat

Interesting Question (glad the "group selection" post got you thinking!)
Me and two friends thought about your question during our Biology BSc at ICL (in fact we also thought about an even more puzzling phenomenon called "bacterial transformation" which is like conjugation, but they incorporate genes from dead bacteria!!) our first year course convener recognized our answers as "most likely candidates" so here they are:
1. Stress-induced Experimentation Hypothesis
The likelihood of conjugation/transformation occurring may change for a bacterial population as a whole depending on how stressed it is (or perhaps how unfamiliar the environment is?). Stress signals could cause the population to be more "risky" and take up the DNA from surrounding living/dead bacteria and incorporate it with its own genome: "the hell, we're out of options.. lets transform into something that resembles the indigenous species of this strange ecosystem!". Indeed Bacteria have memory (see: chemotaxis) this means that perhaps they can be able to tell whether they have been receiving more stress now as opposed to before, meaning they can "trial and error" with various genes that have been imported within their plasmids! — "Let's try this gene, oh wait... I'm dying, hmm let's kill off this plasmid and take some more genes!".
In reply to this my course convener said:

"ah yes, a switch from asexual to sexual reproduction occurs in
  many organisms under stress. The genes that cause the
  sex/transformation to occur may gain a net benefit from recombination
  with genes taken from other organisms/the environment."

2. Diversity Plagarism Hypothesis
If we look at the entire population of conjugating bacteria as a single competitive unit itself (e.g. like a tissue is a coordinated group of specialized cells) that can compete with other populations of bacteria who cannot conjugate the conjugating population will "win". This is because a conjugating population will always have much higher phenotypical diversity as it can mix traits between the individuals. This means a conjugating population is much more efficient at undergoing natural selection for beneficial traits or trait combinations.
Think of natural selection (coupled with mutation) as an inventor... something that helps you invent much "fitter bacteria" is the ability to pull things apart from this bacterium and that bacterium and glue them together, this is essentially what conjugation/transformation does!! it allows you to pull bits from this bacterium and stick it to bits from that bacterium to get a "super-bacterium". It's like open source technology (free to share) as opposed to patented technology!! Conjugation is immediately a good thing because it means you can "steal" cool technology from living/dead bacteria and incorporate it into your population's gene pool!
Hope this was helpful!

An  idea- What if the bacteria who is going to get the plasmid actually "compels" the other to give it the plasmid. We can think of it as "asking" by bacteria 2 rather than giving by bacteria 1.

I think  I said in the comment prety much the same thing as the last para  but with a slightly different perspective.

Awesome, well I have to say I know quite little about the mechanisms and mechanics of the conjugation process. But it would be interesting to know whether conjugation is "consensual". At least for transformation it is clear that there is no need for "compelling", the bacterium merely steals the DNA from the "corpse". A really interesting alternative answer is that the genes themselves are selfish genetic elements that can express some mechanism that allows them to infiltrate the bacterial genome.

Check out the Homing Endonuclease Genes (HEGs) http://bit.ly/puyHda  - HEGs literally make cuts in DNA and insert themselves into the genome.

Oh yes..I think The alternative will definitely be advocated by Dawkins. And yes, I thought of that too and I have written that in the question and in the comments. (It isn't an original idea as I have read the selfish gene !)

The other link seems pretty cool ! And i understand that it is difficult to prove that the other bacteria "compells" the 1st one. But thinking wild things is my hobby :)

I really need to finish that book (logs into amazon) but yes, if you are interested in the mind bending but beautiful collection of selfish elements you should read http://bit.ly/182xVzh, im working on research that uses HEGs to genetically engineer malarial mosquito populations!

Yes I accessed your website yesterday (got the link from your profile) and it definitely sounds amazing. Best luck !

Ah cheers, wild thinking is the best.. hope I didn't sound like I was disagreeing - I genuinely am interested in whether conjugation is either: a mutual agreement, a "giving", a "taking" (stealing). If it is the mutual agreement, then your suggestion comes into play! that you can "compel" or persuade or trick the other bacterium into giving the "blueprints to their technology" (DNA)


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Confused at what is happening with these action potentials
Ok so for a bit of a background, I am doing a science project looking at the action potentials of the earthworm. I anaesthatized the worms then hooked them up to a spiker box (http://backyardbrains.com/products/spikerbox) and stimulated them.
This is an average result:

What I am confused about is why the action potential goes negative first before then going back up. From my readings online, I thought that the action potentials were meant to go up first then travel down and then continue on its course. If it helps I used a program called audacity to record the action potentials.
Thanks very much guys. Sorry if I'm not being clear. Just ask anything if you need more information!

Nice graph. What happens when you reach the top of the potential (when you depolarize the membrane) that you need to go back to a resting potential to be able to stimulized again. The membrane gets "neutralized" and this reaction often over-shoots and goes below the resting potential, which is quite normal. Before reaching the normal resting potential there will be no further activation. The Wikipedia article on the "Action Potential" contains a more complete explanation.

This answers why it hyperpolarizes after reaching the peak but why does it hyperpolarize BEFORE the action potential ?

In the graph above? My guess would be that two pulses of activation come directly behind each other.

Sorry for not responding (christmas stuff). @Chris - could you please expand that a bit more? Oh a bit more information about the earthworm incase this influences how it goes negative first: they have 3 main nerve cords carrying the action potentials, 2 of them carrying the signals down the worm and the other transmitting them to the front. Would this at all influence it?

Do you record the impulse from one isolated nerve or is it possible that you record more than one?

Hm that is possible. Because the equipment I was using was not specifically "designed" for worms (it was designed for cockroaches) I have no way of knowing. If you go to the website that I have put here it has a photo of the pins which you put into the worm. However, if it is true that the results are being influenced by the other nearby nerves sending their signals, why is it the same for all the action potentials I recorded? I have around 50 photos which are almost identical to the one above (length wise).

Ok, that makes it unlikely. I was simply thinking about explanations for this signal.

Hm damn. Im really trying to figure this out I'm presenting this project at the national science fair in  2 weeks and I need an explanation :/  is it at all possible that it is just that the earthworms nervous system acts differently? Could it possibly be that (just making something up here) in the earthworm there isn't that polarity that is present in other axons? Maybe there is an even distribution of sodium and potassium ions on either side of the axon?

Did you ever get an answer to your question? I know this may be too late now, but I was noseying around and spotted it, so I'll take a stab nonetheless. I could be wrong, but I suspect what you're seeing here may be an extracellular representation of an action potential (and/or it could be a filtering artefact, see below). From the video on the spikerbox website, it looks like you place the electrodes (nails?) into the animal and hope to get close to axons and see spiking activity. Correct me if I'm wrong.
From a brief reading of the literature it would appear, under optimal conditions, the waveform of the extracellular action potential (EAP) is dependent on the cell type and location of the electrode along the neuron (this paper illustrates this nicely). As you move away from the soma and down the axon/dendrites, you tend to see this more prominent initial spike, as you see in your recordings. This is due to the ionic conductances and timings of channel openings. So that's one possible explanation...

Here's the other: the signal is filtered in some way. I notice in your figure your signal is very smooth without any noise and your EAP very long (assuming your x axis is seconds), which suggests to me your acquisition rate is quite low and/or being filtered. I've attached an image of an EAP I acquired (from a cell soma) a while back (with an acquisition rate of 10Khz, i.e. I 'sampled' the signal 10000 times per second to get the trace). They're all the same EAP on the same scale with different types of filters applied. The original signal is the one on the left; note all that baseline noise. The middle one is a low pass filter of 2KHz (gets rid of signals higher than that). The right hand one is a 750 - 1000 Hz band pass filter. This type of filter does funky things to signals if used incorrectly (such as in this example!). It basically only allows signals within a given region and gets rid of signals outside of it. What you end up with is the signal on the right, which looks suspiciously like yours!
So I'd hazard a guess and say it's a problem due to how the system collects and filters data. BUT, there could be a biological basis for it too.
However, there is one thing that does confuse me, and that is the polarity of your waveform. I would normally expect the prominent point of your EAP to be pointing downward. I have two suggestions as to what may be the cause of this:

You're actually measuring currents here; the units for your Y-axis would help answer that one.
Some grounding issue.


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How do TLR1/TLR2 activate the MyD88 dependent pathway
Recently, I've been reading about the MyD88 dependent signalling pathway, with particular reference to its activation in Macrophages and other cells of the immune system on recognition of a pathogen. I understand that when a PAMP (Pathogen Associated Molecular Pattern) binds with a PRR (Pattern Recognition Receptor), the receptor undergoes a conformational change, which precipitates a cascade of chemical reactions between various proteins, which eventually leads (inter alia) to the translocation of NF-κB to the nucleus, which leads to the production of cytokines. My question is about the finer points, particularly with respect to TLR1 and TLR2.
My reading suggests that these generally form a heterodimer - is this always true? Are both required for a pathogen to be recognised and an immune response produced?
Upon the pathogen binding with TLR1 (whether in a complex with TLR2 or not) what precisely happens to the receptor. I understand that MyD88 is, ultimately, recruited, but by what means?
I believe I understand everything that happens after the recruitment of MyD88, but I am less clear on everything before that. I had initially understood that the recruitment of MyD88 was the immediate next step, but other sources make reference to two proteins which I was initially unaware of: TOLLIP and TIRAP. What, if anything, is their role?
I'm still a little new to stackexchange so I apologise if this question is not up to standard, in which case, let the question simply be: 'How do TLR1/TLR2 activate the MyD88 dependent pathway?'

The TLR are usually working as homodimers (Toll-like receptors), although TLR2 can cooperate with TLR1 or 6.
Upon binding of its ligand (this is called pathogen associated molecular pattern) the receptors change their conformation and allow binding of TIRAP (TIR adapter protein) to their Toll-interleukin 1 receptor (TIR) domain. TIRAP then recruits MYD88, which then recruits IRAK1 or 4. The signal is then passed down the pathway as shown in the figure below (taken from the Wikipedia article on TLR).

Pretty good, but a correction - MyD88 recruits both IRAK1 and IRAK4. 4 then gets phosphorylated, and in turn phosphorylates 1 at Thr209 and Thr387. This in turn activates 1's kinase activity, and it hyper-autophosphorylates. 1 (and maybe 4) then dissociates from the complex, becomes ubiquitinated, and goes on to recruit the membrane-bound TAB/TRAF complex, which facilitates activation of TAK and RIP, leading to the NF-kB, PI3K/Akt, and MAPK pathways.

Thats correct. I updated the answer. Thanks for it.

I really enjoyed your link but I remain a little confused by sentences such as "Lipopeptides and other components of Gram-positive bacterial cells activate TLR2 in conjunction with either TLR1 or TLR6." Should I understand by this that you either have two TLR1 monomers which, together, form a homodimer, or you have a TLR1 monomer and a TLR2 which, together, form a heterodimer? Also, does dimerization occur only after binding with the ligand?


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Exocytosis of mast cell secretory granules
I've been doing a bit of reading about mast cell degranulation and have become thoroughly lost while trying to understand how the secretory granules are actually secreted.
I understand that there are many ways in which mast cells can be stimulated to degranulate, but I have been focusing on the example of IgE bound to FcεRI receptors. I believe I'm right in saying that antigen binding causes cross-linking of FcεRI receptors (since the antigen epitopes bind with the IgE paratopes and the IgE antibodies are themselves bound to the FcεRI receptors.) This recruits Lyn which phosphorylates ITAM motifs on the β and γ chains of the FcεRI receptors. This recruits Syk which is phosphorylated and activates LAT. This phosphorylates PLCγ which catalyzes the breakdown of PIP2 into IP3 and DAG.
All of this leads to the activation of PKC. I understand that PKC is (at least in part) responsible for the exoctyosis of SG but my question is by what means? Wikipedia, KEGG and this handy resource are all very cursory, whereas the academic papers which google turns up are way over my head.
So, if I might, what is it that PKC does and, in general, how are the secretory granules transferred from within the cell to the plasma membrane and out into the environment around the cell?

SG = secretory granule(s). I'm sure you already knew that if the above made sense to you, but I think it's good to be clear

You might be right about that, that was certainly not my intention in asking the question, really, though; I don't know very much about cell biology and don't particularly want to, I'm writing about immunology. I just didn't want to simply finish my paragraph with ...which leads to degranulation, I was hoping for merely a 'bare-bones' description of what PKC then does, whatever it reacts with and a simple description of how exocytosis happens

You've already learned much more than I know about cellular cascades in mast cells, but I wanted to be sure you knew about this handy resource - a free, searchable "Molecular Biology of the Cell" textbook: http://www.ncbi.nlm.nih.gov/books/NBK21054/
For general explanations about cell biology, it's thorough and readable. For instance:

Transport from the Trans Golgi Network to the Cell Exterior: Exocytosis
B Cells and Antibodies

Carry on learning.

Here is a paper reviewing PKC action in exocytosis. Although it dates from several years ago it should be a good start for accessing the literature on this topic since it has been cited 90 times.

Morgan A. et al. (2005) Regulation of exocytosis by protein kinase C. Biochem Soc Trans. 33:1341-4.
PKC (protein kinase C) has been known for many years to modulate regulated exocytosis in a wide variety of cell types. In neurons and neuroendocrine cells, PKC regulates several different stages of the exocytotic process, suggesting that these multiple actions of PKC are mediated by phosphorylation of distinct protein targets. In recent years, a variety of exocytotic proteins have been identified as PKC substrates, the best characterized of which are SNAP-25 (25 kDa synaptosome-associated protein) and Munc18. In the present study, we review recent evidence suggesting that site-specific phosphorylation of SNAP-25 and Munc18 by PKC regulates distinct stages of exocytosis.

Having returned to this topic, I found this very handy journal article:
http://journal.frontiersin.org/Journal/10.3389/fimmu.2012.00130/full
Much of it, I'm afraid, is very difficult for me to follow, but I still managed to take a lot from it and I hope others may find it useful. I would summarise what I have found thus:
PKC and the increased levels of Ca2+ combine to direct the reorganising of the cytoskeleton through various intermediaries. The cytoskeleton is like the skeleton of the cell and it also provides the structure along which the secretory granules move to the cell membrane. The vesicle will bind with the cell wall and disperses its contents.
I have read suggestions that PKC may be involved in the process of the secretory granules fusing with the cell membrane. Wikipedia suggests that PKC is involved in severing the links between the surface of the secretory granules and the exoskeleton, allowing it to merge with the cell membrane.
Any corrections are obviously welcome.


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How specific is the adaptive immune response?
When you read about the adaptive immune response, you are often told that the response is specific to each pathogen - that the response is tailored. My question is - to what extent is this really true? And if it is true, how is the response tailored?
I understand that the B cell receptors (and, consequently, the antibodies produced by plasma cells in response to a pathogen) are highly specific. A pathogen will bind specifically to a B cell receptor on a particular B cell and particular antibodies will be produced for that pathogen. Again, T cells are specific for each pathogen.
But, it strikes me that there doesn't seem to be that much variation in what antibodies do. Each antibody is particular to its pathogen, but all antibodies work by doing the same few things, e.g. opsonisation, or inhibiting viruses from infiltrating cells. Yes the antibodies may be specific, but to what extent is it true that the antibody will produce a specific response to a specific pathogen? I mean, does the antibody for staphylococcus affect staphylococcus differently from the way the antibody for listeria affects listeria?
Again, each CD8+ Tc cell is specific to its pathogen, but they then seem to go about killing their target pathogen in very similar ways - inducing apoptosis or lysis via perforin and various cytotoxins. So, again, would the CD8+ Tc cell for influenza respond differently to the CD8+ Tc cell for norovirus?

You are correct, specificity is in the antibody etc, but the killing/clearing mechanisms are the same in all cases.

The adaptive immune response is highly specific and is made to fit a specific antigen. The antigen binding sites are located on the ends of the two short arms of the Y-shaped molecule, as seen in the figure below:

The recognition site is made of the ends of one short immunoglobulin chain and one long chain. The ends (shown in yellow in the figure) are also called variable regions and are the key to the big variety of different antibodies.
When B cells develop, there B cell receptor (which is basically a membrane bound antibody) is tested if it reacts to components from the own organism. If not, they are released into the periphery (blood stream). These B cells are then called naive, since they haven't come in contact with an antigen. They express a B cell receptor which usually only has a weak affinity to an antigen - but the body produces quite a wide variety of these cells. (see the second figure).

When the body comes in contact with an antigen (like a virus), it is taken up by the so called professional antigen presenting cells (dendritic cells, macrophages, B cells) of the immune system, broken down into small pieces and these are presented to the immune system. This activates the affinity maturation of the B cell receptor, somatic hypermutation and finally the clonal selection of the cells, which produce the antibodies with the highest affinity (the strongest binding) to the antigen.
There are estimates that the human immune system can produce around 10 billion different antibodies. This variability is achieved by the genetic variability of the mutation of the variable region of the antibody (the whole process is nicely explained here).
For further information on this topic I can recommend reading the following articles:

Development of the immunoglobulin repertoire.
Immune receptor editing: revise and select.

The reaction of the body afterwards is always the same, as you state yourself. The specificity of the adaptive immune response is "only" mediated by the specificity of the antibodies. This also makes the system very strong against new pathogens, since only one part of the system needs to be adapted, while the cascades behind it (like apoptosis) are always the same and can be activated fastly if needed.
This can cause some problems, too. Think about self-antibodies, which occur in autoimmune diseases. Here the body can not distinguish between a legitimate immune response against a foreign antigen and those, which are from the own body.

Rather than saying that it is specific for an antigen, won't it be better to say that it is specific for an epitope ?

To make it more prescise: It is specific for an epitope of a specific antigen.


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Can more than one antibody bind the same antigen
I'd like to clear something up about antibodies that I'm not sure I've understood in the articles I've read. Looking at concepts such as "affinity maturation", "monovalent antigens" and "polyvalent antigens" it seems as if there are multiple antibodies which can bind to the same antigen. (Although I think I'm right in saying that individual antibodies can only bind to one antigen?) However, when I read sentences like "It has been estimated that humans generate about 10 billion different antibodies, each capable of binding a distinct epitope of an antigen" on the Wikipedia page (for antibody) it does make it sound like it's one antibody per antigen? Is this the case? Or is it one antibody per epitope. Either way, to put this question in a nutshell:
Is it true to say that the same substance could bind with (and, therefore, be recognised by) more than one antibody, or not?
Also, if the answer is no, does that mean that antibodies with different binding affinities are classed as the same antibody or not?

Let's clarify the terms. An antigen is a molecule that can be associated with a particular substance (virus, pollen, dander.) When an immunoglobulin or antibody recognizes an antigen it binds to a specific epitope. An antibody recognizes an epitope using its paratope.
Some antigens have multiple epitopes; this means that different antibodies can simultaneously bind to them (if the epitopes are far-enough apart from each other so that binding to one doesn't preclude binding to the others.)
An example from my work is influenza (flu) hemagglutinin, which is a major viral coat protein. Here's a low-resolution structure showing a "head-binding" antibody fragment (actually three of them), and here's a similar structure showing a "stem-binding" antibody fragment. Our immune repertoire (and physiology) greatly predisposes us towards producing head-binding antibodies over stem-binders. Note that each structure has three antibody fragments bound in the same state. Because the head-binder and stem-binder antibodies are well-separated in space they can both be accommodated in a single complex (as is experimentally confirmed.) In this case, up to six antibodies, using two distinct paratopes, could simultaneously bind to a single antigen.
For matured (high affinity and high specificity) antibodies, each binds a specific epitope. The typical state of affairs is then explained "one antibody per epitope" which is overly simplistic because some epitopes can be recognized by multiple paratopes (which would be found on different antibodies.) So a given epitope can be recognized by no antibodies (a new antigen, or one that is poorly immunogenic) or by multiple ones.

Is it true to say that the same substance could bind with (and, therefore, be recognised by) more than one antibody, or not?"

Yes, that's true.

Is it, then, true that one paratope could bind to more than one epitope?

Yes. The process of affinity maturation starts with low-affinity and low-specificity interactions, with the paratope getting progressively improved with respect to affinity and specificity.

Yes, this idea is called a polyclonal or polyspecific antibody. It is known that antibodies before they are fully matured are polyspecific. That is how we can recognize nearly limitless 'things' with only a limited number of antibodies. This is because each antibody you initially make can take on the job of binding more than one epitope.

Yes -
Its all binding kinetics - even a monoclonal antibody will bind many different antigens. The affinity/avidity will be different depending on the interactions. The target antigen may have the lowest known K_d, but antibodies will still bind to many many other antigens. This is why when doing research using antibodies you often have to "block" your specimen with something like BSA or milk to try and reduce the "non-specific" binding.

Although right in principle, this idea is misleading. Yes it is true that at some equilibrium that you can bind anything, even if the Kd is 20 grams/ mL, but that's not adding to the discussion and really diluting it with semantics of concepts that are not physiologically relevant.


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Does lower stomatal conductance of water influenced by elevated CO2 decrease overall evapotranspiration?
From what I understand, elevated CO2 levels decrease the stomatal conductance of water in plants. What I remember from irrigation sciences, higher temperatures should be more demanding on evapotranspiration. What will be more decisive for (evapo)transpiration of Canopy - higher temperature or higher CO2 levels?
Thank you!

Still not quite sure about this topic - some new article about it...
https://modernfarmer.com/2022/12/plants-have-mouths/


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Share of water usage by plants
From the total water absorbed by the root system, how much water does the plant use for transpiration and how much water does the plant use for photosynthesis?

This seems like a homework question. Can you provide more information regarding your thoughts on this or any efforts towards finding this particular statistic?


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Do spring varietes of cereals have a process of vernalization?
I was wondering about this question - Do spring varieties of cereals have some process of vernalization?
It would be nice to have some description of the main processes' differences of spring and winter varieties.
Thanks!

The answer depends to some degree on what you mean by "some process of vernalization". As far as I know, the difference between winter and spring varieties is a matter mostly of how strong the response is, not whether the response exists.
One paper writes in the abstract:

Wheat cultivars are classified as two general types: winter wheat with variable low temperature requirement for a proper flowering time (vernalization) and spring wheat without the requirement, based on their qualitative vernalization requirement. Winter wheat cultivars are classified as three types, weak winter, semi-winter and strong winter, according to their quantitative vernalization requirement to reach a vernalization saturation point or achieve the maximum vernalization effect.

The difference is not whether vernalization exists as a process, so much as whether it is required for timely reproductive transition.
See the figure below (from this paper), showing spring (LEG) and winter (MIR) varieties of wheat after various vernalization periods. Basically, even the spring variety has a weak vernalization response; it's just much less notable than the strong response of the winter variety.

With legend:

Frost tolerance (LT50), apical development (DC = decimal code) and days to heading of ‘Mironovskaya’ (MIR) winter wheat and ‘Leguan’ (LEG) spring wheat plants during 12 weeks of acclimation at 2 °C and two photoperiods, 16 h (long day) or 8 h (short day). Vertical bars indicate LSD0·05 and asterisks indicate that the plants had not reached heading by 100 d.


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Single wire pacemakers
There are single wire pacemakers used for regulating heart beat. The wire will conduct pulse to the heart. How can one wire be enough? Where is the reference wire for the stimulation of heart?

Hi, welcome to BIO.SE! What research have you already done on the topic? We ask that all questions here provide some evidence of previous research. Thanks


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Can immune cells be recruited to an area of inflammation, and later go on to a second?
With regards to innate or adaptive immune cells... can naive/immature cells such as neutrophils, monocytes, macrophage/dendritic cells or adaptive T-cells be recruited to an area of inflammation, for instance an infection in the gastric mucosa, then leave that area and be recruited to another different area of inflammation? Or once recruited to a site are they unresponsive to other events?


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What is neuronal computation?
Can someone give me a good explanation of what is neuronal computation and some examples of its use in neuroscience investigation?

Hi Welcome to Bio.SE! What research have you done on your own? we ask that all question askers provide evidence that they've tried to answer their own question. Piccinini & Bahar (2013) seems like an ok start to get you some citations to explore...

The term neural computation is basically synonymous with computational neuroscience.  It is the science of studying how the brain processes information by creating realistic mathematical models. Unlike general study of artificial neural networks (ANNs), neural computation heavily relies on biological accurateness. However, it may use models from ANN research, and vice versa.
Also see this course description of the PhD level course "Neural Computation" at Carnegie Mellon University  (CMU) :

Neural Computation is an area of interdisciplinary study that seeks to
  understand how the brain computes to achieve natural intelligence. It
  seeks to understand the computational principles and mechanisms of
  intelligent behaviors and mental abilities -- such as perception,
  language, motor control, and learning -- by building artificial
  systems and computational models with the same capabilities. This
  course explores how neurons encode and process information, adapt and
  learn, communicate and compute at the individual level as well as at
  the levels of networks and systems. It will cover basic concepts in
  computational and neuronal modeling, information theory and coding,
  neural networks and learning, neural data analysis and decoding,
  signal processing and system analysis, statistical learning and
  probabilistic inference.

(Emphasis mine)


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Why do I have super vision in purely red light?
I installed some RGBW led strips in my apartment recently.. by some I mean everything is now lit by led strips and there isn't a single light bulb left.
One thing I've noticed over the last few days is that my eyesight is significantly sharper in pure red light. Historically I've had pretty good sight but reaching 30's I've developed some nearsightedness. I don't wear glasses since I can still see things up to ~2m from me as clear as ever but reading street signs now requires me to get closer and stuff like that.
Things that require me to squint and really try hard in daylight (or white light emitted by the led's) are really easy to look at in red light. My vision is worse in blue light and worst in green light. Is there any kind of common explanation for this?


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Are there any animals that get smaller as a normal part of their life cycle?
It seems that at any given moment in a creatures life, it either grows bigger or has stopped growing.
The only exceptions I know of are extreme events like insects undergoing metamorphosis or evolutionarily irrelevant effects like humans shrinking a bit at old ages due to their spine getting compressed (I consider it irrelevant because for most of human history, people old enough for this effect to be significant enough were either dead or long done with reproduction).
Are there any animals that are known to "grow smaller" over some period of their lives as a purposeful part of their biological functions?

Are you asking about decreases in length, volume, weight, or all of the above?

In holometabolous insects it is quite common for the final larval stage to be heavier than the adult stage. For instance, Goliathus beetles, which are among the largest insects on earth, the adult stage often weighs about half of the final larval stage (which weigh 80-100 grams).
The same situation can be seen in the Hercules beetles, which this picture of both larvae and adult of Dynastes tityus clearly shows:
.
(picture from http://harrellhouse.com/in-the-museum-eastern-hercules-beetles/)

Sorry, I just saw that you mentioned metamorphosis in your question, which I managed to overlook. I'm leaving the answer either way, since some might find it useful.

here's some, a jellyfish and a frog: https://www.reddit.com/r/askscience/comments/5lse3t/are_there_any_animals_that_get_smaller_as_a/

Animals behaviour may lead to a weight reduction, although this is not a reduction of the structure itself: the number of organs (for sure) but also of sub entities within organs (number of brain lobes e.g.) remains the same but some of these may reduce in size in a regulated manner.
This is most obviously the case in hibernation, but has also been evidenced in non-hibernating mammals and is termed Dehnel's phenomenon.


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Why would you plate cells at different densities in a colormetric assay?
The aim of my experiment is to see if a kinase inhibitor reduces cancer cell viability. I am using 2 different cell densities 50,000 cells/well and 100,000 cells/well and different doses of the kinase inhibitor.

What sort of research or thinking have you done? What could be some possible reasons for different plating densities?

I have been told to plate some of the wells at 50,000 cells/well and others at 100,000 cells/well, but haven't been told why. In all the papers about colormetric assays I have looked at only one plating density is used.

I have read that the lower the cell density per well, the more greater the effect of drug treatment.

Also at higher cell densities the metabolic state shifts from proliferative metabolism to quiescent metabolism.

The comments you have given are some reasons, although they also depend on the confluency of the cells. Your teacher/professor/advisor is also making sure that you can see an effect at low levels of drug, as well as making sure that changes in the signal are visible - for example, does a 50% reduction in viability due to drug activity give the same drop in signal as reducing the number of cells by 50%? You don't say what kind of assay you're running, but a fairly common and inexpensive one is the MTT assay, with some kits nowadays switching to XTT for greater sensitivity and a reduction in the number of steps in the assay (example kit from Cell Signaling compared to an MTT assay kit from ThermoFisher), as the final colorimetric product does not require solubilization before reading. Finally, depending on the lab you're in, the conditions for the assay may not have been optimized yet, so your instructor wants you to test a couple of different densities to see what works best.

Firstly thank you for answer, I really appreaciate it. I am still a little confused though, are you saying that if there is a 50% decrease in viabilitiy in 50,000 cells/well experiments at a given drug dose, then there should also be a 50% decrease in viability in 100,000 cells/well experiment at the same drug dose? In both my experiments (50,000 cells/well and 100,000 cells/well) I haven't reached a 50% reduction in cell viability.

@Bio124 no, what I meant was if there was a 50% reduction in viability of the 100k wells, the signal should be the same (or very similar) as the control 50k wells. It was just an example, don't worry if you're not treating with a high enough concentration of drug to hit 50%. If you click on the Cell Signaling link and look at the first data figure, you'll see how the viability curves vary at different plating densities, although in this case they're looking at signal over a period of time (as the cells grow and multiply) instead of varying the drug concentration.


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Mapping ATC codes to names (Computational Pharmacology)
From Wikipedia:

The Anatomical Therapeutic Chemical (ATC) Classification System is used for the classification of active ingredients of drugs according to the organ or system on which they act and their therapeutic, pharmacological and chemical properties. It is controlled by the World Health Organization Collaborating Centre for Drug Statistics Methodology (WHOCC)

The WHOCC Website has a manual search. But I'm looking for an automated way to map ATC Codes to their names. I'm currently interested in mapping third-level ATC codes. For example:

N03A → ANTIEPILEPTICS
C03B → LOW-CEILING DIURETICS, EXCL. THIAZIDES

In addition to third-level codes, an ideal solution would map codes of any level to their name. After lot's of Googling, I've yet to find a dataset (such as a JSON or TSV file) that contains both ATC codes and their names.
Fingers crossed I don't have to write a web scraper.

You can download their database and parse your list. It seems to be not free (they take ~200 Euros). I would say that it is not really worth 200 euros. You can automate the search by appending the search term to the address https://www.whocc.no/atc_ddd_index/?code=N03. Anyway, this is not a biological question in a strict sense and would be put on hold.

I'm voting to close this question as off-topic because it is not about biology or bioinformatics.

Thanks @WYSIWYG—sorry I overlooked the Order page. I wasn't expecting the United Nations to sell access to data that's part of essential biomedical infrastructure.

After some more intense Googling, I found a TSV that did the job:

versioned blob link

You can access the file as raw text with the URL https://raw.githubusercontent.com/OHDSI/Vocabulary-v4.5/661804cf3c17add61b02e2e83e477f48acb011d5/21-ATC/atc_code.txt.
Thanks OMOP Standardized Vocabularies V4.5 for making this file available on GitHub!
This file was last updated on Aug 24, 2014 and is not actively maintained. It would be much more preferable if WHOCC hosted their datasets in a machine readable format. Furthermore, WHOCC should openly license to their content.
I'll keep this question open in case anyone knows of a better solution.


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Why do veterinary vaccines have shorter effect?
In humans activated T-lymphocytes persist until end of life, and activated B-lymphocytes persist many years, so most vaccines don't need to be reapplied and the few that do are reapplied after 10 to 15 years (recommendation varies slightly by country).
However cats (and dogs) are vaccinated every year, with individual vaccines reapplied after one, two or three years.
Does the immune system of cats differ so that it loses the activated lymphocytes faster? Or why are the vaccines (recommended to be) reapplied so often?

Can you give an example of the same vaccine that is recommended every year for dogs/cats but only every 10-15 years for humans?

I get an influenza vaccine every year, and now expect to get a COVID booster after 6 months.  Tetanus is 10 years, or if you have a wound that might result in an infection.  (I'm human, BTW :-))  Perhaps one reason canine vaccines are given more often is that your dog can't really tell you when s/he's sick, until it's too late.  Some are for things that are invariably fatal and/or easily transmitted, like rabies.  So perhaps one factor is "better safe than sorry".

@jamesqf, Influenza is a different vaccine every year. Tetanus is bacterial, so 10 (but it's 15 here) years make sense as it relies on B-lymphocytes only. What's going on with the covid one is not yet understood, so I'd leave it out for now.

Unfortunately rabies vaccines decline in effectiveness over time.
The first key study was by HN Johnson in 1954. He tested 25 dogs 1 and 2 years after receiving a vaccine. The dogs in the control group all died. The dogs inoculated at 1 year had a 100% survival rate. The dogs challenged with rabies at 2 years had an 88% survival rate. So, apparently there was some degredation in the vaccine effectiveness after a year.
Rabies vaccine duration effectiveness was also studied in the following experiment:
Dodds WJ, Larson LJ, Christine KL, Schultz RD. Duration of immunity after rabies vaccination in dogs: The Rabies Challenge Fund research study. Can J Vet Res. 2020;84(2):153-158.
In this study the effectiveness of the vaccine declined over time. All of the beagles in the control group died. In the 6 year group, survival was 80%, but it dropped to 50% in the 7 year group and only 20% in the 8 year group.
So, given these kinds of numbers the tendency has been to try to do an annual vaccination to maximize the level of protection.

But is there any idea of the underlying mechanism why that happens?

@JanHudec According to current knowledge, the only long-lived immunological cells are long-lived bone marrow plasma cells which can drip out serum antibodies for years unlike other immunological cells which are mostly dead after a month or two. So, if a vaccine loses effectiveness over the course of years, the only apparent cause would be a gradual decline in bone marrow plasma cells which are producing rabies antibodies.

And memory T cells, no? Those should be even longer lived given thymus shrinks with age. And the question than basically boils down to how long do the two kinds of memory cells live in carnivores.


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Energy efficiency of muscles and animals as a whole
When human or animal do some work, they use energy from their food. What is known about overall efficiency of this process?
Say a horse is turning a winch and does 10,000 kJ of work. How much more food will it eat to sustain that effort (compared to when it just stands around)?


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Flow Cytometry to learn about Cell cycle
I am posting my Flow Cytometry data here again because I realize that there are many people who are willing to help me, and I can learn a lot from you guys.
In this cell culture Lab, we use Cell U-937 Lymphoblast. And we want to learn how can we analyze cell cycle by using flow cytometry.
Could anyone help me to explain how to read the flow cytometry result related with cell cycle? I will be very glad to learn from you guys.
Thanks in advance!

The basis of analysing flow cytometry data in regard to the cell cycle is the fact that DNA synthesis occurs in S-phase and therefore cells before S-Phase (G0/G1) have half the amount of DNA compared to cells after S-phase (G2). [M-phase lasts to short to be of any relevance for this kind of analysis]. Signals that have less DNA than the cells from G0/G1 phase are either artefacts or apoptotic cells with fractured DNA (these are labelled as sub G1).
In order to measure the amount of DNA per cell the dye PI (propidium iodide) is used, since its quantitatively binds to DNA. Therefore the distribution of the PI signal can taken as a distribution of the different stages of the cell cycle.
This wikipedia article also explains the analysis in more detail and provides further references.

Thanks for your response! And may I ask what represent the 100% Sub G1 in Unstained control? Is it also dead cell? or just a population of cell before undergoing cell cycle? @Nicolai

@Sokviseth In an unstained sample none of the PI dye was added. Therefore you can not detected any DNA in these cells (even if it's there), so you can not say in which part of the cell cycle they are. This control is only done to check for problems with the PI staining.

Ah, I see :-). And i wonder one more thing why the amount of cells in (Dot Plot diagram) None is lower than that of Rapamycin (87.8 Vs. 91.4). Since the Rapamycin can inhibit the cell cycle, why the amout of cells do in crease? @Nicolai


text:
Identifying mutations in a yeast strain

Cells of a triple-mutant yeast strain (leu- his- trp-) were spread
either on minimal medium or on minimal medium supplemented with
various combinations of histidine, leucine, or tryptophan. The
cultures were grown at either 25C or 37C for 3 days. Colony numbers
in each plate were counted, and the data are listed in the following
table.

What kind of mutation most probably causes the his- phenotype?What
kind of mutation most probably causes the leu- phenotype?
A.Point mutation
B.missense mutation
c.nonsense mutation
d.conditional mutation
e.deletion mutation

My questions : What is the meaning of confluent in this context ? Can anyone give me a hint to solve this question ? I have no clue how to solve this.

For starters, you can just google "confluent".  It means that there are no colonies, but that the cells cover the whole plate.
So when you provide all three amino acids, the cells fill up the whole plate.  If you leave His out, but keep the plate at 25 degrees, the plate still fills up with cells, so the His- allele isn't hurting the cells at all at 25 degrees, but it's pretty nasty at 37 degrees.  That makes it conditional; the mutation only impairs His metabolism at some temperatures.
There is not a single cell which is surviving a lack of Leu, but there are some which are surviving the lack of Trp, and the lack of His at harmful temperatures.  Presumably, those are the small number which are lucky enough to acquire mutations which compensate for the original deleterious alleles, but NO cells were able to overcome the problem with the Leucine metabolism.  This suggests that the Leucine mutation might be a total deletion.

Just to add a useful term to this answer: the rare colonies on the -Trp plates and the -His at 37C are called revertants. Mutation classes (a), (b), (c) and (d) as listed in the question are all capable of reverting. A deletion cannot revert.

@AlanBoyd Why can all the others revert but not deletion ?

Most deletions cannot revert because they represent a large loss of information. A deletion of a single base would cause a frameshift, and that could revert as a result of a compensating insertion (or two more single deletions) that restored a functional reading frame.


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Is female the default sex in humans?
I was taught in school that female is the default sex in humans based on the following logic:

Development into a human male requires the activation of the SRY gene in the foetus. If that doesn't happen (because there is no Y chromosome, or for some other reason) then development into a female occurs.

For historical context on the use of the term default, please see this article:

Female sexual development ... was thought to proceed as a “default” in the absence of Sry.
The English word, “default,” means “failure to act; neglect” or “a preselected option adopted […] when no alternative is specified” (Oxford English Dictionary, 2011). In the case of sex determination, “default” became the prevailing model for female pathways—i.e., an ovary results in the absence of other action...

Is it reasonable to say that female is the default sex in humans? If so, is the SRY gene all there is to it?

What if I say the same thing about FOXL2?

In the same vein you could argue humans have tails by default as embryos develop a tail before white blood cells break it down again. It really depends on your perspective in my opinion.

If a whole bunch of genes didn't activate in proper order in the human foetus it would result in abortion or stillbirth. Is the default state of humans inviability?

Please define what you mean by “default sex”. Despite the extensive answer by @canadianer the term by itself does not mean sufficient to me to be the basis of a discussion. It is not clear to me whether you are asking any more than whether it is true what you were taught about the SRY gene at school. Too many questions on this list end up as semantic arguments because of imprecise formulation.

I think the answer is Yes, the difference between male and female is that females can reproduce, it easier to not do something than always doing all the work, so genetically, males are a subset of a female without the reproductive features.

Summary:
The idea that primary sexual determination defaults to female was proposed several decades ago and is primarily based on the observation that, in the absence of Sry, ovarian development takes hold. However, more recent models suggest that both ovary and testis development require complex genetic regulation and neither can really be said to occur by default. Furthermore, maintenance of sexual determination is apparently a life-long process.

Quote from a Review (Yao 2005):

We have just begun to glimpse into the mechanisms underlying ovarian development. Convincing evidence challenges us to reconsider the existing paradigm that describes ovarian development as a default system. The default concept was first proposed in the early 1950s when Jost performed the groundbreaking experiments to demonstrate mechanisms of sex differentiation of reproductive tracts (Jost, 1947, 1953, 1970). The term “default” was not originally intended to describe the developmental status of the ovary. Instead, it is referred to the female reproductive tract or the Mullerian duct based on the fact that the female reproductive tract forms in both XX and XY individuals in the absence of gonads. Indeed, now it has become evident that early ovarian development is an active process involving intrinsic cell fate decisions and complex crosstalks between germ cells and somatic cells. Most intriguingly, the appearance of testicular structures in XX individuals where Sry and its downstream components are absent further raises the improbable question: Could the testicular development be default after all?

Some Details:
Sex determination in mammals involves the development of a bipotential gonad into either a testis or ovary. Sertoli cell differentiation and thus testis formation is under the control of the regulatory gene Sry (Koopman et al. 1991). The Sry gene product was later shown to upregulate the expression of Sox9, which is key in testis development (Sekido and Lovell-Badge 2008). On the other hand, ovarian development is centered on β-catenin stabilisation by WNT4 signalling, which is thought to inhibit Sox9 expression (Bernard et al. 2012). Because Wnt4 is expressed basally in the genital ridge and testis development apparently depends on Sry expression, the ovarian pathway has often been described as default; in other words, the pathway that the gonad would take in the absence of Sry.
However, ovarian development is in fact an active process requiring the correct balance of many factors, including a transcription factor called forkhead box protein L2 (FOXL2) (Yao 2005). Studies in mice showed that Foxl2 is expressed in the ovary, both during development and in adulthood. Knockout of the gene prevented granulosa cell differentiation during development, leading to ovarian failure (Schmidt et al. 2004) and increased expression of markers for the testis development pathway (Ottolenghi et al. 2005). Furthermore, mutations of this gene are responsible for XX sex reversal in goats (polled intersex syndrome, PIS) (Pailhoux et al. 2001). Taken together, these experiments indicate that Foxl2 is required for ovarian development and that its absence can favour testis formation.
Many developmental process are dependent on correct timing of gene expression. Sry, particularly, must be expressed within a specific time interval or ovarian development will take hold (Bullejos and Koopman 2005; Hiramatsu et al. 2009). Research by Uhlenhaut et al. (2009), however, shows that this is not necessarily the case for Foxl2 mediated ovarian development, maturation and maintenance. A homozygous floxed Foxl2 mouse strain that expresses Cre under tamoxifen induction allowed conditional knockout of Foxl2. Three weeks after induction, cells of the ovary had transdifferentiated, adopting a morphology and gene expression pattern consistent with Sertoli and Leydig cells (which are normally found in testes). Notably, Sox9 expression increased drastically. Immunostaining showed that, while Foxl2 expression expectedly decreased after Cre induction, the increase in Sox9 was not observed until a day later, indicating that the expression of both is mutually exclusive and that FOXL2 may directly regulate Sox9.
This research presented a novel model for the maintenance of female ovary differentiation. During primary sex determination in females, activation of WNT4 signalling stabilises β-catenin allowing expression of female specific genes and the inhibition of Sox9 (Bernard et al. 2012). In adulthood, FOXL2 actively represses Sox9 expression in gonad cells, maintaining the granulosa phenotype. A similar model of maintenance has been proposed in males due to evidence that the loss of the transcription factor Dmrt1, which normally represses (and is also repressed by) Foxl2 expression, induces transdifferentiation of male mouse Sertoli cells to granulosa cells (Matson et al. 2011). In the case of both males and females, primary sex determination is not just a process that occurs during development but rather requires active regulation for the duration of adult life. This involves collective antagonism between various female and male sex determining factors, including Foxl2 and Dmrt1, and may dispel the notion that ovarian development occurs by default.

Further Reading:
The Genetics of Sex Determination: Rethinking Concepts and Theories
Genetics of sexual development: a new paradigm (Blecher and Erickson 2007)

References:
Bernard P, Ryan J, Sim H, Czech DP, Sinclair AH, Koopman P, Harley VR. 2012. Wnt signaling in ovarian development inhibits Sf1 activation of Sox9 via the Tesco enhancer. Endocrinology 153:901–912.
Blecher SR, Erickson RP. 2007. Genetics of sexual development: a new paradigm. Am J Med Genet A 143A:3054-68.
Bullejos M, Koopman P. 2005. Delayed Sry and Sox9 expression in developing mouse gonads underlies B6-YDOM sex reversal. Dev. Biol. 278:473–481.
Hiramatsu R, Matoba S, Kanai-Azuma M, Tsunekawa N, Katoh-Fukui Y, Kurohmaru M, Morohashi K-I, Wilhelm D, Koopman P, Kanai Y. 2009. A critical time window of Sry action in gonadal sex determination in mice. Development 136:129–138.
Koopman P, Gubbay J, Vivian N, Goodfellow P, Lovell-Badge R. 1991. Male development of chromosomally female mice transgenic for Sry. Nature 351:117–121.
Matson CK, Murphy MW, Sarver AL, Griswold MD, Bardwell VJ, Zarkower D. 2011. DMRT1 prevents female reprogramming in the postnatal mammalian testis. Nature 476:101–104.
Ottolenghi C, Omari S, Garcia-Ortiz JE, Uda M, Crisponi L, Forabosco A, Pilia G, Schlessinger D. 2005. Foxl2 is required for commitment to ovary differentiation. Hum. Mol. Genet. 14:2053– 2062.
Pailhoux E, Vigier B, Chaffaux S, Servel N, Taourit S, Furet JP, Fellous M, Grosclaude F, Cribiu EP, Cotinot C, et al. 2001. A 11.7-kb deletion triggers intersexuality and polledness in goats. Nat. Genet. 29:453–458.
Schmidt D, Ovitt CE, Anlag K, Fehsenfeld S, Gredsted L, Treier A-C, Treier M. 2004. The murine winged-helix transcription factor Foxl2 is required for granulosa cell differentiation and ovary maintenance. Development 131:933–942.
Sekido R, Lovell-Badge R. 2008. Sex determination involves synergistic action of SRY and SF1 on a specific Sox9 enhancer. Nature 453:930–934.
Uhlenhaut NH, Jakob S, Anlag K, Eisenberger T, Sekido R, Kress J, Treier AC, Klugmann C, Klasen C, Holter NI, et al. 2009. Somatic Sex Reprogramming of Adult Ovaries to Testes by FOXL2 Ablation. Cell 139:1130–1142.
Yao HH-C. 2005. The pathway to femaleness: current knowledge on embryonic development of the ovary. Mol. Cell. Endocrinol. 230:87–93.


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Flow cytometry data Analysis
everyone.
Since I am new in the flow cytometry technique, I am not really sure how to analyze the result.
We use cell U-937 Lymphoblast.All Cells

Could Anyone help to explain me this one?
Thanks in advance!

Please explain what your study is about. We can't just guess what you are doing

Disclaimer: Assumes you know how flow cytometry works.
You've done a flow-based AnnexinV apoptosis assay here.
Annexin A5 (AnnexinV) protein binds to phosphatidylserine (PS), which is typically in abundance of the inner leaflet of live cells. Upon the initiation of apoptosis, PS is known to flip to the outer leaflet. Thus, you can use AnnexinV conjugated to a fluorescent molecule such as fluorescein isothiocyanate (FITC) to look at externalized PS.
7-Aminoactinomycin D or 7-AAD is a fluorescent intercalator that can be used to detect DNA and is excited on the 488nm laser (emits on a 650nm longpass filter or the like). The dye is not permeable to live cells, and so for dead or dying cells with compromised membrane permeability, it binds freely to DNA.
The problem with either alone is you cannot say a 7-AAD+ cell is apoptotic and you cannot say an AnnexinV+ cell is apoptotic, because we know that you have early apoptosis and late apoptosis, and in either the cell isn't wholeheartedly dead, yet. You also have necrosis.
And so on a dot plot of 7-AAD and Annexin V, you can create 4 quadrants based on the mechanism of the two components:
Double-negative: No external PS or DNA binding means these are viable cells.
Double-positive: Both external PS and membrane instability means late apoptosis.
AnnexinV single-positive: Undergoing early apoptosis, nucleus isn't yet permeable.
7-AAD single-positive: Completely dead or necrotic, membranes have probably disintegrated.

The basis of the assay is you're trying to determine at what stage of cell death your cells are in.
The unstained control is a way of looking at your cells alone, and allows your to correct for autoflorescence, florescence generated by your cells just from excitation alone. You also want to run single-stain controls to see where your positive, and negative populations lie. Without FMO (fluoresence minus-one, basically your full staining panel minus a color) controls, it's hard during gating to confidently say where your positives and negatives are delineated, due to the effects of spillover and noise.
A note about the AnnexinV single-stain control: You can see that in the untreated sample, there's basically no AnnexinV, but in the control it's 22.0% of the cells. Single-stain controls where you assume positives exist have to have positive and negatives. Without positives, where do you set the gate for them? What if the population shifts during acquisition? They probably used cells that were dying on purpose to generate confident controls for that sample.
That's the left half of your data. The right half are treatments. Basically you've stained the cells for both markers and then treated them with Torin2, Rapamycin and Mitomycin to see how those compounds affect the viability of the cells. There's a control where you added nothing.
Based on the gates set with the controls, you can see that the mitomycin sample has the greatest effect: The cells are 6.54% AnnexinV positive, undergoing early apoptosis, and 14.3% are double-positive, undergoing late apoptosis, and 8.09% are dead or necrotic.
The conclusion you'd derive is that mitomycin, but not the other compounds, has a profound effect on the viability of the cells.

Thanks So much for your explanation. I did learn a lot from you. :-) @CMosychuk

And in the 7-AAD single staining, we did not put Annexin V, why we can see the amount of cell death in the annexin V quadrant?

The laser is still collecting in the annexin channel, the author simply didn't stain that marker. So it could just be noise, or autofluorescence, or spillover in some cases (I don't know what fluorophore they used to stain annexin). If you saw something significant there, you could subtract that background from your treatments to get a more accurate readout.


text:
What goes wrong in the immune system that leads to autoimmune diseases
As far as I understood so far, B and T cells are produced in the bone marrow, and during their maturing process in the bone marrow or Thymus, the are "programmed" to react to certain proteins. It is like giving them a particular key.
As I also understood, these "keys" are entirely created by random. Which means, that also "keys" are generated that match cells of the "host body."  Hence, if released into the bloodstream/lymph system, those B and T cells would attack the cells of the "host body."
As I understood further, there is a kind of a "security system" which checks if B and T cells are produced that would attack cells of the "host body." This security system would intervene and destroy those B and T cells before they are released into the bloodstream/lymph system.
As read lately - and I am not sure if I did understand this correctly - it is also possible, that B and T cells could also react to other cells even if the key doesn't match perfectly.
Now my questions.
Firstly, being an SW engineer interested in this topic is my understanding above correct?
Secondly, is it correct to say that autoimmune diseases are mainly caused by the following two points:
1. the "security system" in the bone marrow / Thymus failed, and therefore "bad" B and T cells were released into the bloodstream/lymph system
2. B and T cells react to other cells, even if the "key" does not match perfectly.

Welcome to Biology.SE! You need to keep in mind that this is one of the (many) riddles in biology which aren't completely solved yet. So, although you might get answers to many of your questions, don't expect an answer to everything

This will be a fun read for you. Note the publishing date: this is still a hot area of debate. Also note that there's another security system, clonal anergy, meant to stop rogue cells from responding to autoantigens: T cells require 2-3 signals during Ag stimulation for conventional activation, as do B cells require Th or Tfh cell co-stimulation. Otherwise they're made to become quiescent and die in the periphery.

There's also this notion that B or T cells regularly need to get survival signals, often times from very weak self-pMHC signalling that doesnt activate them, but says stay alive (ref). Whats interesting about B and T cell maturation is they need enough binding for self-pMHC at selection checkpoints that they don't bind too tightly, but also that they bind at all.

Consider you're a software engineer, consider an autoimmune disorder the equivalent of a bad antivirus update causing your AV to recognize C:\Windows\system32 as a threat and "quarantine" it.

Your understanding of the process is basically correct. There are of course a lot more details to it, but that wouldn't be in the scope of the question. Do note that only T cells mature in the thymus (that's where the T comes from ^^), whereas B cells mature in lymph nodes and the spleen.
As for why autoimmunity occurs you also understood the basics, however the devil is in the details: wikipedia does have a much longer list of mechanistically different causes. While its often sufficient to explain immune recognition using 'keys' (T cell receptor / B cell receptor = antibody) and their respective 'locks' (peptides bound to MHC / antigens), the exact process of immune cell activation becomes important in autoimmunity, where cells are wrongly activated. This means that there are many possible points at which the 'security system' of the immune cell maturation can (or rather has to) fail to allow autoimmunity.
As for the cross-reactivity of cells: the difference between the binding of B cells (via antibody/B cell receptor to protein surfaces) and T cells (via T cell receptor to peptide sequences) means that in general T cells are much more likely to show cross reactivity - just because the possibility space of a 10-12aa peptide is much smaller than that of a protein surface (even though the probability is still very low).
Additionally - as stated in the comments to your question - both the immune activation pathway and the issue of cross reactivity, while principally understood, are not 'completely solved'. The immune system is insanely complex just by itself and the addition of interactions with both almost all human proteins AND proteins any kind of pathogen, mean that it will take quite a lot of time until researchers can figure out all the weird quirks caused by the 'wrong' combinations.


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Is Race the Result of Microevolution
I've been studying evolution for some time and was wondering whether the emergence of different races is an example of micro evolution within our species?
Bonus Question: is it impossible for homo sapiens to undergo to split into separate species via macro evolution?  I think it's impossible since were so interconnected (due to globalization and transportation), therefore speciation could not occur.
Thanks

Welcome to Biology.SE. If you don't mind me asking the question, what source (websites, books, etc...) did you use to study evolution?

I took Gr. 11 biology.  As for internet sources I used 'Understanding Evolution' and 'Talk Origins'.  I also glanced at the occasional youtube video.

Racial differentiation is illusory. We form a continuum that is currently understood better by some sociologists than by most biologists, regrettably.

Yes, but no humans are not plausibly going to diverge into separate species based on pre existing races.

Micro- and macro- evolution are terms vaguely referencing to arbitrary time scales
The terms microevolution and macroevolution have rather arbitrary and unclear meaning. For this reason, they are rarely used in the scientific literature. When they are being used, it is often in the first part of the introduction where general statements for which inaccuracy matters little are being made.
Typically, the existence of lineages called races (but see below) within a greater lineage called a species are limit cases between what one would want to call macro evolution or micro evolution. But in essence, it really does not matter where such arbitrary boundary is put, it changes nothing to evolutionary processes at play.
The concept of ethnic group
Note also that the concept of race (generally called ethnic group) is a human made concept that sometimes fail to match the reality of population structure in humans. If we were to name lineages based on genetic differentiation rather than socio-cultural cues, we would, if I am not mistaken, end up with a reasonably different result.
Bonus question
For your bonus question, you'll probably want to have a look at the post Does it make sense to classify all humans in a single species? and the post How could humans have interbred with Neanderthals if we're a different species? who discusses the concept of species.
You are right that the increased migration rate brought about by globalization causes increase interbreeding between humans lineages and will therefore rather prevent any further population structure that would have otherwise eventually lead to an event of speciation. There is, for the moment, no sign that any human speciation would evolve any reproductive barrier with any other human lineages. We are for the moment far from any speciation event in humans.

For the bonus question, would Homo floresiensis qualify as a species evolved from H. sapiens, or did both evolve from some precursor species?

I guess it is mainly a matter of what you decide to call Homo sapiens. As H. floresiensis is not called H. sapiens floriensis, I must be considered as a a sister lineage of H. sapiens and not a subspecies.