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The human brain in numbers II-A: synaptic connections per structural type
The overall number of synapses in the human brain is roughly 1,000 trillion, i.e. 10,000 synapses per neuron.
I assume that each structural type of neuron (basket, pyramidal, ...) has a somehow characteristic average number of in-coming and out-going synaptic connections, i.e. not every type of neuron will have the same roughly 10,000 in-coming and 10,000 out-going synaptic connections.

I am looking for a thorough overview of these characteristic numbers
  by structural type.

Ideally as a link to an existing resource, but if someone with a good overview over the literature would take the effort  to compile such an overview (like user another 'Homo sapien' thankfully did in his answer to The human brain in numbers I: neurons), it would be even greater.
What's for sure: such an overview will be a) not complete and b) only estimates, so don't worry about that.

Please don't keep reposting effectively the same question. This is almost identical to the one that was closed last.

Also, very importantly, we actually gave you some great resources on the last question you asked to follow up on, and you seemed entirely disinterested and expecting people here to do your work for you. I found that really rude actually. It's like you are going to StackOverflow and asking somebody to write you a sorting algorithm.

I don't understand your discontent.. I just ask for specific references which seems perfectly ok at other SE sites. "BRAIN project's web site" is not a specific reference in my humble opinion.

Concerning your first comment: I was explicitely advised to split up my question  (to make it less broad) and followed this advise. What's wrong with that?

Your new question is absolutely not any less broad than the last one, it just reflects a basic misunderstanding of neuron morphology. If you plan to make 2 more versions of this question, still asking the same question in different angles, those will also be too broad.

To give you an idea of what is acceptable, see something like https://biology.stackexchange.com/questions/57495/cortical-projections-from-layers-2-3-back-to-4/57519#57519 This is asking about just a single pathway, between two layers of cortex, only talking about excitatory cells, and I wrote a multiple page answer.

Would you please be so kind to correct my basic misunderstanding. Aren't synapses something one can count? And why shouldn't there be a difference in number between different morphological types of neurons? I just have no clue where my basic misunderstanding lies.

Let us continue this discussion in chat.


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Help! What kind of spider is this?

Can anyone tell me what kind of spider this is and if it might be poisonous?

Welcome to Biology.SE! Please provide the location and an approximte size of the species. A close-up photo would be much better.

looks like it was a broad-faced sac spider, or something related

source: Stack Exchange

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

sort: votes


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What is the average speed of human sneeze?
I sneeze a lot, at various times and various "volumes", and often wonder about the speed of the sneeze itself, i.e. the speed of the air coming out of the nose while sneezing.
What is the average speed of that, in humans? Are there any records for such a thing?

Mainstream understanding is that a sneeze is 100 mph, or ~45 m/s. However, this isn't even close to being true..
A study in 2013 (see link below) was conducted where they investigated the airflow dynamics of sneezing and breathing, and discovered that the highest velocities of a sneeze are around 10 mph, or 4.5 m/s.

...the maximum sneeze velocity derived from these measured distances was 4.5 m/s.

So, about 1/10th the value of what most people believe.. just like the 10% use of our brain misconception, but reversed! (we use 100% of our brain.. not necessarily all at the same time, but we do utilize all parts of our brain)
Airflow Dynamics of Human Jets: Sneezing and Breathing - Potential Sources of Infectious Aerosols

While this is a good study, my understanding is that they looked at the extent of the propagation of the sneeze 'plume', based on Schlieren imaging of the turbulent flow.  It's quite possible that the flow through the nose (which might still be laminar to some extent) has a higher velocity.  That wasn't an item of interest in the study (since they were looking at sneezing in its role as propagating an infectious aerosol), but a simple argument from volumetric flow rate necessary to expand the plume suggests that through-nostril velocity should be higher than plume velocity.

Yes, the air velocity coming out of the nostrils is greater than the plume velocity.. you can safely make this assumption solely by considering Bernoulli's principle, and the fact that airflow outside the nostril has more interaction with it's surrounding atmosphere than it does inside the nostril. Regardless, the difference in velocity would still only be 10-15% at most. To get a more precise idea though, you could consider the rate traveled of sneezed particulate, and account for air resistance, to then derive some kind of initial force and velocity. We're still talking under 20mph though.

About 35-40mph
According to the Mythbursters who subjected this to their tests showed that their own sneezes went around 35 to 40mph. This is anecdotal since it only has a sample size of two persons, but it at least gives an indication about the speed of a sneeze.

Mythbusters is absolutely terrible in how they conduct their "experiments", and 99% of the time, its not proper science.Sorry, but this answer is inaccurate.

@Charles depends how the measure the speed, which we don't really know

@Shadow Wizard I would rather trust a recently published study that was conducted by multiple PhD's and peer-reviewed by a scientific community, than a couple guys on a TV show just looking to entertain.
And why would we not know how they measured the speed? It was a TV show, I'm sure they showed it.. and if they didn't, that just even more supports my argument that Mythbusters isn't real science.

@Charles sure, but wait a minute, "velocity" is not always "speed". Maybe with such velocity, it reach a final speed of 35-40 mph. Sure they mean actual speed in that article?

It also depends what exactly has been measured. The air moves fastest, the smallest aerosol particulates are a bit slower and larger liquid particulates move slower again.

@ShadowWizard Are you serious? The absolute, only difference between velocity and speed is that velocity also describes direction, whereas speed doesn't. That being said, your statement doesn't makes any sense. Please don't try to discuss things that you're not familiar with. And yes, I'm sure they're talking about "actual speed" in the scientific, published study..lol.

@Hyfnae The OP asks what the speed of the air is.. " and often wonder about the speed of the sneeze itself, i.e. the speed of the air coming out of the nose while sneezing."
The answer I provided addresses air dynamics; the particulates aren't germane to the question.

@Charles not native English speaker, for some reason I confused velocity with acceleration. All clear now, thanks and sorry!

@ShadowWizard No worries! If you were thinking acceleration vs velocity, then yes, the two are completely different. All the best.

@Charles Fair enough, I upvoted your answer anyways, it provides a much better source than mine.

Yup, the "common belief" vs. "scientific research". Both have value.

@Charles: While I agree with your point regarding the accuracy of Mythbusters' experiments, I feel obliged to add this xkcd link: https://www.xkcd.com/397/

@tonysdg Sometimes it's a shame I'm restrained to only one upvote per post. Yours is one of those occasions.

@tonysdg Haha, it has Richard Feynman. That comic is right on, however, I'm not sure how successful Mythbusters is in actually motivating people to stop watching TV, get off the couch and do their own experiments. Also, to me that comic suggests the argument of what is the bare minimum of an experiment, and what is considered to be just fooling around. I think Mythbusters is a successful TV show because it walks the fine line between those two concepts. +1 to your comment though.

Results seem to vary wildly depending on the methodology. Charles' article on plos.org seems to be serious, and is very complete. Still, looking at an earlier study of Penn State University published by LiveScience, they measured speeds of up to 200 miles per hour.
See it here: https://www.livescience.com/3686-gross-science-cough-sneeze.html
As mentioned in the article:

"The smaller and lighter particles are less affected by gravity and
  can stay airborne almost indefinitely as they are caught up in and
  dispersed by the room's airflow. [...] Some of [these particles]
  rocket out at speeds greater than 200 miles per hour."

It does not go into details of how the Penn State University experiment was measured, but it clearly shows that you would have to agree on a methodology and which particles' top speed to use to get some consistent results.

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

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


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Are all animal species prone to cannibalism induced prion infection?
Humans have the tendency to get certain prion diseases when eating human flesh. It's known animals can get prion diseases as well.
Does cannibalism among other animal species also make them more susceptible to get a prion disease, and are there distinctions between mammals doing so and other orders like reptiles, birds, fish etc.?

Perhaps worth noting that BSE wasn't caused by cannibalism, but rather because cattle were fed with material derived from sheep.

I'm not aware of prion diseases in non-mammals. It isn't clear whether this is because of differences in their PrP homologs or for some other cause.

It is perhaps worth looking into more historically established prion diseases in noncarnivorous animals, like sheep. If prion diseases were only transmitted by consuming prion-rich brain tissue, then they should be extremely rare (produced via unique misfolding events or mutations in affected individuals) or completely absent in wild herbivores and domestic herbivores which are not being fed meat meal.
In fact, I mention scrapie because it predates the practice of supplementing livestock feed with meat-derived protein. (The first documented mention of the disease dates back to about 1772 and mentions that the disease is about 40 years old at that point.) As it happens, the earliest mention of livestock feed or feed supplements being composed of meat and bone meal I can find dates to about 1890. Prion diseases also appear in wild populations of elk and deer in the form of Chronic Wasting Disease, currently a big problem in the northern US and Canada, as well as in cattle and sheep.
So how did scrapie come to be such a problem for European sheep farmers?
Well, for one thing, scrapie (and CWD) can be transmitted via ectoparasites. But the most common culprit probably lies in the soil. It turns out that infectious prions can survive for years in soil once they're deposited. Not only is the decomposition of a carcass a way to infect the soil with the misfolded prions, but CWD proteins are also present in the excreta of infected animals and even antler velvet.
This is a problem, because both scrapie and CWD can be acquired simply by consuming infected soil or grazing on grass containing it. This is most likely the most common way that these prion diseases are acquired naturally--not cannibalism at all, or at least not the sort we commonly think of! It's a simple fecal-oral route of transmission, albeit one with an alarmingly long potential incubation period.

An individual (animal or human) acquires a prion disease when they consume meat that contains prions (proteins that are mishapen enough to drastically change their functionality), which subsequently causes proteins within the individual to misfold into the same shape as the prion, resulting in a whole slew of problems.
As of right now, there is little knowledge of where prions come from/how they're formed. Also, there is little knowledge of how inter-species infections/transmissions occur. Researchers are currently investigating various combinations of inter-species transmissions, such as humans eating infected horse meat, or cats eating infected chicken meat, but still know only very little about this phenomenon.
To say which species have higher rates of prion disease when looking at a cannibalist communities within that species, I don't think we're anywhere near close to making those conclusions, and the same goes for inter-species transmissions.
All the best.

Too bad there is so little known about this. Are there any places were a layman like me could gather some more information about this subject?

Dr. Dean O'Del was on radio with a syndicated health show in the 1990s during the BSE/Mad Cow scares, where he cautioned that the use of bone meal on roses or plants as the heat of making bone meal did not destroy the prions until it was burnt to charcoal carbon.
Given scant evidence for  grass from contaminated soil might also have the prions in the grass for how sheep might get and transmit it, lowering the odds of eating prions still would require a totally plant based diet given the vast numbers of animals mixed into processed meat products like Pink Slime and deviled meat or ham, & a  organic diet given that,  only a spontaneous and rare mis-folded protein would start the 40 year incubation towards Alzheimer's and vCJV.
Both scrapie and CWD can be acquired simply by consuming infected soil or grazing on grass containing it. This is most likely the most common way that these prion diseases are acquired naturally--not cannibalism at all, or at least not the sort we commonly think of! It's a simple fecal-oral route of transmission, albeit one with an alarmingly long potential incubation period.

It would be handy to get some supporting references or even wikipedia links in this post, though it looks like it might be somewhat informative. Note that the other answers, which contain similar messages, do have such links.

This non-answer blatantly plagiarises the existing accepted answer and the external source without citation. Whilst this is an incomplete explanation on how non-cannibalistic and indeed non-carnivorous species could come into contact with prions it does not address the question about if those animals might be prone to infection from such contact. The first 2 paragraphs should really be a supporting comment on the accepted answer, or a community edit.


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I found this bug in my closet. Could someone help me identify?
It looks like it recently died. The shell was shiny and smooth and fairly brittle. I've been having trouble identifying what it is because it doesn't quite look like any of your common house pests.
The bug is at most 4 mm. I live in a relatively old apartment in New York City and my best guess is that this guy crawled out of a crack in my closet wall.

Welcome to Biology.SE. Can you please add 1) approximative scale 2) where do you live (country and lower scale information about the ecology around your place) 3) How is your house (do you live in an old wooden house or in a modern concrete building)?

I've updated the original post. Thanks in advance :)

I agree This is definite a spider beetle

The image you provided isn't the best of quality, but I really think it looks like a spider beetle. Anyone else agree?

I looked up a few more images of these guys and I think you're right on the money.

Glad to hear it, and best of luck when trying to get rid of them!


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How many almonds a day can cause toxicity for vitE?
Vit E in high doses is dangerous for tissue. How many almonds a day taken regularly can cause this?
RDA
Males : 10mg/day
Females : 8mg/day
Pregnancy : 10mg/day
Lactation : 12mg/day
15 mg = 33IU for vit E
Requirement increase for higher intake of pufa
Pharmacological dose: 200-400 IU/day

Almonds contain  hydrocyanic acid, apparently as much as 25 mg/kg (8mg/kg standard deviation). However, it would take at least 2 kg of almonds (roughly 1650 kernels) to reach a lethal dose, which is highly unlikely to be digested unintentionally. You may die before vit e toxicity.

You can eat bags and bags of almonds every day for years and not be in any risk of vitamin E toxicity. There are many, many cases of adults consuming 500+ mg of Vitamin E every day, for years on end, with no signs of harm.
In general though, the max daily recommended value of vitamin E consumption is 1000mg. One cup of almonds (100g, or ~100 kernels) contains a little under 30mg of vitamin E. That being said, you can consume over 30 cups of almonds in one day before reaching the daily recommended limit.
You would have to eat tens of hundreds of thousands of almonds for there to be any kind of health concern.. at which point, you would probably suffer from other conditions than vitamin E toxicity.
You (should) have nothing to worry about.

EDIT: Here are a couple sources...
This page has everything about recommended limits, research that has been done, tables with daily limit values, etc.
US Department of Health and Human Services - National Institutes of Health

Research has not found any adverse effects from consuming vitamin E in food.

This page contains basic nutritional facts for almonds. A 95g serving is about 90 whole kernel almonds. Nuts, Almonds - Nutrition Facts

Serving size 95 g ... Vitamin E (Alpha Tocopherol) 24.9 mg


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Does sperm weight causes sex ratio?
Chromosome X in female sperm is heavier than male Y chromosome. Does it causes difference in fertility of sperm and heavier female sperm is unable to fertilize better than male sperm?
This is given in AK Jain of physiology, chapter on reproduction.
I doubt this explanation.

Probably not! There are certainly some physical reasons to doubt it. Looks like the mass difference between X and Y sperm is on the order of 0.1 picograms: X chromosome "weight"?
First, mass differences are not likely to affect swimming and motility of sperm, because sperm are at low Reynolds number -- the forces of fluid drag vastly overwhelm inertial forces. See, e.g. Purcell's lecture "Life at Low Reynolds Number" (http://aapt.scitation.org/doi/abs/10.1119/1.10903 but also available online). For this reason, even much larger differences in mass are not likely to matter to swimming.
If motility is not the issue, you could imagine that, during the fertilization or insemination process, sperm might be under the force of gravity, leading to different sedimentation rates. A sperm's sedimentation speed is equal to the force on it divided by its friction coefficient $\gamma$,
$$v_{sperm} = \frac{(m_{sperm}-m_{displaced}) g}{\gamma} $$
where $g$ is the gravitational acceleration and $m_{displaced}$ is the amount of mass displaced by the sperm. You can estimate $\gamma$ with Stokes' law (https://en.wikipedia.org/wiki/Stokes%27_law) as about $6\pi R \mu$ with $R$ being the sperm size and $\mu$ the fluid viscosity. We're interested in the maximum possible difference in speed, so we'll choose $R$ to be at the small scale of sperm size, $5$ microns and $\mu$ to be that of water $\mu \approx 0.01 \frac{g}{cm s}$. This gives us $\gamma \sim 10^{-4} g/s$. The difference between $v_X$ and $v_Y$ is then
$$v_X - v_Y = \frac{(m_X - m_Y) g}{\gamma} \approx 0.01 \,\textrm{micron}/s$$
This means, for there to be a significant difference between X and Y sperm you'd have to keep them sedimenting under force for quite a while. This can be used (especially in a centrifuge, where you can increase the gravitational force) to select between genders - but it seems unlikely to happen in vivo.
To see why this is a small speed in practice, you have to ask whether the sperm would also have diffused a larger distance or managed to swim while it was sedimenting. Sperm velocities are on the order of tens of microns per second, so anything that changes the sperm swimming speed by even 0.1% is more important than the mass difference in sedimentation.
Putting this together, it suggests that mass differences are not a likely origin for sex ratios slightly deviating from one - if they are tuned, it would make more sense to change sperm length or swimming stroke. In fact, I believe there are some small geometric changes between X and Y sperm - but could those geometric changes happen simply because there is less chromosomal material in the Y? That, I'm not sure.

It would be better to add this : https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1440662/

Thanks JM97 for link. I would have accepted that as answer.


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Wikibooks claim that it is difficult to find two texts that agree on the definition of an animal
In this entry of Wikibooks we find the claim

It is surprisingly difficult to find two texts that agree on a precise definition of an animal.

Is this true?
[I know nothing about biology, but I find this claim perplexing.]

Definition of Animal
Animal is typically defined phylogenetically (just like any other monophyletic taxon; see here for intro to phylogeny). Any lineage part of the taxon Animalia (aka metazoa) is an animal. This is the definition given by wikipedia > Animal. You can find the animals here on the tree of eukaryotes.
Issue with the claim

It is surprisingly difficult to find two texts that agree on a precise definition of an animal.

This claim is pretty clumsy in my opinion. It sure can be hard to find a set of phenotypic traits that would group all animals together but it does not mean it is hard to define 'animal'.
IMO, what they meant is

It is surprisingly difficult to find a set of phenotypic traits the are shared by all animals and by none of the living organism that is are not animal.

This claim would make more sense. It is indeed true that it is hard to make such set of phenotypic traits. There are plenty of non-animals that are heterotrophic eukaryotes (such as fungi), there is at least one animal that is (at least partially) autotroph (Elysia chlorotica), not all animals have a nervous system, etc...

Thanks! +1. I tried to edit your answer by changing "triats" to "traits", but the software told me that edits must be at least 6 characters long.


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Can a hemorrhage occur after death?
Can a hemorrhage occur after death?
Specifically lung hemorrhages. Can an organ hemorrhage after death and, if so, how long for?

Under certain circumstances, yes. Can you add more detail to clarify exactly what you're looking for? Because the general answer is "no".

Hi there, thanks. I'm doing some looking over an autopsy of a celebrity for personal interest as the cause of death is uncertain. The person in question had appeared to have hung themself and CPR had been attempted around 30 minutes after the person had hung themselves. The autopsy later revealed that "the lungs had focci of hemorrhage" and if the hemmorhages were unlikely to have been caused post-death then this makes foul play more likely.

To summarise though, the person examined had been dead for a good time when CPR was attempted.

Usually,blood moves through the body by force from the contraction of ventricles, the contraction on muscles, gravity, or other forces. At death, the only force left is gravity, which is why we see lividity (or livor mortis -pooling of blood in dependent positions) after death. This continues for ~8-12 hours (depending in part on temperature).
The blood in the arterial system at the moment of death is still under pressure because arterial wall musculature has not relaxed yet. (I don't know how long this takes, to be honest.) If an artery is pierced (say, a bronchial artery, e.g. by a knife), blood will flow from a high pressure area to a lower one (e.g. into non-inflated lung tissue, the abdominal cavity, or the outside or the body) So post-mortem hemorrhage can occur until the arterial musculature has completely relaxed. After this relaxation, stabbing a corpse will produce a small amount of oozing at most, unless pressure is applied somehow, e.g. during CPR. CPR may make small petechiae larger.
Livor mortis can occur in the lungs post death as well.

as the blood accumulates in the dependent areas, the pressure of the settling blood can rupture small vesslels, with development of minute hemorrhages (petechiae)... This usually takes 18-24 hours... and is more common in (asphyxia).

Hanging is death by asphyxia, and is known to be associated with lung hemorrhages, but very small ones.
Forensic Pathology, Second Edition By Dominick DiMaio, Vincent J.M. DiMaio, M.D., pp.22-25

Thanks for the great answer! One last thing, as my knowledge of biology is limited, could the "Focci of hemmorrhage" been as a result of CPR (IE pressure on the chest causing lungs to be damaged)?

It's possible but very unlikely. CPR does cause damage: bruised muscle, broken ribs, etc., but it's not common. The petechiae in the lungs after hanging take hours to form as the blood settles in the lower parts of the lung. If the person was only hanging for 30 minutes and CPR was started, the blood is moving, not pooling. Hope that helps.

@Charlie - Here is a list of things CPR can do to screw up autopsy results: Forensic aspects of complications resulting from cardiopulmonary resuscitation.

Would it be possible to discuss this further with you in a chat? It would be great to get a knowledgeable person's opinion on the matter and look into more details the autopsy if it would be too much trouble.

that is if I can even start a chat, as I'm not entirely sure how to do it without spamming a conversation in chat for ages.

@Charlie - As I'm not a coroner, I don't think I can be of much more help. Sorry. :-/

that's fine, thanks for your help thus far anyway. Feel free to contact me if you change your mind though as any medical experience would be very valuable. :)


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What purpose does the wax coating on blueberries serve?
What purpose does the wax coating on blueberries serve? Is it some sort of protective layer?
A search on the web reveals that it is called "bloom". But the source is not a credible, scientific source. And it doesn't explain in detail what the coating does.

My uneducated guess is that the wax is called Epicuticular wax.

The main functions of the epicuticular wax are to decrease surface
  wetting and moisture loss. Other functions include reflection of
  ultraviolet light, assisting in the formation of an ultrahydrophobic
  and self-cleaning surface and acting as an anti-climb surface.

It would seem that your uneducated guess is in fact correct. This kind of cuticular wax is also found on other fruits, such as bananas, grape berries, and (I think) tomatoes.

Years ago my wife and I made  grape juice that turned to wine. This happened because the bloom on the grapes harbors yeast cells. The same situation occurs with other berries including blueberries.  Organisms living on the surface of other organisms are usually symbionts


text:
Which grows slower: the thumb nail or the pinky nail?
I notice that thumb nails and pinky nails grow slower than the 3 other fingers in the middle. But which one is slower, the thumb nail or the pinky nail?

This isn't at all my experience - it seems this may vary. I'm sure apparent growth also depends on "usage".

Biology Stack Exchange is a question and answer site for biology researchers, academics, and students. This question is of freak-show triviality. I have voted to close it.

@David There are many papers on the subject. Bean wrote 4 papers on fingernail growth that are considered important medical findings.

Which one is slower? "Important medical findings"? Mr Bean?

Your question would be better if you summarized relevant said research. It's also probably prudent not to call other people sssholes.

I did some research and found out that it is actually the pinky that grows the slowest. See the decadal reports of Bean on fingernail growth or:
Gupta, Gita Rani, et al. "Human nail growth pattern and medicolegal aspect." (2005).

So how are you going to use this information? If you really think it is worthy of anyone's attention, cite references it in a way that someone else can consult them. You need proper journal etc details with a link of some sort.


text:
How do our eyes detect light at different frequencies?
Here is my confusion: we can see colored light of different wavelengths: form red to violet. To my understanding, these stimuli cause a confirmational change in the photoreceptors in our eyes and results in a STP that eventually leads to an "all or nothing" action potential that sends another signal, again an all or nothing action potential through the optic chiasm to the occipital lobe and we perceive the colors as we see them.
My question is *how does this signaling work? *; How can a minor stimulus, resulting in an "all or nothing" chain of action potentials be converted into something as specific as the vision of color?
Asked another way, how does variation in a confirmational change at a receptor that results in "all or nothing" signaling lead to specific signals being sent such as colored vision ?
PS: I dont know jack about sensory physiology

Short answer
Action potentials generated to different colors are indeed similar throughout the nervous system and do not encode color as such. Instead, the different color- sensitive cells in the retina are connected to different neurons and these color-specific signals are kept segregated up until the higher visual cortical areas.
Background
Action potentials are indeed pretty similar throughout the nervous system. However, the color-sensitive sensory cells in the retina, called the cones, come in three flavors: red, green and blue. These colors form the RGB system just like in your LED TV and can together make all the available millions of colors. These three cones synapse ultimately onto color-specific secondary sensory neurons (Fig. 1).
Hence, R, G and B cones indeed generate identical action potentials in downstream neurons, the trick is they do so in different retinal ganglion cells, and at different firing rates depending on the intensity of light that particular cone is sensitive to. These different classes of retinal ganglion cells project onto different classes of neurons in the brainstem (lateral geniculate nucleus, or LGN) and ultimately onto different neurons in the higher cortical visual areas in the brain.

Fig. 1. Different classes of cones synapse onto different classes of secondary sensory neurons in the retina. source: Discovery Eye Foundation
The reason why we can differentiate millions of colors can be explained by the Hering model of color vision (Fig. 2). Basically, the different cones converge pairwise onto opponent color-sensitive cells. The red-green opponent system, for example, operates by weighing the amount of red and green in the incoming signal. This weighting results in an analogue system that can code millions of colors along the red-green axis (Fig. 3).

Fig. 2. Hering model of color vision. source: Webvision

Fig. 3. Red-green color axis. source: SO

Beat me to an answer - glad yours came up before I got too far in to mine. You might add something about the nature of communicating via action potentials: that although they are all-or-none, the rate of APs can encode intensity, and a brief mention of how photoreceptors themselves don't have action potentials but rather drive their targets to fire at different rates.

@BryanKrause - thanks. The question is so broad I decided to give a simplified, short answer. However, I do not think rate coding applies to color vision; the message is that the pathways are seggregated spatially (still working on the answer though).

Yeah, I don't think it needs anything but a brief mention, but I disagree that rate coding doesn't apply to color vision. The relative rates of cells affected by different cone types is what gives a broad spectrum of possible colors.

Also related: https://biology.stackexchange.com/questions/52315/photoreceptors-and-light-with-mixed-frequencies?rq=1 though I don't think that question answers this one well, this one goes more toward the basic physiology.

@BryanKrause - I've added the Hering model. How's that?

Added to one of your sentences, feel free to review and revert if you don't like it. Otherwise I think it's great; Fig 3 might not be necessary. Already gave you an upvote so here's an extra 5 Internet Points.

You can also give name of this principle : labelled line principle.

@AliceD Is there any reason for Blue cone not having a connection to Greenness-Redness neural stage? The other two cones are having connection to all neural stages though.

How can a minor stimulus, resulting in an "all or nothing" chain of action potentials be converted into something as specific as the vision of color?

Visual phototransduction is the one of answers to your question.
It is a process by which light is converted into electrical signals in the rod cells, cone cellsand photosensitive ganglion cells of the retinaof the eye. This cycle was elucidated by George Wald (1906-1997) for which he received the Nobel Prize in 1967. It is so called "Wald's Visual Cycle" after him.
Overview
The visual cycle is the biological conversion of a photon into an electrical signal in the retina. This process occurs via G-protein coupled receptors called opsins which contain the chromophore 11-cis retinal. 11-cis retinal is covalently linked to the opsin.  When struck by a photon, 11-cis retinal undergoes photoisomerization to all-trans retinal which changes the conformation of the opsin leading to signal transduction cascades which causes closure of cyclic GMP-gated cation channel, and hyperpolarization of the photoreceptor cell.
Signal Transduction
In dark
glutamate is continually being secreted at synapse between photoreceptors and bipolar cells.
In light

1)A light photon interacts with the retinal in a photoreceptor cell.
The retinal undergoes isomerisation, changing from the 11-cis to all-trans configuration.
2) Retinal no longer fits into the opsin binding site.
3)Opsin therefore undergoes a conformational change to metarhodopsin II.Metarhodopsin II is unstable and splits, yielding opsin and all-trans retinal.
4)The opsin activates the regulatory protein transducin.

5) This causes transducin to dissociate from its bound GDP, and bind GTP, then the alpha subunit of transducin dissociates from the beta and gamma subunits, with the GTP still bound to the alpha subunit.
6) The alpha subunit-GTP complex activates phosphodiesterase or PDE.PDE breaks down cGMP to 5'-GMP.
7)This lowers the concentration of cGMP and therefore the sodium channels close.
8) Closure of the sodium channels causes hyperpolarization of the cell due to the ongoing efflux of potassium ions.
9)Hyperpolarization of the cell causes voltage-gated calcium channels to close.As the calcium level in the photoreceptor cell drops, the amount of the neurotransmitter glutamate that is released by the cell also drops.
10)A decrease in the amount of glutamate released by the photoreceptors causes depolarization of On center bipolar cells (rod and cone On bipolar cells) and hyperpolarization of cone off-center bipolar cells.
Impulse conduction
As is explained by AliceD above via CN 2 using labelled line principle.

thanks anubhav!! I never knew they worked by hyperpolarization

How do our eyes detect light at different frequencies?

Different frequencies are recepted via different photoreceptors i.e. different pigments in cones. Tricolor mechanism being the most famous.
Here, our eyes can detect three different colours Red,  Green and Blue. These are mixed in appropriately for detection of different colours.
For eg: 99:42:0 will give you perception of orange color. Which means 99% Red 42% Green and 0% Blue.

Don't add another low-quality answer on top of an existing post - please write a single answer and edit it instead.

@AliceD Madam, I knew your answer was perfect for question. If you had not written that,  I would have had written same. But, when we look at question, what comes in mind at first glance is Tricolor mechanism. This is the only answer any examiner will write in response to question like How do our eyes detect light at different frequencies?. So, I gave the same, so that anyone who searches for this question on internet, shall find an answer, an answer which OP does not want.

Firstly, you shouldn't write answers which OP doesn't want... You should write answers that target the question. Secondly, I'm a bloke 8-)


text:
Identify this insect - genus, species
Please help identify this insect - genus, species and anything interesting about it.
Note, this is posted separately due to comments in this other thread.

I'm

Please add the location where it was found. That helps with ID

Locations are not available :( - there's very little data associated with each one other than additional photos

This one is most probably a longhorn beetle (Cerambycidae). The long elytrae (protective forewings) and the long curved antennae are quite typical.
Yours looks a bit like this one: https://en.wikipedia.org/wiki/Rosalia_longicorn
It is probably a different species, though.

do you have further advice or methodology insight on identifying the species

@ina The way that is taught at school is to use a determination key, but in practice, identification often starts with a familiarity with the group of interest. I would advise to browse an insect identification guide, where species are grouped in families, and get an intuitive feeling of what insects in a given family look like, alongside with general description that the guide gives. Then, to get more precise ID, one has to find a determination key that covers the group of interest. Often, these documents are specific for a region. Some technical notions are often needed.


text:
Identify this insect - genus, species (orange, black)
Please help identify this insect - genus, species and anything interesting about it. Do the colors matter in the identification?
Note, this is posted separately due to comments in this other thread.

Any idea where the species is from (country / type of ecosystem / ...)? Did you capture / find this insect yourself? What is its approximative size? (you can consider answering to these questions to your related posts as well)

i did not capture these - they were sent from the artist. i'll try asking, but not sure if they know where the original source image was from

The colours usually matter, but there can sometimes be variability within a species.

This looks like a Weevil. Specifically it looks like a red/orange-spotted lily weevil

Here is some more information on it:
https://en.wikipedia.org/wiki/Brachycerus_ornatus
though the information is very limited.

are they always colored like that?

its a general weevil. this one is just stopped but many arent spotted


text:
Can cognitive enhancement from exercise be replicated/replaced through prolonged standing?
Can cognitive enhancement from exercise be replicated/replaced through prolonged standing?
Like, will BDNF be released from prolonged standing.  I would prefer to use a standing desk than exercise (due to wanting to save time).

Short Answer
Probably not.
Slightly longer answer
This fairly recent review shows little positive effect of standing desks and mixed results of treadmill desks for cognitive outcomes (note: this is a summary of 23 full studies). Only treadmill desks were actually studied for cognitive performance, and even those showed no effects.
There were some positive physiological outcomes for both standing and treadmill desks, but much more consistent with the treadmill desks. The treadmill desks seemed good for weight loss, though, especially in obese participants.
All in all, it doesn't seem like a mere standing desk is known to give direct cognitive benefits, though the existing studies are all fairly small. It probably won't hurt, although standing for long periods can be problematic, too.
None of these studies compared the effects of the standing desks to the effects of exercise.

References:
MacEwen, B. T., MacDonald, D. J., & Burr, J. F. (2015). A systematic review of standing and treadmill desks in the workplace. Preventive medicine, 70, 50-58.

There are studies, however, like this one:
Mehta, R. K., Shortz, A. E., & Benden, M. E. (2015). Standing up for learning: A pilot investigation on the neurocognitive benefits of stand-biased school desks. International journal of environmental research and public health, 13(1), 59.
...that purport cognitive benefits of standing desks. However, it is important to note that one of the authors has patents on standing desks that are licensed by companies that produce them, including some of the desks used in the study.

Re "standing for long periods can be problematic", for some people (I'm one), even short periods of standing in one place can be problematic - though walking long distances is no problem at all.  I would also greatly doubt the idea that standing is at all similar to exercise.

@jamesqf You might not be standing correctly.  I use some of these techniques: https://www.youtube.com/watch?v=kNFsdGsaB2s  It might just be a placebo effect, but I've noticed more muscle tone when I started standing.  But definitely don't stand if it hurts.


text:
What is this spider from Arizona?

I live in Phoenix, Arizona, USA. Can you please identify this spider for me. Is it dangerous?

It's hard to judge from a single photo but it appears to be from the Family Theridiidae (cobweb spiders). Spiders in this family have long front (first legs)and much shorter third legs as the spider in your photo seems to have. But the perspective may be off. You don't mention the size which would help.
I enjoy photographing insects and spiders in my area. One thing I found when I was trying to identify spiders is colour and pattern can vary quite a bit from different locale. Sometimes two spiders of the same species could look like two completely different species.
So please bear this in mind. All I am is an arthropod enthusiast that has benefited from some more skilled and knowledgeable people helping me out. With that in mind, I wonder if your spider might be Phylloneta pictipes (syn. Theridion pictipes).

Source: http://bugguide.net/node/view/2209
I should've said but the two spiders above are the same species; male on the right and female on the left.
You can check out more spiders of this species at http://bugguide.net/node/view/49080/bgimage and see how they vary.

The spider is a spotted orbweaver (genus Neoscona)

Probably of the species: Western Spotted Orbweaver (Neoscona oaxacensis)
This photo I attach came from a gallery of western spotted orbweaver observations filtered on only observations from Arizona:
https://inaturalist.ca/taxa/123713-Neoscona-oaxacensis/browse_photos?quality_grade=any&place_id=40


text:
How long can Vibrio cholerae live in its ambiental optimal context?
How long can the Vibrio cholerae live in its ambiental optimal context?
Thank you in advance. My problem is that i can't find this information. I did some research on google, but nothing was retrieved, I even used other search engines. Thank you very much for your help.

I Found It!!!!    SURVIVAL OUTSIDE HOST: Cholera can survive in well water for 7.5 ± 1.9 days and the El Tor biotype can survive 19.3 ± 5.1 days(Footnote 21). The bacterium can survive in a wide variety of foods and drinks for 1-14 days at room temperature and 1-35 days in an ice box(Footnote 21). It has also been found on fomites at room temperature for 1-7 days(Footnote 21).
Source>>http://www.phac-aspc.gc.ca/lab-bio/res/psds-ftss/vibrio-cholerae-eng.php


text:
Why are the granules of pancreatic beta cells larger than those of alpha cells?
Why are the granules (insulin) of β cells larger than the granules (glucagon) in α cells in pancreatic islets of Langerhans?
Also is there any size difference between alpha cells and beta cells?
Source: Inderbir Singh , Text book of Human Histology. Ed 8. Ch-16. Pg 202.

This may help: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2909340/#!po=55.1282  smaller granules=>more precision. Large granules=> more economy is excreting large quantities.

May be thats the case here as well as..


text:
What is the name of this tree with compound leaves?
Can anyone tell me what is the name of this tree?
It was found in Northern US.
(click on image to enlarge it)

Is it a tree or a shrub? (I can't tell if that's a pot or a trunk.) Whatever, that's one of the prettiest leaves I've ever seen. I hope someone can identify it.

You have the tree in a pot 1) so is it a native tree you found and replanted? 2) Or did you buy it at a nursery or had it given to you? 3) Did it stay outside through the winter? 4) If not, has it been subjected to below freezing temperatures - at least briefly? 5) What part of the northern US as in location (which won't matter if this isn't a native tree or survived the winter)?

It is Cussonia spicata,  It is one of the favorite foods of wild elephants.
The attractive leafs grow from the end of thick branches to form rounded heads.

Source
Wikipedia

Wonderful that you identified it! I figured it couldn't be any native tree that in NA as its leaves are so unusual, otherwise I'm sure I'd remember seeing it online. I love the leaves but considering it's a tropical tree, not likely to find it in garden shops either. Curious how you knew it - have you been to Africa and saw it there?

The image you put doesn't have the same type of leaf as in the question. You should argue why you think it corresponds nonetheless. Are the leaves of this plant variable in shape? (I know this is the case in Hedera helix, another Araliaceae).

This Cussonia leaf looks more like the one on the photo: http://www.zimbabweflora.co.zw/speciesdata/image-display.php?species_id=142930&image_id=6


text:
What is this flying bug in Denver, CO?
It seems to be a flying insect about 2-3mm in length. It also doesn't seem like it's very good at flying. They seem to crawl around my desk until I try to hit them, which is when they'll start flying.
Location: Denver, Colorado, USA
They seem to come out more at night.

Can you get a better image? Also, a description of the environment?

@arboviral that's about the best pic I can take with my iPhone, sorry :( the environment is my computer desk, it's pretty bright as I have a few monitors that are on all  the time

Could you get one with the wings in focus? Without some idea of wing patterns and venation there will be serious limitations on what we can do, I'm afraid.

@arboviral I added another picture with the wings spread. Hopefully that helps? :)

A little - but unfortunately probably not enough, I'm afraid! Based on the activity period, size and photos I had been wondering if it was a biting midge (Diptera: Ceratopogonidae) of some sort - take a look at some sample photos here: http://www.padil.gov.au/maf-border/pest/main/140521/49023 - but I'm now much less confident about that; the head looks too big and I can't see the distinctive antennae.

@arboviral they don't bite though. I think they are some sort of fly? I put apple cider vinegar into a cup and they all flew into it. does that give you a clue? I don't think they are fruit flies, they don't have red eyes.

These are Scuttle Flies (Order Diptera, Family Phoridae) (the wing venation, best seen on the lower left individual of the top photograph, is characteristic); the group has several hundred species in America north of Mexico.  So far as I am aware, the generic key in Manual of Nearctic Diptera, Volume 2 (available online here, pages 25 to 48) will still yield useful results, but cannot be used on these photographs.  The 30 pages in bugguide.net's gallery (starting here) eliminate a few of these, but not nearly enough to go further on the evidence we have.


text:
What is an in-frame activating fusion?
In [1] it is written that:

Whole-genome and RNA sequencing identified recurrent in-frame activating FGFR3–TACC3 fusions

What is a recurrent in-frame activating fusion?
[1]   Cancer Genome Atlas Research Network, “Comprehensive molecular characterization of urothelial bladder carcinoma.,” Nature, vol. 507, no. 7492, pp. 315–322, Mar. 2014.

This is explained in the linked article.

We found several recurrent translocations of likely pathogenic significance, including an intra-chromosomal translocation on chromosome 4 involving FGFR3 and TACC3 (n=3). The breakpoints were in intron 16 (2 cases) or exon 17 (1 case) of FGFR3 and intron 10 of TACC3 (confirmed by DNA sequencing and RNA-seq). All three lead to fusion mRNA products whose predicted proteins include the N-terminal 758 amino acids of FGFR3 fused with the C-terminal 191 amino acids of TACC3 (Fig. 2a). Based on the structure of the FGFR3-TACC3 fusion protein, we predict that it can auto-dimerize, leading to constitutive activation of the kinase domain of FGFR3. FGFR3-TACC3 fusion, which was recently described in both glioblastoma21 and bladder cancer7,8, represents a promising therapeutic target.

FGFR3 is a member of the fibroblast growth factor receptor family. It is a transmembrane kinase that is normally activated upon ligand binding which triggers dimerisation. TACC3 is a protein that can dimerise through a coiled-coil domain.
The FGFR3-TACC3 gene fusion that is generated by the reported intra-chromosomal translocations thus generates a version of the receptor that is predicted to be constitutively active because it can dimerise in the absence of the growth factor.
Recurrent means occurring frequently.

Just one little comment: in-frame means inside introns or exons, but not within inter-genic regions?

in-frame means anything that  generates an open reading frame in the mRNA so that a fusion protein will be produced. Te endpoint in TACC3 was always in an intron, and in two cases the FGFR3 endpoint was also in an intron. This will generate a gene fusion with a hybrid intron. In the other case they say that the FGFR3 endpoint was in the next exon. Since all three fusion proteins have the same structure that means that the exon interrupted by the translocation must have become part of a hybrid intron. If you draw yourself a diagram it will become clear. But yes, not in intergenic regions.


text:
Why do flowers naturally reproduce with their own species?
I have always wondered why flowers reproduce with the same species naturally. Why can't the pollen grains get to a different species flower through via the wind, water, or insects?

Sometimes they do.  There are many naturally-occuring hybrids of (close) species where their ranges overlap, and many more produced by human intervention.  But in a sense the question is backwards: things become different species because they can't easily interbreed: either by geographic or temporal separation (that is, they bloom at different times), or perhaps some biochemical incompatibility.  If they could easily interbreed, they'd be the same species :-)

I know with cactus at least some self-fertile plants will ripen the male and female sex parts at different times. The female parts will mature and accept pollen from nearby neighbors, then the male parts mature and provide pollen to any plants with mature female parts (possibly even itself.

The pollen from a given species of flower does get transmitted to other flowers of different species (like you said, through air, insects, etc.)..the problem though is that those two species of flowers are just that!: they are two different species, and by definition, aren't able to reproduce amongst one another.
I would recommend looking into the definition of a species. There isn't a single, blindly-conformed-to definition, however, its most commonly accepted that a species can be defined by the "boundaries" in which that species can or can't produce offspring with other organisms. Organisms that can produce offspring together are generally considered to be of the same species.
There are odd cases though where some interspecies reproduction occurs, such as a donkey and a horse producing a mule. Yet, if two mules were to attempt sexual reproduction, they wouldn't be successful in producing offspring (mules are sterile). So, this is a tricky situation to define, in terms of if the donkey and horse are the same species or not, since they can produce offspring, yet that offspring is a dead-end, so to speak.
A different example.. if (somehow) a chicken attempted sexual reproduction with a pigeon, the sperm would reach the females egg, however, no offspring would occur.
A major impedence of offspring occurring for interspecies reproduction comes down to the mechanics of meiosis, and how chromosomes match up with each other throughout the process. Chromosomes need to be of similar size, shape, etc., in order to properly pair with their complement during meiosis. Also, the correct number of chromosomes need to be present. These dynamics, as well as many others, get messed up when interspecies reproduction is attempted.
I hope this addresses your curiousity.. All the best!

It's even more blurry - mules aren't always sterile. The definition really is more along the lines of "their offspring aren't easily capable of having their own offspring". And while donkeys and horses are considered separate species, mules (and honkeys) aren't. Humans like their nice little categories, but nature rarely fits those boxes :)

I don’t think this is a helpful answer; it just falls back on an unhelpful and inaccurate “definition” that isn’t definitive at all.

To complement what Charles (Darwin is it you? :)) said, and JM97 hinted at the comments, there is also another factor impeding the cross pollination between different species, that is the pollen-pistil interaction.
Basically whichever pollen can come in contact with the flower but only pollens carrying specific recognition signals (I'm not an expert but I suppose is specific compounds on the coating of the pollen that are recognized by the pistil) can actually start the fertilization process.
This has of course interesting consequences, namely self-pollination incompatibility: some plants are more than happy to self pollinate (e.g. barley or Arabidopsis) but some others use this same process to exclude the pollen coming from the same plant and only allow fertilization from pollen coming from other plants of the SAME species (basically what most European royal families were NOT doing...)


text:
How is the human oxygen absorption dependent on the concentration of oxygen in respiratory air?
I just wanted to calculate the theoretical time span in which I could survive (conscious) in my apartment without letting the air on the inside exchange oxygen/carbon dioxide with fresh air. During my calculations I came to the point where I was unsure, if the oxygen amount already consumed, influences the future O2 absorption and consequently the CO2 production.
In this hypotetical scenario, I assume that the air in my apartment is homogeneous and ideally mixed, thus measuring the same level of oxygen anywhere on the inside. Furhter I assume that all of my rooms are completely empty, hence having volume of the living space * room height * oxygen concentration as my initially available oxygen amount. (I tried to be independent of the air pressure by using standard values for consumption depending on concentration and calculate how long it would take for the oxygen level to drop below/carbon dioxide to rise above a specific threshol (depending on what gets lethal first) ).
I asked this particular question and not "How long can one survive in a closed room...", because I have not found a useful answer yet considering the oxygen/carbon dioxide concentration, but the absolute amount of these gases in it.
In case it would be helpful/necessary: I am not familiar with biochemical, metabolic reactions and have not studied in this field before.
Thanks in advance.
PS: If you think, another stackexchange community would be more appropiate, please comment.

If you read about the effects of high altitude you should be able to map this on to your question in relation to oxygen requirements. However, in a closed room you would also have to consider the toxicity of accumulated carbon dioxide

As @AlanBoyd suggests, carbon dioxide will be a problem before lack of oxygen is. Read up on the Apollo 13 mission.

Related: https://biology.stackexchange.com/questions/53107/sitting-in-a-closed-room-filled-with-regular-air-for-how-long-will-the-air-las

@Alan Boyd: Would the effects of high altitude be the same?  There you have a 80/20 N2/O2 mix, but at lower absolute pressure.  In a closed room (assuming a good CO2 scrubber system) you would maintain a higher pressure, but decrease the percentage of O2.

@jamesqf I admit that the physics of gases was never one of my strengths. At high altitude the partial pressure of oxygen is lower because of the reduced overall pressure. In the closed room the partial pressure of oxygen falls because oxygen is consumed. Isn't it possible to use the fatal partial pressure derived from knowledge of altitude effects to deduce the fatal partial pressure in the closed room since it is the partial pressure of oxygen that determines the loading of haemoglobin in the lungs?

Please include your precise question in your question text. A title is quite separate. In your case your long "question" does not actually include your question and I am unclear what you have tried to calculate or wish to know.

@Alan Boyd: Well, that's what I'm wondering about.  Is it simply the partial pressure that matters, so that breathing a 100% oxygen atmosphere at 20% of sea level pressure would be the same as normal air at sea level?  Or are there effects from absolute pressure, the way there are effects from increased pressure when scuba diving?


text:
What exact characters determine an animal's Genus?
I do know that if two animals cannot naturally reproduce, they are said to be of two different species. But what determines the genus?
Just for example, the African elephant belongs Loxodonta but the Indian counterpart belongs to Elephas , despite the fact that they are so similar, as opposed to say, the fact that, the Bengal Tiger and the Snow leopard despite being so different , are placed in one genus, Panthera ?

I don't think there is any non-arbitrary concept being used to tell whether two species belong to the same genus or not. The same goes on with any other taxonomic rank. Systematicists build some intuition within each clade about what a genus could mean and use it to argue what is the most strategic grouping but the concept of genus may well vary a lot from clade to clade (from spiders, to mammals or to flowering plants, ...).
Note that even the concept of species is not as nicely defined as you may think. Have a look at How could humans have interbred with Neanderthals if we're a different species? for discussion on the concept of species.

What also SciShow forgot to mention is that, by the very definition of evolution, taxonomy is just a handy way that we invented to simplify our life (or complicate, if you ask me). As they pointed out, categorizing and identifying appeals to our brain. But it's just a photo of a runner; if you snap it a few seconds (or geological eras) apart then you get the runner in a different position.
Reminds me of a riddle I was told some time ago: "where was the men when he jumped off the bridge?". If your answer is "in the air", well that's AFTER he jumped... likewise "on the bridge" is BEFORE he jumped.
So what we today identify as a specific species or genus might very well change in the future decades or even years and taxonomy is full of cases in which species where "relocated" and renamed. Sometimes changing the parameter on which you build the taxonomy (mostly now is gene based, before it was morphology based) might completely turn the tree upside down from the roots. Plant taxonomy (being a botanist that's what I'm familiar with but I suppose it happened also with animals) was revised multiple times because some clades would change position depending which gene was used as reference.


text:
Is this a bed bug?
This insect is ~7mm long, it has a dark strip on the body and I found it in Spain. Is it a bed bug?

See this thread for a genuine bed bug; given the less than ideal focus of your photographs I can't do more than guess at what you actually have, beyond "probable Heteroptera nymph" (a bed bug it isn't).

Looks the wrong colour to be a bed bug to me, they've been reddish brown when I've caught them (3 times in the last 5 months in India)...

For me I think it is a nymph of Centrocoris variegatus. But I am not 100% sure beacause the photos are unclear. The facts lead us to that Heteroptera species, and surely it isn't a bed bug. Also here are and some photos of a nymph and of an adult Centrocoris:
Nymph-to-adult:

Adult:

I hope I covered your question! :)


text:
What is this red and white striped wasp?
I saw this dead wasp in a park in Hong Kong.

Looking at what I can see of the wings and antennae I'm more inclined to believe this is a true bug; a look at the animals topside (its upside down in these photos) would confirm that (but I suppose the corpse is no longer available for additional photos).

@ArthurJFrost We can also guess the rostrum on the photo, that is also a good hint that this is a hymenopteran.

First of all, it isn't a wasp, but a true bug. After a long search in the databases about Hong-Kong's insects, I found that it is a red cotton stainer. Wikipedia says "Dysdercus cingulatus occurs in Sri Lanka, northeastern India, Bangladesh, Thailand, the Philippines, Sumatra, Borneo, Papua New Guinea and northern Australia".  iNaturalist.org has a number of photos, including some that match the one in the question, and confirms that the bug occurs in Hong Kong.
These insects are serious pests of cotton and there are several other species of them, some of which occur in North America:

The cotton stainer is most common in southern Florida and in Cuba. It has been reported in Jamaica and Puerto Rico, Alabama, Georgia, and South Carolina. In view of its scarcity in north Florida, it must be presumed rare in the other three states mentioned. Dysdercus andreae ranges from southern Florida to most of the Antilles and Surinam. Dysdercus mimulus ranges from southern Florida, Texas, and Mexico into Central America and the West Indies. The fourth, undetermined species is known in the United States from two specimens taken at Key Largo Key and Homestead, Florida.

--University of Florida
Here are some pictures to compare with these one in the question:

To clarify, it's not a beetle which form the order Coleoptera but a true bug comprising the order Hemiptera. Beetles undergo metamorphosis from egg to larva to pupa to adult. True bugs undergo incomplete metamorphosis.

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


text:
Can nerves in the human body be spliced with a form of electric wire?
This may be a ridiculous question, and is hypothetical, but I'd like a well-supported answer.
Is it possible to splice copper wire (for example) into the human nervous system? Would the charge carried along the nerves then travel into the wire?
Say for example that I wanted my reflexes to be improved (because I know electrical current travels significantly faster through copper wire than our nerves), and wanted to replace a section of my nerves with copper wire. Would it work?

No, it wouldn't work.

Actually 'current' (in biological context impulse) moves faster with nerves (https://hypertextbook.com/facts/2002/DavidParizh.shtml) than copper wire (http://hyperphysics.phy-astr.gsu.edu/hbase/electric/miccur.html#c1).

Bryan - I appreciate your answer, but do you have a source to back up your claim?


text:
How to calculate RPM?
I´m just starting my postdoctoral fellow and my new project involve sRNA Deep Seq. I´m having problems with the data normalization.
I´ve been reading papers about it and the variety of normalization method is huge!
The simplest one that I found is by TPM or RPM (transcript per millon or reads per millon), in which each raw read count is multipled by 1 millon and then divided by the total read count of the whole library.
The question is: which library?
I have 3 treatments. In one of them, the number of raw seq were 10 millons. After filtered of adaptor, length < 15nt, # <3 count, we generate 8 millons of mappable reads. Then, once we mapped against Arabidopsis genome, 3 libraries were generated. The mapped mRNA, tRNA, rRNA, RFAm, Repbase library (5.7 millon; 72%); the custom virus we sent library (20; 0%) and the miRNA (sRNA) library (2.3 millon; 28%). On the 3 treatments the numbers were diferent and always the miRNA library was smaller than the mRNA library.
In order to a direct compare between data set, we have to normalized the counts.
If I want to do it with RPM, which library do I have to use? The total mappable reads (including mRNA, tRNA, etc) or only the miRNA library?
I have noticed that the result is very different with one or the other, because the percentage of the libraries are not the same between treatments.
Any hint you can provide me will help me a lot.


text:
How can I describe running a solution four times through a chromatography unit (in an instruction)?
I'm translating a document from Russian:

The mean retention time for the first four injections of RNase should be (40.8± 2) min. If the mean RT is beyond this range, adjust the gradient system (change the content of acetonitrile within the 20% - 32% range) and chromatograph the RNase solution four times.

I'm aware that we don't use chromatograph as a verb in English usually, but we do use it in Russian this way. What would be the generic English expression for this, usable in a procedure description? I know that we have the word run but this might be too colloquial for an official paper.

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

@terdon -  it's about terminology used in biotech, as pointed out by one of the tags. Had I asked it on ELL SE, it would have been voted for closure as off-topic too, or the replies would have been not very professional.

I feel it is more about the use of a specific word and not jargon. I just don't think this sort of question is on topic here since it isn't really about biology but about English. By the way, have a look at yesterday's chat transcript, we did find a few examples of its being used as a verb. Personally, I would say and run the RNAse solution through the chromatographer four times, but this isn't really my field.

@terdon - I see. I decided to bring it out from the chat area to help out (possibly) some fellow translators, web surfers etc.

Sure, and only one user so far feels it is off topic. I need to get another 3 to agree with me, and perhaps I'm alone in my opinion. Also, argh, typo in my previous comment. I meant . . .  run through the chromatograph, not chromatographer.

"Pass", "transit", "process"

I would say simply:

repeat the chromatography four times

or less formal, but quite acceptable:

re-run the column (or whatever it is) four times

This puts the emphasis on the process.
But I’m not exactly sure what’s happening. You have four injections of RNAase. If they are not right are you repeating each once or what? If the former, then it would be:

repeat the chromatography (or re-run the column) for each sample

It sounds to me as written that the intention is to attain accuracy via averaging a set of four runs, and if target value not attained, make adjustment and repeat another set of four runs until mean is within desired range. Perhaps state as "... then repeat another set of four runs.  Repeat as needed until the desired mean retention time is achieved."

@N2ition — Could be. But your use of "runs" suggests that is the most natural term to employ.

I would continue to use inject to describe loading samples into the liquid chromatography system and replace

chromatograph the RNAase solution four times.

with

inject the RNAase solution another four times.

Thank you! Will inject always imply ..and record the chromatogram in this context?

I think one can do better than this. The emphasis shouldn't be on injection but on repeating the process of chromatography.


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Is there anything that tells me how Lichens Grow?
I've done a lot o research about this matter but I could not find anything relevant. So I'm doing a Computer Science project where, using AI and Computer Graphics, we try to predict the growth and aging of lichens on a stone, and at this moment I need some "academic validation", so is there any way like a formula or something that tells me how lichens evolve and grow on stones? Thank you so much!
This image shows what I've accomplished:

In real Life:
https://i.stack.imgur.com/7S7E5.jpg
So is it possible to predict how are they going to spread along the stone in a period of time? Do they start by growing in small colonies and then tend to get together to create a bigger colony? I don't know if this makes any sense, anyway thank you for your patience!

Welcome to Biology.SE. The questions How do lichens evolve? and How do lichens grow? are both extremely broad and rather undefined. Are you interested in the effect of phosphorus on lichens growth, in whether a logistic model fits lichen population growth, in wether the fungi or the algae is the growth limiting factor in case of low nutrient, in whether this symbiosis first evolve from a parasitic relationship, for what selection pressures exist on genes explaining this symbiosis, in whether there are gene cluster for the symbiosis, etc... You should boil your questions down.

It may help if you could explain exactly what you are modelling with your AI. Also you say I've done a lot o research, if you could link to what you looked for, it may help us to understand which direction you're heading to. Did you find anything of interest to you on the wikipedia article

If you're doing some kind of predictive AI (which usually involves machine learning), you should be working off experimental data sets (in this case) in order to train your AI properly, to then make accurate predictions. Also, what aspect(s) of growth are you trying to predict?

I edited in the image for the model, but the "in real life" link is not correct.

Just from conducting a Google search using the phrase, "lichen modeling pdf", I was able to find several studies/publications that address your need(s). Though its dated 2004, this article seems extremely relevant to your application.
Simulating and Modeling Lichen Growth

In this paper, we present a system for modeling lichens
  and simulating their propagation and growth in a virtual
  scene.

In the article, they mention:

Aging and Weathering
Ecosystem Simulation
Lichen Seeding and Propagation
Environmental Charateristics
Theoretical Aggregation
Complex Modeling

And here are (a few) examples of what they produce:


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Popular science on carcinisation
Carcinisation is described succinctly in a Wikipedia entry. The entry references few scientific publications regarding the subject. But are there any popular scientific articles describing and giving examples of carcinisation in the layman's terms?

GoogleScholar > Carcinisation

This is the most cited publication regarding the topic: http://research.nhm.org/pdfs/11727/11727.pdf


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How did the orchids evolve to support pseudocopulation when they do not have any organ for vision to see how insects look like?
How could they guess so perfectly how a moth or whatever the pseudocopulating organism looks like. They do not have eyes to see the shape or structure. What could possibly be the reason they evolved with such accuracy to deceive an animal?

plants don't consciously control their shape why would they need eyes?

Evolution does not work based on an organism (or designer) "seeing" a problem and seeking a solution. Evolution via natural selection works when members of a population that have a certain heritable trait are better at reproducing than other members of that population. Because they are better at reproducing, subsequent generations of the population have a greater percentage of individuals that have that heritable trait, and the process continues, sometimes to the extent that all the individuals of that species have that trait (this is called "fixation").
The way something like this would evolve is that some predecessor to modern orchids has some morphology or chemical secretion that was particularly attractive to insects. This increased the ability of that predecessor to reproduce. Over generations, any other random mutations that further promoted attraction of insects also were selected for, until they accumulated all of the adaptations we see in a modern orchid.
Today, we can study that process and realize post facto that "Oh, these adaptations worked because they tricked the insects into thinking they were copulating, when really they were just dispersing pollen."
However, the flower never needed any knowledge of insect copulation, it just happened that flowers that had those traits did better at propagating their genes to the next generation.
These types of questions are more easily understood with a broad understanding of evolution. One great resource is Understanding Evolution from Berkeley.


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Do ants really dispose of their own dead, and how/why?
I just read this from Wikipedia's Swarm Behavior article:

Despite the lack of centralized decision making, ant colonies exhibit complex behaviour and have even been able to demonstrate the ability to solve geometric problems. For example, colonies routinely find the maximum distance from all colony entrances to dispose of dead bodies.

There was no citation.
Is it true that ants dispose of their own dead? If so, how and why? I would've though it would be much better to just eat their own dead, which would be a "free" food source allowing the colony to reclaim some protein and nutrients. It would cost much more energy (and risk) to transport dead ant carcasses away from the hive.

If you want to watch something scary, google for "youtube cordyceps" for a clip from "Planet Earth".

Eating the dead makes far more likely you will catch whatever killed them. They transport and dispose of the dead for the same reasons we do, to reduce disease vectors. They dispose of their garbage for much the same reason, in fact they often dispose of both in the same place even if they separate the two in distinct piles. Hygiene is very important is colonial insects because you are constantly surrounded by other ants which makes disease transfer very easy. Fungal infections are particularly problematic. They also have specialized toilet sites for the same reason.
Note only some ants transport the dead outside, other put them is special chambers far from normal traffic and reserved for that purpose and refuse disposal. In either case they are moving them away from casual contact.
Source
Source 2

Humans do not transport their dead for the same reasons that ants do.. the theory of germ disease wasn't established until a little over 100 years ago, yet we've been making graveyards and burying our dead for thousands of years. Ants do not have emotions, or spend time remembering their dead. It's completely different.

Ants do of course have emotions, emotions are the basic way the brain functions, but no they do not "remember the dead". humans bury their dead because being around the dead make us uncomfortable, our brains evolved to make us feel uncomfortable around corpses because they are disease vectors. So yes it is ultimately for the same reason.

I would like to see supporting literature that addresses the neurological systems that are activated upon a person encountering a human corpse. In the case of the ants, they are specifically triggered by the detection of oleic acid. And you say for humans, it's most an emotional response that has an evolutionary advantage of circumventing the propagation of disease vectors? Again, literature please.

And ants most definitely, absolutely, do not experience emotions. Fight or flight, and/or a mixture of the two when panicking, does not constitute emotion, nor does the activation of some reward system.

pleasure and aversion are the basic building blocks they underlie all learning, emotions exist in any creature capable of learning. as for the human corpse, I am unsure what you mean by "it's most an emotional"  but corpse aversion it is the explanation for why the uncanny valley  a well documented effect http://www.sciencedirect.com/science/article/pii/S0747563210001536

You can also consider things like the disgust/revulsion reflex triggered by decaying corpses, which is as universal https://www.ncbi.nlm.nih.gov/pubmed/17630362 it is not hard to see how it would evolve as part of our behavioral immune system. Feel free to open a discussion to explore this further.

I'd like to add a +1 to John's comment re: animal emotions. Charles, you just specified that a physiological response while panicking was not an emotion. What do you think panic is?

Yes, ants do in fact relocate their dead away from the nest. This is because when an ant dies it releases oleic acid, a chemical that is strongly associated with death. Upon detection of the oleic acid, ants will move (carry away) their dead as to avoid contamination within the nest, just in the same way they do with their waste (ants are actually pretty "clean").
What's kind of funny is that, even if the ant is still alive, if a single drop (relative to the size of the ant) of oleic acid is applied to an ant, the colony will still move that ant to the graveyard/dumpsite (midden).
The common term that refers to these ritualistic behaviors is "necrophoric behavior".

Good to see some cover the proximal reasons and mechanics of the behavior

"A single drop" sounds pretty huge compared to an ant... even bigger than the ant itself. If I had 100L of liquid smelling like a dead body dumped on me I'd want to go bury myself too.

@Mehrdad The single drop is meant to be relative to the size of the ant. Thanks.

Interesting. What happens to that ant after it's dropped at the graveyard? Does it commit suicide? Does it wait a while then walk back to the nest?


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Tick Identification
While enjoying the outdoors in mid-Missouri and Northern Iowa, I came across this tick in my belongings. I can't distinguish whether it is a dog tick, a rocky mountain tick or some other species.

The tick you found is a female American dog tick (Dermacentor variabilis) and not a lone-star tick (Amblyomma americanum). Female lone-star ticks do not have white coloration towards the head and only a round dot in the middle of their body. The following PDF document offers a visual comparison of the two species:
https://store.extension.iastate.edu/Product/pm2036-pdf


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Cleanliness of cast iron never cleaned between meals
Cast iron cookware has unique benefits. One difference between cast iron and most other cookware is that many people advocate for not cleaning it with any soap between uses, because the soap can degrade the seasoning which protects it. I wonder, how hygienic is that?
The way I understand it, the seasoning on cast iron cookware is a smoothed layer of polymers that prevents food (and bacteria) from contacting and sticking in the iron cookware. Simply scraping it clean, maybe rinsing with some hot water briefly and drying off immediately after, is generally considered enough to 'clean' the cookware.
How is it that bacterial growth on the cookware is never a problem, given they are not washed with soap for long periods of time? I'm under the impression that most kitchenware - pots, pans, dishes, utensils - are susceptible to bacterial growth that could make you sick or transfer illness if you eat with them and don't properly wash off all the food, oils, etc. that gets on them. Does the layer of polymer on cast iron protect it from such growth? The main question here is: Does other cookware really need soap any more or less than cast iron to be used hygienically, and why or why not?

I assume that during the cooking process, if you're using a cast iron skillet, you typically get it hot enough to kill most pathogens on it! Not sure how that relates to other types of cookware but I cast iron skillets get VERY hot when used.

I think we could argue a negative here.  That is, if not washing cast iron cookware was unhealthy, there'd be a lot of sick people :-)

Soap or detergent does nothing to kill organisms. Instead each detergent molecule has two ends, one being hydrophobic (meaning it's repelled by water) and the other end is hydrophilic  (attaching the end to water). When anything is washed with soap or detergent, the oils and dirt on the object - whether it's a dish or your hands - can combine with water as an emulsion and be rinsed away.
Dishes and utensils are only susceptible to bacterial growth if there's traces of food on them. Washing is meant to remove traces of food and oil so bacteria can't multiple on them. The conditions must be right for bacteria to multiple. If traces of food were to be completely dry and hardened on a dish and someone ate off it, the likelihood of any bacteria present on it is close to nil. They need moisture to grow. If dishes had no oily food on them, washing and rinsing with very warm water would be sufficient. I've seen people from other cultures wash dishes with traces of food that are soluble in water. They come out perfectly clean. (As an aside, using a tea towel can often spread bacteria when they're not used properly.) Towels top kitchen contamination hazards list
Bacteria can't multiple in oil. For example, ordinary cooking oil doesn't need to be refrigerated although it can go rancid. A cast iron frying pan is properly meant for frying foods only. No watery sauces should be cooked in them. Even "scraping it clean" shouldn't be done with a sharp metal object as it can remove some of the polymerized hardened oil layer.
I have several cast iron pans that I don't wash. I wipe them out after each use, then I add a little oil nd roughly a teaspoon of salt. With a paper towel, I rub at any bits of stuck on food. If done within a few hours of being used, it effectively removes any food traces, leaving a smooth surface. I usually rinse off the salt in warm water, dry it and then apply a very thin film of oil. I've been cooking in cast iron pans for decades and have never gotten sick or had mild food poisoning (what many people call a 'stomach flu').
Cast iron pans with a layer of proper seasoning and treated like this will definitely not cause sickness. It can't support bacterial growth and as @jeanquilt mentions, the pan gets very hot - enough to blister your skin if you touch them with a bare hand.

'Soap or detergent does nothing to kill organisms.' is incorrect - see https://biology.stackexchange.com/q/39894/1320

@Jude can the alkaline pH of soap or detergents not cause any damage to microbes?


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How did fig tree take root in trunk of palm tree?
Please see pictures below.

I never saw anything like this.  Do the roots of the  fig tree penetrate the trunk of the palm tree?  Is there a symbiotic relationship between the two?

I won't write an answer because I couldn't identify the small plant (whom you are telling as 'fig') so couldn't search its behaviors. However such association is called epiphytic relation. Epiphytes usually could be of various grades between  commensal (such as many orchids) to parasite(such as Cuscuta) Also at the crevices on tree-trunk, soil and rotten organic matters accumulate where non-epiphytic plants sometimes grow if somehow a seed reaches there.Some figs like Ficus benghalensis and F. religiosa  common example, of that incidence and may cover up and kill the host plant.


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Identification of a bug in Vasai, India
Can someone please let me know what insect this is?
This may be something very common, but this is the first time I have seen them and that too suddenly in a large number.
They were mostly on plants, but the only clear image I got was of the one sitting on this bike. Image captured in Vasai, India

(Brought into Biology SE from https://i.stack.imgur.com/RHcrg.jpg)

It looks like Oides andrewesi.


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All somatic cells contain the same genome, then how does it knows that it should develop into a specific organ?
All somatic cells contain the same genome, then how it knows that it should develop into a specific organ. In https://www.youtube.com/watch?v=aeAL6xThfL8, Joe Hanson says that each cell has the same book that each has 20,000 same instructions. And each cell has bookmarks, where it finds which instructions to read.
Can you tell me where these bookmarks are stored in the cells? Is it outside the chromosomes or outside nucleus?

The answer to your question is not really know yet and there is whole scientific field dedicated to it: developmental biology. I'll try to explain the basics however:
Like you described the identity of a cell (its cell type; which organ it belongs to) is dependent on which of (actually) ~30000 human genes are activated (or read) in that cell. There are two fundamentally different ways this is done in cells:

Transcription factors:

These are proteins that bind to specific (regulatory) DNA sequences and thereby lead to the activation (or repression) of certain - usually nearby - genes. Since they are proteins, their own genes have to be activated in the first place, so we already at a 'chicken or the egg' type of problem. In principle proteins can 'survive' outside the nucleus of the cell for some time, but they are usually degraded within a few hours, so I guess the remaining factors from the mother cell are not very important (I have no idea if anyone ever checked this).
Additionally many transcription factors are not constitutively active, but are waiting for some outside (from the perspective of the cell) signal. These could be certain developmental signals, growth factors, hormones or environmental factors like nutrient availability (the list goes on ...). During embryo (& therefore organ) development not only the presence of these signals (morphogens), but also their intensity are a very important factor in determining the 'fate' of a given cell.

Epigenetics

The term epigenetics describes genetic regulation that does not happen on the sequence level. Instead the accessibility of the DNA is regulated through modifications of histones (which are part of the chromosomes) and the DNA itself. Thereby the cell can almost permanently shut down certain genes. Since epigenetics are also inherited during cell division, this regulation affects whole cell lineages and is therefore very important in regulating which cells are active in certain organs or tissues.

Do you have a citation for the number of genes?

@canadianer I had the number in my head from working with NCBI data. I just looked for references: the often cited ~20000 is for protein-coding genes only, so I guess that why so different numbers are used. I tried to get the number of annotated genes from the human genome from NCBI but couldn't find it. This older book say 30k-40k genes (scroll to 'The functions of human genes'), I didnt find a better source at NCBI right now.

Thanks. I had always heard ~20,000 genes as well, but if that is just protein coding then a higher figure makes sense.


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Is it true that the human brain has not evolved in 100 000 years?
I read that the human brain has not evolved in 100 000 years and that's why there are no genes for intelligence.

Can you please cite your source for that claim?

Perhaps "there are no genes for intelligence" because intelligence isn't a simple trait like eye color or blood type.  Multiple genes likely control various factors that affect intelligence, and these gene probably affect other things as well.  Then too, there's the nature vs nurture aspect.  How much of intelligence is inherent, and how much is developed?  For instance, my genes might allow some maximum muscle development, but if I choose not to exercise, I will never come close to that max.

tl;dr
Here are the two claims you make

human brain has not evolved in 100 000 years

Wrong!

there are no genes for intelligence.

Wrong!
The claim there are no genes for intelligence. is unclear though (see below) but if rephrased in the most intuitive correct way, then the claim is wrong!
Are there genes for intelligence?

[..] there are no genes for intelligence.

The claim there are no genes for intelligence is unclear. Does that mean there is no genetic variance in the human population for intelligence? To understand why the claim "gene for something" makes no sense, please have a look at this post
Make sure to read this post..... Done? Now you understand why the concept of heritability is key. So let's rephrase the question so that it makes sense and can be answered
Is Intelligence heritable?
Well, the issue here is to define the term 'intelligence' in a way that is non-arbitrary and yet match our intuition of what we like to call intelligent. A number of studies have investigated the heritability of intelligence, often using different definitions / metrics for intelligence.
All these studies agree on one point. Yes, intelligence is heritable! How heritable it is varies a lot from one study to another (because those studies vary in the population studied and in the definition of intelligence). See the wikipedia article on Heritability of IQ for more layman information.
Has the human brain evolved in the past 100 000 years?
First you need to understand how evolution is defined. Here is a commonly used definition

Evolution is a change of allele frequency through time in a population

Have a look at the post What is meant by individuals do not evolve, populations do? to understand what this definition mean.
Well... first. Everything evolve. You can't stop evolution from happening on any phenotypic trait or on any genomic region. So, of course it evolves. But let's not stop there.
There is still one issue with this question. The saying brain characteristics rather vague. But I'll deal with it as I can.
Is the brain still evolving - phenotypic evidence
Spoting changes in brain structure through time is not easy, as brains don't preserve well. Over such a short period of time (100,000 years) it will be even harder to detect much difference on gross metrics we can use such as cranial cavity.
We can compare the volumes of cranial cavity. Neanderthals interbred with humans (see this loosely related post) with Homo sapiens and Nanderthals had a cranial cavity that is bigger than Homo sapiens, so this gene flow would very likely affect H. sapiens cranial cavity.
Is the brain still evolving - genetic evidence
Consider for example Evans et al. 2005 showing that the allele coding for micro-encephaly at the gene MCPH1 is currently increasing in frequency in the human population.
This article from NewScientist also reports the findings of Evans et al. 2005 in layman terms.
Is the brain still evolving - current selection pressures
You should have a look at the post Is intelligence declining due to the lack of selection pressure? and eventually on the wikipedia article for the Flynn Effect.

Every part of the human genome is constantly evolving - but at a VERY slow rate. Therefore there are only a few changes from the last 100k years (This article describes this quite well).
Intelligence is a very complex characteristic, which is therefore influenced by many different genes. Most of these influences are only minor, so that scientists are arguing whether the influence is real or not (pro, uncertain, contra). Additionally there are a lot of genes that are just necessary for the brain to function the way it does - you could argue that all of these are 'genes for intelligence, since without them we would not be intelligent.

Not every part of the genome is evolving at a slow rate. Every part of the genome is evolving, most of them at a slow (although this is relative) rate.

I'm curious to where you read that b/c its simply not true. Remember that evolution is driven by selection pressures. Also known as evolutionary pressures, they drive a reason to evolve. The stronger the pressure the faster evolution takes place. An easy way to spot this pressure is by looking at the range in ability, skill or adaptation of a trait. The larger the range the stronger the pressure.
With that in mind, can you think of any selection pressures that the human brain might had to face over half your given time, lets say the past 50,000 years?
The human brain has had to adapt to entirely new environments in that time frame.
Within that time-frame is all of recorded history. How about the adaptation to formal education? That might be one. Also during this time think of the explosion in languages. Consider how different we all are in our ability to be educated and to pick up languages. Or how some of us can cognitively operate effectively with wildly different amounts of sleep debt or calorie intake.
Also there are many genes that influence intelligence since intelligence is multifaceted and can be expressed in many ways. You also need to remember that  these pressures can influence how genes are turned on or off. This is known as epigenetics. You might have a gene but your cells could simply not use it.
There have been theories of autism being a result of an evolutionary pressure.
With all of this in mind the last thing you need to remember is that the human brain is evolving in other ways than simply via its genes or their expression. The human brain exists in a space shared by other human brains and we have the ability of sharing our ideas with others. This allows for groups of people to share a selection pressure and thus evolve as a group.
Do you know what this is called? I know you know.
Culture. In many ways human evolution has moved on from the biological to the cultural space. And I find that quite fascinating.
https://www.timeshighereducation.com/features/human-evolution-has-moved-on-from-the-biological-to-the-cultural-arena/169440.article


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Analysing papers and providing search
Suppose I want to provide "smart" (AI, meaning extraction etc.) search over many published papers (specifically, biological) to simplify researchers' live.
Now, I have access to my university library that contains text of many papers from different sources, including those with payed subscription.
Is it legal to download all papers, analyse them and provide search without disclosing full text of the paper, only small part of text or image and with proper citation?

You need a legal opinion, not one from a biologist. Your question is therefore off-topic and I have voted to close it. However, apart from the obvious step of looking at the conditions associated with download of papers from (?) — probably through — your library, you should consult your University librarian. I seem to have read that many journals do not allow such data mining. You are certainly not the first to think of doing this.

I'm voting to close this question as off-topic because this is a legal question, not one about biology.

Can we talk about this? contact me at http://Keybase.io/gabefair

Could Academia stackexchange would be a better fit for migration?

I don't have enough reputation on biology exchange so I'm unable to close the question myself. If somebody can close it, please do, I'll ask it on Academia stackexchange as @AlwaysConfused suggested

@AlwaysConfused https://law.stackexchange.com/ would be better.


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How can a waterborne disease be transmitted
If a disease is waterborne [as in it is based in the digestive tract], what ways can it be contracted other than the obvious drinking of infected water?