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How can humans hear low frequency sounds using the cochlea which is tiny compared to wavelength?
Humans can reportedly hear sounds as low as 31 Hz. If we consider the speed of sound in air to be 1125 feet per second, then a sound at 31 Hz will have a wavelength of about 36 feet.
Normally, to capture a sound or other wave, we need an antenna that is at least as long as the wavelength of the signal we are attempting to receive.
But with the ear this is plainly not possible. If the cochlea of a human ear were to be unrolled, it would have a length of about 1 inch. Thus, in the sense of being an "antenna" it would seem to be far too short to be able to receive a 31 Hz signal, yet somehow it does.
How does the ear sense such low frequency sounds?

"to capture a sound or other wave we need an antenna that is at least as long as the wavelength of the signal" - this is definitely not true for sound, it doesn't have to be anything special about an ear. I am also guessing your laptop/headset/cell phone doesn't have a 15-meter long antenna.

Possible duplicate of What causes the tonotopic organization of the inner ear?

Yep, no idea where you got that quote from, but obviously we can hear low frequency sounds. Try googling "basilar membrane dynamics", which should explain how sound frequencies are separated within the ear.

Besides that misconception, I voted to close as duplicate because another question asks about tonotopic organization in the ear and how different frequencies are 'mapped' to the basilar membrane. I think that answer is sufficient to answer your question.

I don't think this question is a dupe from What causes the tonotopic organization of the inner ear?. It has overlap, but the focus is different here. Overlapping questions scopes are fine and should not be closed.

You are thinking of antennas for EM signals such as the dipole antenna. In this type of antenna, an external field (EM waves) excite the antenna (creating an electric current) which you then measure. There is thus something like a transduction step, which is more efficient if you can use the spatial scale of the wavelength.
In the case of hearing sound waves, the ear does not transduce the mechanical signal into another modality, but is directly modulated by the hair cells.


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Why do people feel shame when exposed nakedly?
Why do people feel shame? Meaning the kind of shame specifically related to exposing 'private parts'.
Where does it come from (i.e. social factors due to upbringing, inherent in our genes etc.)?
What is its evolutionary purpose?

Is your question specific to nakedness or was that just an example?

Note the field of knowledge you question fits in is called evolutionary psychology which is very theoretical and very little empirical test were actually perform. So, one can, at best formulate a hypothesis but you will hardly find any evidence for one or another hypothesis in this field.

Not a native speaker. I meant the kind of shame specifically related to exposing private parts. I'll adjust the question.

You should know that evolutionary psychology is very controversial, in part for the reasons @Remi.b states and in part because of the potential for misuse of those hypotheses, in particular to defend as "natural" certain behaviors that are deemed socially unacceptable. I think the field of eugenics is a reasonable historical analogy. In other words, tread lightly and skeptically.

@Bryan Defending certain behaviours as "natural" on the basis of evolutionary psychology is not "misuse". You may not personally like the idea of promoting certain behaviours on the basis of their theoretical naturalness, I'm not entirely keen on it either, but it's just as valid a hypothesis for how to decide what behaviours to promote as any other. If we wish to oppose horrors like eugenics we do not not need to pretend their hypotheses are invalid, it's enough that we don't agree with their conclusions. Pretending they are invalid just plays into their hands.

@Isaacson The problem isn't the hypothesis, the problem is the use of unscientific arguments posing as scientific ones. I'm not against responsible evolutionary psychology, either, but I meant to caution the OP, who is a novice to the field, to tread lightly and to be aware there is controversy and inconsistency of quality.

Probably a cultural effect
In many tribes, people are naked. Also, the naturist movement is very popular in the western culture and they don't feel shame. In northern Europe, it is common to be naked in spas.
I would guess it is mainly a cultural effect and there is little heritability for this trait. I doubt you'll find a study on this particular question, so the best one can do is just to formulate a guess here.
If you don't quite understand why I talk about heritability here, then you should have a look at Why is a heritability coefficient not an index of how “genetic” something is?. In layman terms and in vague terms, I meant that there is probably little role of genes to explain why we feel naked.
Yes, but let's assume it was selected for...
If we were to assume that feeling of shameful in front of nakedness had been selected for, one may hypothesize that it could be due to sexual selection, where rich and wealthy wear clothes. It could also be due the social presssure of showing off what you are worth as sexual body parts are likely under strong sexual selection as well.

I'd say the ability to feel shame is physically (genetically) determined. The object/issue of shame may be culturally determined (what we learn what is to be shamed off). In that sense its likely like disgust. Specifically on nakedness I remember from lectures of "Eibl-Eibesfeld, Human Ethology" that there are almost no ethnic groups really completely naked. He mentioned one (Amazonian?) tribe who only wore a single small string around their waist, but fell terribly ashame when someone saw them without that string. So maybe the shame object nakedness itself is even genetically determined?

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What are the exact reason causing missing calls in a VCF file from exome sequencing?
My data is a VCF file from exome sequencing variant call. I'm not very familiar with the sequencing process and variant calling process. I noticed that there are some missing genotypes, which is recorded as "./." at the GT field. From googling I learned that they're not homozygous reference genotype ("0/0"), but missing calls due to some sequencing ignorance.
In order to make my data "cleaner", I thought it's better to filter out the loci with missing calls if there're not too many of them. I also checked the corresponding "DP" of the loci with and without missing calls. For example:
chr1:123 GT:DP 0/0:2 1/1:4 ./.
chr1:234 GT:DP 0/0:10 1/1:11 1/1:20
chr1:345 GT:DP 0/1:40 1/1:37 0/0:78
chr1:456 GT:DP 0/1:7 0/0:23 ./.
chr1:567 GT:DP 0/1:34 1/1:39 0/0:58

In the above toy example, there're 3 people and 5 loci. I checked the mean DP of all 5 loci and I found that the mean DP of loci with missing calls (1st and 4th loci) to be significantly lower than the mean DP of loci without missing calls (2nd, 3rd and 5th loci). Is that a coincidence? Or are there any specific reason that the loci with missing calls have lower coverage than the "normal" loci? Thanks!

Have you looked up in the software that made the vcf what ./. means?  I would guess it means 0 coverage in that sample at that locus.

Not that this isn't a useful question here, but there's a newly-started Bioinformatics SE that might like to have a whack at this: https://bioinformatics.stackexchange.com/

@swbarnes2 In the documentation, "./." simply means no call. In literatures, there're several different reasons causing this. This could be due to 0 coverage, and also other reasons, which I'm not so clear about. But let's assume that they're caused by 0 coverage, I still don't know the answer to my question. Do you have any ideas?

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Carbohydrates- D-Glucose & L-glucose , alpha and beta
What's the difference between D-glucose & L-glucose ?
Yes , I know that L-glucose is an isomer of D-glucose . But what differences do they have ? They are the same , they are glucose .
Similarly for alpha and beta glucose ?
Sorry I just started learning on carbohydrates and I'm a little confused about these 2.

Welcome to Biology.SE! What research have you done before asking it here?

They are not the same. Because they are enantiomers, they do not have the same shape. Because they do not have the same shape, enzymes in metabolism that have evolved to use D-glucose cannot work on L-glucose.
L-glucose is not synthesized by organisms because life on earth shares a lineage using the R-enantiomer, so organisms don't encounter it, so there is effectively zero selective pressure to evolve the ability to metabolize L-glucose.
For alpha and beta glucose, see this question on Chemistry.SE; those terms refer to anomer forms of glucose that can interconvert in solution. Given enough time, glucose and similar molecules in solution will form an uneven but consistent ratio of alpha and beta forms.


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Why is carbon dioxide produced in alcohol fermentation but not in lactic acid fermentation?
From my understanding, alcohol fermentation takes place in yeast and lactate production takes place in humans.
These two pathways take place only when there is insufficient oxygen, because the other parts of metabolism (TCA cycle, ETC) can't take place as they happen in the mitochondria, which requires O2.
For alcohol fermentation, there is production of carbon dioxide while lactic acid fermentation does not produce carbon dioxide. CO2 is produced when there is an oxidation of one carbon molecule. So my main question is: since there is a lack of O2, how does yeast produces CO2 while humans do not?
Also, how does NAD+ recycle all the time when glycolysis is happening?
Thanks!!!

Glycolysis needs a steady supply of NAD+ to happen - this is the driver for the anaerobic oxidation to lactate and ethanol, although this is energetically much less favorable than the complete oxidation. But without oxygen there is no other way to keep the glycolysis active for at least some energy supply.
The difference is located in the enzymes available for the conversion of the pyruvate. This is the Lactate dehydrogenase in humans (and other mammals) and the Pyruvate decarboxylase in yeast. The first catalyzes the reaction from Pyruvate to Lactate, the second from Pyruvate to Acetaldehyde and CO2, the Acetaldehyde is subsequently converted to Ethanol. Only the second step produces NAD+.
See the illustration (from here) for further understanding:

The CO2 produced in this reaction does not occur due to oxidation, but is released from the decarboxylation of the Pyruvate. See the illustration below (from here):

In the production of lactate no decarboxylation is happening which allows the backreaction from lactate to pyruvate once enough oxygen is present again.

Where the 2 NAD+ accepts electrons from to recycle back to NADH ?

You might want to add that since there is no decarboxylation in production of lactate, there is no CO2 evolved. Also that glucose already contains oxygen, so there is no need of O2 in producing CO2 from pyruvate (just saw that you missed these points from the question :)

@user307640 Each molecule of glucose makes two molecules of pyruvate, which allows to run the process twice.

@another'Homosapien' Good point.

@another'Homosapien' You don't need to shift around O2 in the molecule, you cleave off CO2 from the molecule by the decarboxylase.

@another'Homosapien' Then I misunderstood your comment. But I hope it is now clear, where the CO2 comes from.

Just to add, no offence, 'twas already clear to me, I just wanted you to add this point in your answer ;)

@another'Homosapien' None taken, that's ok. Something clear for yourself is not necessarily clearly explained for somebody else. Criticism helps here.


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What is the best solvent for Mutagen X?
Many solvents can be used for mutagen X (3-chloro-4-(dichloromethyl)-5-hydroxy-5H-furan-2-one), however, long-term stability is not specified. Which would be the best solvent for long-term storage? Once dissolved, can it be stored at RT or -20ºC?
Thanks


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Why does K+ move out of the cell?
I was reading this page: Equilibrium Potentials when I found the following example at the end of the page: "If the K+ equilibrium potential is –90 mV and the membrane potential is –70 mV, in what direction will K+ move through open K+ channels?".
The site gives the answer, and it turns out that K+ moves out of the cell. I'm not entirely sure if I understand why this is the case.
(1) Because the equilibrium potential for K+ is –90mV, this means that the intracellular region must be negatively charged, at –90mV, to have zero net flux of K+ across the membrane. Therefore K+ would leave the cell, making the interior more negative from –70mV to –90mV.
(2) But the resting membrane potential is still –70mV. Will this membrane potential be established by other ions? If not the case, K+ will be pulled inside the cell again, then we wouldn't be able to tell that K+ goes out.
(3) I find the starting conditions somewhat confusing. "K+" goes out means that there needs to be a potential difference. Is the question assuming we have, as starting conditions, the same concentration of K+ at both sides? Otherwise it is not clear why K+ should stop leaving the cell at any moment (even when it is at the state of equilibrium).
(4) Can we conclude, as a general rule, that if MRP is the membrane resting potential and EP is the X+ equilibrium potential, then X+ leaves the cell if EPMRP. Would the roles be reversed for X–?

The other answer is a bit misleading.

"Another cause is the the intracellular K+ concentration"

No, this is exactly the same cause, the differing concentrations is what causes the equilibrium potential. You can think of the equilibrium potential for one ion as "how much voltage does there need to be to prevent this ion from flowing down its concentration gradient." The Nernst equation gives you the equilibrium potential for any one ion. The equilibrium potential is also known as the "reversal potential" because if the voltage exceeds the equilibrium potential, ions will flow the opposite way, against their concentration gradient.

Don't get confused by the resting potential, because it is only a potential that the cell arranges for itself to maintain a stable environment. This cost a lot of energy and attention in form of protein synthesis to keep this potential. This mechanism is achieved by the Na+-K+ ion-pump

The resting potential is not to "maintain a stable environment" or anything like that. The resting potential is the net potential that a cell reaches due to all of the conductances of various ions and the flowing current of each ion governed by its own equilibrium potential.

This mechanism is achieved by the Na+-K+ ion-pump, which exchanges those two ions

This is partly true, but again, misleading. The Na+/K+ pump establishes the relative concentration of ions, which only leads to a certain resting potential because the conductances of different ions vary at rest. Because the conductance of K+ is higher at rest than the conductance of Na+, the resting potential is closer to the equilibrium potential for K+. If the Na+/K+ pump was functioning exactly as it does, pumping Na+ out and K+ in, but the membrane was more permeable to Na+, then the resting potential would be positive rather than negative. All that matters for resting potential is relative ion concentrations and conductivity. The Goldman equation is the way to calculate this resting potential.
What is happening to K+ when a cell has a resting potential of -70mV but a K+ equilibrium of -90mV?
Because you need -90mV to 'hold in' the potassium against it's concentration gradient, at -70mV K+ will flow out of the cell. However, by definition, resting potential is the potential at which the net current will be zero. That means that, yes, other ions have to be involved. This is where the Goldman equation is very useful.
Although K+ may be the ion with the highest membrane conductance, there will also always be some leak of Na+ and Cl- ions (usually others ions are ignored because these three are the major players; other ions can be important in some situations). Therefore, if -70mV is rest, there must be at least as many Na+ ions flowing in or Cl- ions flowing out as there are K+ ions flowing out.
You can calculate these currents if you know the conductance of each ion and the equilibrium potential for each ion using Ohm's Law: I = V/R, where R is 1/conductance and V is the difference between the current voltage and the equilibrium potential. Try it out with the Goldman equation! If you use the voltage the Goldman equation gives you (the resting potential) you will find that the net current is zero!
Okay, so far we've answered your questions (1) and (2). Now (3): you state "Otherwise it is not clear why K+ should stop leaving the cell at any moment". It is important to note that equilibrium potential doesn't mean no ions are moving: it means the voltage isn't changing. If you just left the cell at -70mV and waited some time, eventually the concentrations of the different ions would change. This is where the Na+/K+ pump comes in: this ATPase is constantly pumping some K+ out and Na+ in to counteract the leak that occurs at resting potential. Cl- ions move, too, but mostly passively. It's also important to note that very few ions have to move for the potential to change on the order of millivolts. -70mV might sound like a lot, but electrical forces are very powerful, so very few ions relative to all the ions available have to move.
I don't quite understand what you are asking with (4) but if you can edit the question I will try my best to answer that as well. It's possible I already answered your question by talking about what "equilibrium potential" means for one ion. For a Cl- ion, if the equilibrium potential for Cl- is -65mV, then Cl- will flow into the cell when the membrane voltage is -60mV (tending to make the cell closer to -65mV), and it will flow out of the cell when the membrane voltage is -70mV (still tending to make the cell closer to -65mV).

.. resting potential is not to "maintain a stable environment" or anything like that.. isn't resting membrane potential established by cell to make ICF isotonic to ECF?

@JM97 No, and certainly not in this context. An electrical potential won't do anything with respect to tonicity because water isn't charged. Where did you get that impression?

Yes, water is not charged but this unequal charge distribution(made by the cell) helps cell in preventing excess accumulation of osmotically active substances at one side. So resting membrane potential is consequence of cell's attempt to maintain isotonic icf.

@JM97 " this unequal charge distribution(made by the cell) helps cell in preventing excess accumulation of osmotically active substances at one side" - I don't understand the mechanism here. The membrane potential doesn't do anything to prevent movement of osmotically active substances or water. Do you have a reference?

Last paragraph of http://www.preservearticles.com/2011083012499/what-is-the-gibbs-donnan-equilibrium.html   To survive, the Na+-K+ pump in the cell membrane continuously pumps out excess cations.

@JM97 By a reference I mean something like a scientific paper, or at least a textbook reference, not a blog site. And the statement "Na+-K+ pump in the cell membrane continuously pumps out excess cations" has nothing to do with the membrane potential being necessary for survival. It would be possible to pump out excess cations and yet still have a membrane potential of zero.

The Equilibrium potential(-90 mV) of Potassium-ions(K+) will drive the ions to flow out of the cell if K+ channels are opened, because K+ ions try to establish this potential instead of the resting potential(-70 mV). Another cause is the the intracellular K+ concentration that is around 140 mM compared to the extracellular concentration, which is only 5 mM.
Don't get confused by the resting potential, because it is only a potential that the cell arranges for itself to maintain a stable environment. This cost a lot of energy and attention in form of protein synthesis to keep this potential. This mechanism is achieved by the Na+-K+ ion-pump, which exchanges those two ions (pumps K+ in and Na+ out to achieve the -70 mV).
If K+ ions flow out of the cell the membrane potential will get lower than the resting potential, also referred to as hyperpolarisation. This event occurs at the end of an action potential when the outflow of the K+ ions "undershoots" the resting potential.

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What sounds deter sharks?
Have any studies been done to find sounds that alienate sharks?

https://en.wikipedia.org/wiki/Gilbert_Gottfried

If you want to drive away, maybe it would be better with substances that trigger a particular taste.

Have you tried doing any of your own research on the topic??

Sharks hear from 10-800hz.
Sharks jump out of water for fun, which makes  huge noise pressure next to their ears. Sound weapons aren't very renowned in Darpa or defence tech. i'd say, you play any kind of patterns to a shark at any frequency, you'll have a tough time upsetting it.  you may have a very good effect at attracting them from afar and delaying predatory response as they assess/avoid the prey. LF takes huge batteries compared to HF. curiously, dolpins hear up to 100khz, whales as low as 2-3 hz for booming across the ocean. precise answer here : https://scholar.google.fr/scholar?hl=en&q=shark+sonic+deterrent&btnG=&as_sdt=1%2C5&as_sdtp=

Todays best shark deterrents have z range of 5-10 meters and are magnetic and electric: https://prwire.com.au/pr/77309/worlds-first-boat-and-beach-long-range-shark-deterrents

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How to calculate Fst from AMOVA
I calculated an AMOVA from a genind object, with one hierarchical factor. In the table I obtain there are SSD values (for my grouping factor,"Error" and total) and sigma2 values (for my grouping factor and "Error")
I have two questions:

What does "error" stand for?
How do I calculate Fst? Which values do I have to use?

Welcome to Biology.SE. It may help if you could include the AMOVA outputs (or some of the outputs). Also, what software did you use to calculate your AMOVA?

I have never performed an AMOVA myself and I don't know what a genind object is. But ...
Error
Typically, "error" can also be called "residuals". In other words, it is the sum of squared deviation between the data and the regression line (just like in any regression model). You might want to learn a little bit about regression and ANOVA to understand your AMOVA.
Fst definition
From Nei 1973 (very good paper, I recommend reading it),
$$F_{ST} = \frac{H_S-H_T}{H_T}$$
, where $H_S$ is the average subpopulation variance in allele frequency and $H_T$ is the total variance in allele frequency.
What you probably got from the AMOVA output
You should have these info in your AMOVA output. If it only give you the total variance and the between group variance (which is what is used for the F-test), then just remember that the among variance is the total variance minus the between group variance.

Thanks for your input! I found out that Fst cannot actually be calculated from the AMOVA, since I am not given the total variance in allele frequency. As to the error, in the AMOVA it refers to the variance which cannot be explained by the grouping factors I have fixed.
A genind object is an object used by the library adegenet on R, which contains allelic information about a group of individuals. It enables you to carry out many types of analyses such as multivariate analyses. Sorry for not specifying it in my post!

The AMOVA output probably gives you at least 2 of the following 3 statistics: Total variance, between group variance, within group variance. If you have two of them, you have the third one. Yes, exact you got it for the "error" term. As said, you might want to reinforce your understanding of simple ANOVA. Here and here are short videos that may help you.


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Relation between carbon dioxide assimilation and the ambient and intercellular partial pressures of carbon dioxide
So, water-use efficiency (and carbon assimilation rate) is correlated with ambient CO₂ concentration (Ca), and  carbon isotope discrimination Δ is correlated with Pi/Pa (partial CO₂ pressure, intercellular and atmospheric, respectively) in C3 species. If the Ca increased, would that result in decreasing Δ? In other words, would increasing ambient CO₂ levels result in less discrimination towards the ¹³C isotope, in C3 species? And if that's true, is my math sound?

After more research, I've found this to be true and the reason why. Discrimination against ¹³CO₂ isotope comes from two reasons; kinetic effects (diffusion and enzyme fractionation), and thermodynamic effects (1). ¹²CO₂ and ¹³CO₂'s diffusion rates are different, carboxylation reaction's discrimination value is 30 per million, and the diffusivity of ¹³CO₂ is 4.4 per million less than that of ¹²CO₂ (2).
When stomata are fully open

they place no place no limitation on diffusion of CO₂, C3 leaves should discriminate against ¹³CO₂ by 30 per million, with respect to the atmosphere. When stomata are sufficiently closed that they become the sole source of limitation, the discrimination should be 4 per million. Intermediate cases give intermediate discriminations. (2)

It's known that when CO₂ is abundant in the atmosphere, stomata start to close because their job is to balance the CO₂ uptake and water loss by transpiration. This, combined with the previously mentioned information, to my understanding, means that, when they are more closed, CO₂ in the intercellular space gets consumed more. This lessens the carboxylation reaction's effect on the ¹³CO₂ discrimination because the CO₂ in intercellular space becomes more limited compared to the free diffusion of fully open stomata. In other words, carboxylation reaction has less CO₂ molecules to choose from intercellular space because free diffusion doesn't supply a constant flow of CO₂ molecules, making it use more ¹³CO₂.
(1) Farquhar et al., 1989, Annual Rev. Plant Physiol, Carbon Isotope Discrimination and Photosynthesis
(2) Farquhar et al., 1982, Aust. J. Plant Physiol, On the Relationship between Carbon Isotope Discrimination and the Intercellular Carbon Dioxide Concentration in Leaves

"C3 leaves should discriminate against ¹³CO₂ by 30 per million, with respect to the atmosphere." I don't understand the measurement.


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Why don't my ears pop in the morning going through a tunnel?
I drive through a tunnel (morning and evening) on my normal work commute. In the evenings, my ears will pop going through this tunnel, but they do not pop in the mornings. There are actually 2 separate tunnels for the northbound and southbound traffic, but they are right next to each other, with the same elevation changes.
What is the difference as to why the ears only pop in 1 direction?
Here's a short video of tunnel

Presumably the elevation change is in opposite directions.


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Why are many unable to defecate and urinate simultaneously?
Many people (including myself) do not defecate and urinate simultaneously, but rather in succession.  Only after one is completed, the other commences.  I have noticed this in myself, but the internet suggests this is neither unique nor universal: for example, see quora, reddit, grasscity.  I don't seem to find any references explaining why people would be unable to do both at the same time.

Why the downvote?

Probably because we don't deal in personal health questions here. I usually just vote to close in those cases, and usually leave an explanatory comment, but people are free to downvote as well.

@BryanKrause I see.  I never intended to ask a personal health question but I can imagine why it may be perceived as such with the personal introduction.  I have reformulated it to be more generic.

After the edit, this does not appear like a personal medical question. I recommend reopening.

Something related to increasing pelvic/abdominal pressure during urination mandates external sphincter to contract simuntaneously.


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What kind of drain fly is this?
Habitat:  Men's room at a rest stop in Syracuse, New York.
Size: ~1 cm
Based on my limited searching ability, I think it's a type of "drain fly" (Psychodomorpha): https://en.wikipedia.org/wiki/Psychodomorpha
Hard to get a better picture without a macro lens, but is anyone able to speciate this fuzzy urinal-fly?

This is the same species as is featured in the question "What's the name of this bug from Toronto, Canada?" (see: https://biology.stackexchange.com/questions/38665/whats-the-name-of-this-bug-from-toronto-canada); there the question has two answers.  As further support of the answer I gave there, see the diptera.info thread https://diptera.info/forum/viewthread.php?forum_id=5&thread_id=69927, where a European specimen is identified to species by an expert (the species is VERY widely distributed!)

Interesting to hear about it's expanding range.  When I first saw it I wasn't sure if I should call it a moth or a fly, that "moth fly" description fits well. I feel sorry for its sad little life around the urinals :(


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Species identification - what kind of worm is this?
I am finding these worms in my bathroom since summer arrived. I have been finding these on floor, walls and damp towel I left hung overnight in bathroom couple of times. When these worms are squished, a bang like sound is produced. Can you help me identifying this, is it something to be taken seriously & requires immediate action? Average length of these worms is ~ 1-1,5 inches.  Please find a closeup picture I managed to capture with mobile camera.
I moved into this house last winter so don't know previous summer history. Anyways I think I should get bathroom drain cleaned.
Edit: Just noticed it has very tiny hair thin, white/ transparent legs, many of them. These legs are barely seen with naked eye. May be they are just hair like things not legs (I don't know proper terminology).
Edit2: origin is Lahore, Pakistan. It's far from sea, open agricultural terrain. Climate is hot.
About movement, no they don't move like earth worms (shortening in length and then stretching). Neither it's snake like. It kinda straight. They also don't have legs as centipedes do, on their sides.

It might be helpful to include what kind of climate/what region you live in

Do they move by shortening in length and then extending OR in a snake-like motion moving side to side. This could tell us whether they are a worm or closer to a millipede. Also do they have a hard or slimey exterior

definitely looks like a millipede (or some other myriapod) with lots of legs. are they really 3 inches long? (my experience is that things crawling in your house often feel bigger than they really are) i don't know about millipedes being problematic, but i don't really know much about pest control. i think you need a better picture for proper identification.

@hamilthj, origin is Lahore, Pakistan. It's far from sea, open agricultural terrain. Climate is hot. It usually gets as high as 48 degree Celsius in summer. Rains have less frequency (fortnightly, monthly).
About movement, no they don't move like earth worms (shortening in length and then stretching). Neither it's snake like. It kinda straight. They also don't have legs as centipedes do, on their sides.

@picapica, yes you're right. They are shorter than 3 inches, way shorter. It has max length of maybe ~1-1.5 inches. I misperceived it's length before. Didn't have a ruler.

Well, I don't think we'll get much further without much better photos. But my guess is that they just like the damp areas in your bathroom. I doubt they do any harm (other than possibly scaring humans), but if you make it dryer they'll probably leave. Also, you should add the new information to the question to make it easier to find.

It's some sort of millipede. Look closely and you will see hundreds of small white legs sticking out of its sides. Also, you said it goes "Bang" when stepped on; that suggests it has a rigid jointed exoskeleton, something that all millipedes have but, as far as i'm aware, cannot be found in any surviving annelid worm.

This is almost certainly not a millipede as it has no antennae and moves by compressing its body. My money is on insect larva, possibly a drain fly (which would make sense if you regularly see them in the bathroom).
It would be interesting if you could put one in a jar and see what it develops into.


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Do lizards expand in the summer and contract in the winter?

We all know that objects expand on heating and contract on cooling.

Lizards are cold-blooded animals, i.e. they become hotter and cooler depending on their outside temperature. Warm blooded animals like us however maintain a constant body temperature.
This must mean that lizards are cooler in the winters and hotter in the summers, which should mean that they expand in the summers and contract in the winters, although by a very unnoticeable amount.
Does this really happen? How does the lizard or other cold blooded animals accommodate this expansion and contraction?

if expansion or contraction is unnoticeably small then why need for some special mechanism for accommodation?

I think you might be over-extrapolating your knowledge a bit. Animals are mostly made of water, and water only changes density by about 1% between 0C and 37C, so you are overestimating the effects of expansion/contraction due to temperature (and most organisms don't experience such a wide range of core temperatures, outside of special circumstances).
Because water is such an important component of organisms, size would also change with variation in hydration levels (you can easily observe this in plants because many plants use water pressure to support themselves). I would expect this variation to be as great or greater than any expansion/contraction with temperature.
Also note that just because animals are cold-blooded doesn't mean they don't regulate their temperature. Cold-blooded animals move between sun and shade, water and land, etc to regulate their temperature externally.


text:
Why is lower case used in front of a capitalized acronym (e.g. rDNA)?
Examples: rDNA, mRNA, tRNA.
Why do we use small case for "r" in "rDNA", etc? Any particular reason?

I’m voting to close this question because it is about the history or philosophy of coining abbreviations/acronyms rather than a problem in biology.

It's just a stylistic approach because "DNA" or "RNA" is an abbreviation by itself that has become a whole noun. Those terms clearly separate the modifier from the overall DNA/RNA. It makes it easier to read. Terms like DNA and RNA are almost always known just by those acronyms, whereas something like mRNA is known both as "messenger RNA" and "'m' RNA" but almost never as "messenger ribonucleic acid."

These letters are used to indicate the different types of RNA and DNA. Especially RNA has lots of (functionally) different variants, so this helps discering between them.
Your exmaples in particular:
 - mRNA is short for messenger RNA
 - tRNA is short for transfer RNA
 - rDNA could be ribosomal or recombinant DNA (writing rDNA is very uncommon, mostly ssDNA or dsDNA are used)

"For DNA this way of writing is very uncommon." Nope. I often read ssDNA (single-stranded DNA) or dsDNA (double-stranded DNA) or mtDNA (mitochondrial DNA) etc..

@adjan  Ah true I didn't think about that, I edited the answer. rDNA is still uncommon though ^^

I don't agree with that minimized claim, either! I see rDNA used all the time in scientific papers, textbooks, and even informal literature. While it's true that the abbreviation is problematic because of the ambiguity, it is usually pretty clear from context whether they mean "ribosomal" or "recombinant".

The poster didn't ask what the abbreviations meant, he asked why lower case.


text:
Term for timespan between generations
Is there a terminology for the average timespan between generations, like ΔG ?
I mean by that the time from the parental generation being mature to the filial generation being mature.

Note that $\Delta G$ sounds more like a time difference in generation unit like $\Delta G = G_1 - G_0$, where for example, $G_1$ could be the generation at which the state of your model has reached a basin of attraction (or whatever) and $G_0$ could be the initial generation. $Delta t$ would sound a little bit like an actual time (in years or whatever) between two generations (although often the unit of $t$ are defined to the generation time). +1 anyway

You mean generation time?
There are several definitions in use, but one is "the average difference in age between parent and offspring" (or "age at which members of a given cohort are expected to reproduce") which would be the same as the time period you're asking about.
(The difference between these two depends whether the population is at equilibrium or not.)
The two above are 'shortest generation time'; a third definition (which is the first in the link) is a little more complex but is more useful where individuals reproduce over a prolonged period.


text:
Small yellow bug with black head and three black stripes on the back
Can anyone help me to find the name of this small yellow bug with black head and three black stripes on the back. It was found in Jura, France:

It looks like a yellower version of the brown marmorated stink bug (halyomorpha halys) nymphs I've seen in my garden in the US (west Texas). They change colors throughout their life span, so perhaps that's an older nymph that's begun changing to brown. They're prevalent in the US, Europe, and Asia, according to Wikipedia (https://en.wikipedia.org/wiki/Brown_marmorated_stink_bug).
I have no research experience with this insect, and I am not a biologist -- all of my research on this consisted of google searches for variations on "small red beetle three black lines."

it looks like very similar indeed. A friend biologist said it could also be a Troilus luridus. To compare both: https://en.wikipedia.org/wiki/Troilus_luridus and https://en.wikipedia.org/wiki/Brown_marmorated_stink_bug

Following doc http://www.northeastipm.org/neipm/assets/File/BMSB%20Resources/BMSB-IWG-Jun-2013/Invasion-of-BMSB-in-Europe-Haye.pdf explains that the halyomorpha halys was first recorded in Europe during the 90s, starting from Switzerland. And the place we found the bug is very near from Switzerland.

After your addition of locale I think Spined Citrus Bug isn't a possible candidate, from web results there is no sighting of it in France but your insect is of related taxon under the Suborder Heteroptera.

Unfit identification:
It appears a nymph of Spined Citrus Bug, Biprorulus bibax.

Although native to Australia, Biprorulus bibax is considered a pest because it feeds on the fruits of lemons, mandarins and oranges, causing drying and brown staining of the fruit segments, gumming on the skin and premature fruit drop.
Their native host is the desert lime, Eremocitrus glauca.
Late-stage nymphs (IV to V) are mainly green with black markings.
Adults are green, 15–20 mm long, and have a pair of prominent spines on the shoulder of the thorax.
When overwintering tight clusters of up to 50 adult bugs can be found in a single tree. A male-produced aggregation pheromone is responsible for the clustering. The pheromone is attractive to males and females, both reproductive and non-reproductive.

SOURCE: saveourwaterwaysnow, Originally from PRIMEFACT 217, SPINED CITRUS BUG 3, New South Wales Department
of Primary Industries ISSN 1832-6668
I couldn't find any credible source with description of the early instars but the picture of the late instar on the linked website surely shows resemblance with your bug and I think yours is an early instar (any instar below IV).

The egg is 1mm across, almost globular and pearly white when first laid. Red, yellow and black markings develop as the embryo matures.
The first instar is almost oval, 1.5 to 2 mm long, with a short rostrum.

Source: Heteroptera of Economic Importance
This website dedicated to the Biodiversity of Australia has recorded sightings of Biprorulus bibax eggs and hatchlings and the latter strongly resembles your insect.

Very hard to determine the exact species without specifics like which plant/habitat it was found in,...
But one thing is for sure, this is a nymph of the Pentatomidae family.
Given the location this one is found, its size and the most likely encounter due to abundancy I'd say it's an early stage nymph of the Tritomegas bicolor (Pied Shieldbug).

1st instar nymph
https://c1.staticflickr.com/3/2915/14211267059_516d33c90f_b.jpg

Adult specimen
https://www.britishbugs.org.uk/heteroptera/Cydnidae/Cydnidae_images/tritomegas-bicolor_2.jpg
This species is found across North Africa, Europe and Central Asia, although in the British Isles, it becomes rarer towards the north, and is absent from Scotland and Ireland.
(source: Wikipedia Pied Shield Bug)
The adults are 5 to 7 mm in length. Their colour is mainly black with white irregular spots. You'll most likely find them on the ground (as they are burrowing bugs or burrower bugs), but occasionally or during nymph stage you'll find them on dead nettles (Lamium).
Hard to distinguish from T. sexmaculatus.
Extra information:
https://www.britishbugs.org.uk/heteroptera/Cydnidae/tritomegas_bicolor.html
useful classifying guide:
https://www.britishbugs.org.uk/heteroptera/idcards/life_stages.html


text:
Any studies on the effects and/or benefits of oil pulling?
A friend recently recommended me a process called 'oil pulling' for my teeth as I am struggling with my dental health at the moment. The process involves using a tablespoon of some kind of vegetable oil (like coconut oil) and swilling it around in your mouth for 20 minutes without swallowing. This supposedly acts as an anti bacterial and pulls toxins out of the body and helps with dental hygiene.
Are there any studies demonstrating or refuting its validity? Any help would be much appreciated.

This is a classical pseudoscientific claim: It is supposed to help against everything, including AIDS, Diabetes, Bronchitis, Cancer and so on. See for example this table I found online:

First, there is no real mechanism, and it is rather implausible to have an universal cure-all drug for all these completely unrelated diseases. There seems to be some weak evidence for the dental hygiene claims, but as the first reference writes, study groups where too small, not effectively blinded, so there is no final clue if this is true:

Oil pulling’s positive effects are based entirely on anecdote and not
  at all on clinical research – because there’s been very little. Pubmed
  lists six clinical studies related to oil pulling, all performed in
  India, and their quality and results seem all over the map. Some do
  indicate mild improvement in gum health, comparable to mouthwash use.
  But they’re not well blinded, use very small sample sizes and involve
  oil pulling only as part of a proper oral hygiene regimen. So it’s
  impossible to tell what’s causing said improvement.

What clearly does not happen is the detoxification, as this is a pseudoscientific myth itself. Our detoxification is done pretty efficiently by liver and kidney, so there is no need to remove whatever toxin by a treatment.
See references 1-3 (especially 1) for background on the "oil pulling" and reference 4 for the detoxification.
References:

Oil Pulling: Miracle Treatment or Woo Mouthwash?
Oil Pulling Your Leg
Is Oil Pulling Effective for Curing Medical Ailments?
Fashionably toxic

In the scientific world, if there is an absence of good studies does this act as evidence against its validity? I would like to see a professional study done which forever refutes these kind of things so we know with surety that they are ineffective.That would put an end to 90% of alternative medicine.

@Charlie Believers never took care of facts. There are a lot of valid studies showing hemeopathy has no effect beyond placebo, still this idea is around. And you cannot proof the non-existance of a fact - so you can see if you find an effect or if your trials fail to show an effect. This is what happens to pseudomedicine over and over - but the believers still don'T care.

What do you think of the Wim Hof Method (if you've heard of it)? There have been some great studies on that so far and you wouldn't believe how that has quickly gained validity. I practice it myself and it is really powerful.

He gained quite some cold endurance - but the rest (active and willingfull control of the immune system) are pseudoscientific claims without any proof. You can read here about it. Controlling your breath and doing some sort of yoga is fine, but this will not make you immune to diseases.

Not true pal. He's worked with many reputable universities to prove his methods. I'll link them in. I can even explain how it work due to focused hyperventilation. Pseudoscience became science in Wim's case.

Have a read of this:
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4034215/

http://www.icemanwimhof.com/science

And to put it a biit more general: Every time I have seen a persons name followed by method or cure, this was not real. Another red flag should be the lacking of a specific and scientifically plausible mechanism as well as someone claiming to cure everything. This is not possible.

Wim Hof method doesn't claim to cure everything, however, it's being tested as a way of combating autoimmune disorders such as arthritis and Parkinson's Disease. Wim's body has also been proven to be producing an irregularly large quantity of opioids and cannabinoids.

You can have a look at this publication which looked specifically at the guy and his twin brother - one doing this breathing technique, the other not. Both have a comparable cold endurance - because they have a larger amount of brown fat tissue. Nothing too special here. Most of these "proofs" are either claims on fan (or his own) websites or a case study with only one participant. The other one has only 12 and 12. This is by far too low to draw valid conclucions from it.

Let us continue this discussion in chat.


text:
Why bipolar neurons in retina transfer information via graded potentials?
Why should bipolar cells prefer graded potentials to action potentials?
My attempt:
I know that graded potentials are better in processing information since stimulus is directly proportional to response generated unlike action potential where the response is always same.
Reasons:
But I don't understand its need in bipolar cells , because graded potentials  have already been generated in rods and cones. Also the final message coming out of eye is in the form of action potentials from ganglion cells. If graded potentials were of that importance then why they do stop at bipolar cells and continue as action potentials in the later pathway?
Finally, graded potentials are slower than action potentials so latter should be preferred in places like eyes where response is needed to be quick.

"where response is needed to be quick" - note that vision (in vertebrates) is actually incredibly slow.

Relatively it maybe slow but in absolute terms it's still fast. Quick response from rods help a lot in activities like fast car racing, gaming, hunting etc


text:
Cell type that expresses 90% of the genome
Cells that are differentiated express the genes that are necessary for their own usage. I've heard that some cell type expresses about 90% of 30,000 proteins that are encoded in the genome. Can anybody tell me what this cell type is?

Can you point us to a source that says that?

I'm thinking of thymic medullary cells, but I don't know how many genes they express.

I've rolled your edit back because it completely changes the meaning of the question and renders the answer irrelevant. If you have a different question, ask it in a new post.

I'm voting to close this question because the asker stubbornly insists on edits that change the question to something meaningless.

Please stop editing the question so that the answer gets meaningless and open a new question instead. I will roll back it to the last version where answer makes sense and then lock it.

Well, I found this paper:
Danan-Gotthold M, Guyon C, Giraud M, Levanin EY, Abramson J. 2016. Extensive RNA editing and splicing increase immune self-representation diversity in medullary thymic epithelial cells. Genome Biol 17:219.

Medullary thymic epithelial cells [mTECs] express ~85 % of the entire coding genome
...to better determine the fraction of genes expressed in mTECs and other mouse tissues, we took advantage of RNA-seq technology... The analysis... revealed that most of the tissues [see below for those tested] express 12,000–14,000 genes (i.e. 60–65 % of the coding genome). The lung and two immunologically privileged sites, brain and testis, were the only tissues that expressed a larger fraction of the genome, in the range of 70–75 %... In line with other recently published studies, the mTEChi population expressed nearly 18,000 genes, which represents ~85 % of the coding genome, while Aire-deficient mTECs (AireKO) expressed approximately 15,000 genes, suggesting that Aire is responsible for the induction of ~3000 genes in mTECs. Interestingly, even in the absence of Aire, the mTECs expressed a relatively large fraction of the genome (~75 %), considerably exceeding the overall genome expression in other peripheral tissues. Interestingly, neither [cortical thymic epithelial cells] nor [skin epithelial cells] demonstrated higher overall genome expression than other tissues, suggesting that promiscuous gene expression is indeed unique to the mTECs population.

These cells express such a wide complement of proteins because they are involved in T-cell maturation, specifically negative selection.

List of tissues tested in the study:

brain, testes, liver, kidney, lung, colon, skeletal muscle, spleen, cortical thymic epithelial cells, skin epithelial cells


text:
Identify an insect (beetle?)

Body size: 30mm
Location: Poland, in the middle of a large meadow
It was flying and landed directly on my cap :-)

After consulting wikipedia it look similar to some of Tenebrionoidea but can't find an exact match.
Help!

This is a Buprestid beetle, and I think the species is Chalcophora mariana. It doesn't look all that coppery in your photos, but the large size and shape is perfect. Their larvae live mostly on pines, so perhaps there were pines close to your meadow?  (Image from Wikipedia)

(Also I feel a need to say that it's gorgeous and that I'm jealous, they are extremely rare in Sweden so I'll probably never see one)

Perfect match, thank you! And yes, there are pine forests nearby. In the real life it also looked quite gray, like in my photos, with only a slight brownish/coppery tint. I hope you will meet your Chalcophora mariana some day :-)


text:
While preparing Jam we use sugar.Why? (can you elaborate in science language)
Actually I was trying to find out the basic necessity of adding sugar in preparing jam.

Welcome to Biology.SE. Because people like it this way. It is still good with little to no sugar but it then called a compote and not a jam and is typically eaten differently. There is not much science to talk about here! Note that sugar will also increase preservation of the jam but I am not sure this is what you are interested in. Is this a homework question? If, yes there is probably a context in which the question was asked. What is this context?

@Remi.b The sugar is actually essential to the prolonged shelf life of (especially opened) jams, which is the point of making jams in the first place.

Well... the historical interest in making jam should not be discussed here (but I am sure it was not so much your goal). I asked in my comment whether his question had to do with preservation (end of the comment). I suppose the question the OP is trying to ask is "Why adding sugar improve preservation?". The OP would need to clarify that

Someone had asked a Q before and you'll find your answer there.

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


text:
Does osmosis require a protein channel?
Earlier today, I undertook an exam which featured a question regarding the stickiness of mucus in a person diagnosed with CF's. We had to explain why they had stickier mucus than a 'normal' person, given that CF changes the protein channels used for chloride ions to move through osmosis. This confused me, becuase I thought osmosis was through a permeable membrane, and active transport used a protein channel. I have googled it and I have been proved neither wrong nor right.
Basically, I want to know if osmosis requires or uses a protein channel, or the exam board wrote the question wrong and should have put active transport instead.
(Sorry for the waffle, I just felt some clarification is needed)

Normally, epithelial cells of mucous membranes express a chloride ion channel that allows movement of Cl- down its electrochemical gradient and out of the cell. This increase in extracellular electrolytes draws water out of the cells by osmosis, hydrating the mucus.
In cystic fibrosis, this protein is defective, most commonly caused by misfolding and subsequent degradation. Cl- cannot diffuse out of the cell and thus water is not drawn out, leading to thick mucus.

...given that CF changes the protein channels used for chloride ions to move through osmosis.

Water flows by osmosis, not ions.

I thought osmosis was through a permeable membrane...

Osmosis does occur through permeable membranes, but large, bulk flow of water can be mediated by protein channels called aquaporins. Read more here.

...and active transport used a protein channel.

Active transport of solutes does use protein transporters, but they are not strictly "channels": "channel" is the term used for passive transport, also called facilitated diffusion when a channel is involved.

I hope my edit is okay; I usually try not to edit peoples' posts for content but I thought a little clarification was important.

@BryanKrause How dare you?! But actually, thanks.

To my present knowledge, osmosis will occur wherever there is a solute concentration difference across a membrane permeable to the solvent.  It does not require a protein channel.  Not all cells have aquaporins yet all cells have to control their interior concentrations.  Water can traverse the cell membrane by moving through the phospholipids.  This appears to be the most common form of osmosis in very small microorganisms.  My source for this information is an article which I found online on Jan 10, 2019, Verkman A.S. Aquaporins, Current Biology, 2013 January 21, 23(2).  The url is ncbi.nlm.nih.gov/pmc/articles/PMC(3590904)  I realize your test is long past, but for anyone looking for an answer to the same question (as I was) I hope this helps.


text:
How can a species switch from r to K - reproductive strategy in a single generation?
I ask because it seems as though humanity is in the midst of doing exactly this. Only a few decades ago, human population was growing exponentially, and it seemed destined to keep growing until hitting constraints of food supply, at which point we would devolve into resource wars and famine. But then it didn't happen -- over the last few decades, fertility rates in the developed and developing world have plummeted and the world population is expected to stabilize in the second half of this century around 10-11 billion people. Demographers list a number of reasons for this -- education and empowerment of women, urbanization, decreased child mortality and increased life expectancy, availability of safe and effective contraception, etc. The common thread is that these trends encourage people to invest more into fewer offspring. It's as though our entire species is spontaneously deciding to switch from an r-strategy of reproduction to a K-strategy.
My question is whether this is unprecedented or not. I had the impression that r or K strategy was typically a function of species, but here we have a case where humans seem to be switching between the two strategies in a single generation. Are there other species which can change their entire reproductive strategy when the population approaches its carrying capacity? If so, what kinds of environmental cues or epigenetic factors trigger the switch? How do they manifest themselves in the case of humanity's current switch?

The issue in your reasoning is to associate a $r$ or $K$ as being a property intrinsic of the species which, while not entirely wrong, is rather misleading.
The classical and simplistic model of population growth is the model of logistic growth
$$n(t+1) = n(t) + rn(t)\left(1-\frac{n(t)}{K}\right)$$
, where $n(t)$ is the population size (number of individuals in the population) at time $t$, $r$ is the growth rate and $K$ is the carrying capacity. Of course, there exist also continuous time equivalent of this discrete time recursion equation. Here is a quick and dirty R code to compute this recursion equation
r = 0.0004
K = 1e4
f = function(n) {return(n + r * n * (1-(n/K)))}

nbGenerations = 1e5
n = numeric(nbGenerations)
n[1] = 1
for (t in 2:nbGenerations)
{
    n[t] = f(n[t-1])
}

plot(y=n,x=1:nbGenerations)

If you want to compute such function fast you can look for the general solution of the recursion equation (it is a good exercice if you are a little uneasy with recursion equations).
As you can see, the population grows exponentially until some point and then the growth is slower and slower until reaching the carrying capacity. If you look at this species at $t=2000$, then you will deduce that it is a r-strategy species because its growth is dictated by the parameter $r$ (the growth rate). If you look at the same species at generation $t=6000$, then you will deduce that it is a K-strategy species as the population dynamic is dictated by the parameter $K$. Yet, the species has not changed so much.
Being r or K strategic is not a intrinsic characteristic of the species as much as it is a characteristic of the species population size in a given environment.
Now, in my example I chose $r=0.0004$, just pick some greater $r$ value and you'll see that such change from being a r- to being a K- strategy species can change very quickly. Consider for example
r = 0.02 # growth rate
K = 1e10 # carrying capacity
f = function(n) {return(n + r * n * (1-(n/K)))} # recursion function

nbGenerations = 1e3    # number of generations to computer
n = numeric(nbGenerations)
n[1] = 1e7             # starting population size
for (t in 2:nbGenerations)
{
    n[t] = f(n[t-1])
}

plot(y=n,x=1:nbGenerations)

You can now look for realistic estimates of $r$ and $K$ for humans (data from after the industrial revolution), plug them in this equation and see what you get! You can also try to estimate $r$ and $K$ from data (from after the industrial revolution only) of population size over time.
If you play with high values of $r$, you can get overshooting and you can even get chaotic population dynamic.

Are there other species which can change their entire reproductive strategy when the population approaches its carrying capacity?

Of course, this change in a conscious. It is not a decision of the species. It is not either so much an evolutionary process. It is just a consequence of their environment. Yes, all species follow some kind of model of population growth. The famous example of logistic population growth comes from daphnia which growth dynamic has been highly studied. Daphnia can have quite a high $r$ value (depending on the environment) and they can typically show overshooting behaviour of the carrying capacity before settling down back to the carrying capacity.

If you enjoyed this simple models, you'll find another model of population growth with a predator in the post What prevents predator overpopulation?

I see your point -- a simple logistic growth model with constant $r$ and $K$ does seem to fit human population growth pretty well after all. So I think I misstated my question. The logistic growth model doesn't say anything about birth and death rates -- just an overall growth rate. The simplest interpretation of the logistic model is that the birth rate remains constant but the death rate increases as the population approaches the carrying capacity. My question is why that doesn't seem to be the case currently with humans -- for some reason, the birth rates are changing drastically.

$r$ is simply $r = b - d$, where $b$is birth rate and $d$ is death rate as measured at the carrying capacity at which the population growth is maximal (the steepest part of the graph). The realized growth rate at any time is of course simply $b - d$ at that time.

In humans, the death rate dropped like crazy since the industrial revolution. The birth rate is slowly going down to match the death rate. In other words, for humans at the left side of the graph both $b$ and $d$ where large, then $d$ dropped suddenly, population grew like crazy and slowly $b$ is also reducing causing the approaching plateau.

Right, I guess what I'd really like to know is what the actual biological mechanism is which modulates the birth rate in response to the death rate and carrying capacity. As you say, it's not simply a matter of each individual organism consciously estimating the death rate and carrying capacity, and consciously choosing to create the appropriate number of progeny in response. It has to be something more subtle.

Typically, individuals just fail to get enough ressource to produce or feed more youngs. That logic does not really hold for humans though. Many people have asked the question why rich humans tend to produce fewer children than poor humans. I am not sure of what the consensus is if any consensus has been reached.

Okay, maybe that's a better way to frame the paradox I outlined in the first paragraph of my question: it seems that human population dynamics are essentially following a very simple logistic pattern, but not via the simple mechanism motivating the logistic model. As I pointed out, some things are known about the sociology leading to the flattening of the growth rate. But from a biological perspective, it seems very odd that humans and dahlias do the same thing for very different reasons...


text:
Are all phenotypes normally distributed
Reposting from the stats stackexchange.
John Cook, in his blog https://www.johndcook.com/blog/2015/03/09/why-isnt-everything-normally-distributed/, writes that many aren't:

Adult heights follow a Gaussian, a.k.a. normal, distribution [1]. The usual explanation is that many factors go into determining one’s height, and the net effect of many separate causes is approximately normal because of the central limit theorem.
If that’s the case, why aren’t more phenomena normally distributed? Someone asked me this morning specifically about phenotypes with many genetic inputs.
The central limit theorem says that the sum of many independent, additive effects is approximately normally distributed [2]. Genes are more digital than analog, and do not produce independent, additive effects. For example, the effects of dominant and recessive genes act more like max and min than addition. Genes do not appear independently—if you have some genes, you’re more likely to have certain other genes—nor do they act independently—some genes determine how other genes are expressed.
Height is influenced by environmental effects as well as genetic effects, such as nutrition, and these environmental effects may be more additive or independent than genetic effects.

I have two questions regarding this. First, I can't come up with any obvious example of phenotypes that don't follow a normal distribution. Could anyone help me? And second, his claims seem to contradict this other paper: https://www.uvm.edu/~dstratto/bcor102/readings/4_Evol_of_Phenotypes.pdf

To understand the genetic basis of quantitative traits, it is important
to think about the effect of a particular allele, not simply its
presence or absence. A single locus can produce three discrete
phenotypes, but as more and more loci contribute to a trait the
phenotypic distribution comes closer and closer to a normal (bell
shaped) distribution

Who is right here? Does the fact that genes are digital rather than analog really make a difference? And what about the second argument that they aren't independent. Is that really necessary (second paper seems to indicate otherwise if I am understanding properly).

What about the most obvious Mendelian traits? Those would be phenotypes that follow a bimodal distribution, because they are caused by a single gene with just two alleles. Many other phenotypes also follow a bimodal distribution for the same reason. As you add in more modulatory or regulatory genetic variation you will smear the distribution and it will become more normally distributed. That is exactly what your references are telling you.

Many phenotypes might be normally distributed assuming a large enough population size and many QTL (Quantitative Trait Loci) as the normal distribution is a simple result of the CTL (Central Limit Theorem). If it is unclear to you, you should definitely have a look at the central limit theorem.
Typically, if the number of loci is too low, the phenotype may for example follow some kind of continuous approximation to a Poisson distribution. Of course, if the allelic effects are correlated among loci or if there is some linkage disequilibrium or if the phenotype is bounded or discrete, or nominal, you may not end up with a normal distribution of phenotypes but all of that is a discussion for another time.

I can't come up with any obvious example of phenotypes that don't follow a normal distribution

As, the second quote says, think of any phenotype that is discrete. Here are a few examples

sex
right / left handed
eye color

Now if you want a quantitative phenotype that is not normally distributed, then height (which is the bad example of your first quote) is very slightly bimodal due to an average height difference between male and females (look at Are males taller than females in humans?). You can also think of any phenotypes that are bounded. For example running speed. Athletes will cause a very long right tail, while people in wheel chairs will make a big stack of probability mass in 0 km/h.
There is a lot of things to consider when trying to guess whether a is normally distributed or not in a population. It will take some good knowledge of statistics and good knowledge of the genetics of the population.

Thanks for this clear answer! I've never been convinced by the "height can't be normally distributed because it can't be negative" argument, since it can still be approximated reasonably well by a normal. Running speed seems like something you can't approximate with a normal then, but I didn't know it's considered a phenotype! Any explicit example for something that follows a poisson distribution?

Pretty much anything can be a considered a phenotype. A phenotype is whatever effect the genotype has on the world around it which mainly include all the characteristic (behaviour, anatomy, physiology, ...) of the body. I should have said "some kind of 'continuous approximation' to a Poisson distribution'" (now edited). It is just some theoretical reality of a model where there are few loci all biallelic with allelic effect 0 or 1, then you would see Poisson distributed trait. I can't give a specific example.


text:
What species are these baby birds?
I'm trying to save these baby birds' lives, and I need to know their species so that I can know how/what to feed them. Please help me ASAP .

A couple of questions; where did you find them, in what condition? allaboutbirds advises to contact licensed wildlife rehab centre or leave them to the place where they were found to increase their chances of survival. The bird appears to be one from Caprimulgiformes.

I agree they look like Caprimulgiformes. We need more info (where you live, where you found them, why you are holding them, etc.) to answer your question. Also, in the future, if you find baby birds, just leave them where you found them. These look fully fledged, and were almost certainly ok and just waiting for mom to come back to feed them...

If you are in Europe they are juvenile common swift (Apus apus).
There is a website dedicated to them, with a page on how to raise them: http://www.commonswift.org/Hand_rearing_Swifts.html
They are very fragile and with the wrong diet they might develop feather deformations. They also require a continuous effort because they eat very often. I raised them a couple of times and when they take off is magnificent but it is easy to do something wrong. If you have some recovery center or expert nearby  I suggest to hand them over.

+1 For the website you linked. I mistook them for nightjars.


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Gene networks for different tissues?
I currently work on gene networks and specifically, I analyze the brain gene regulatory network of an insect to understand its sexual behaviour. During a recent presentation, I got asked this question which I just couldn't really tackle in a good manner. The question was why do I study the brain gene network to understand sexual activity when I should be studying the gene network of a sexual organ, for eg: the ovary. I got out saying that since the brain decides behaviour, it would be much better to study the brain GRN. However, I got confused and would like to know if different tissue or organs in the same organism have different gene networks? Any idea regarding the theory is welcomed.

Of course different tissues have different gene expression - I'd expect that isn't something at all new to you so I'm wondering why you are asking the question? Your response to that somewhat bizarre question seems fine to me, maybe the question asker was trying to lead you into a discussion of how sex organs also affect gene expression in the brain, e.g. via hormone production.

Check out this heart development paper. What's striking is different programs for varying progenitor cells within the same tissue, and the presence of core elements from other cell types or tissues such as GATA3, working together to perform unrelated functions. Cell have the capacity to express the same gene network, but how they're regulated differs on a number of variables.


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How is "selection" best defined?
There is natural selection but there is also sexual selection which some regard as a category of natural selection.  There is also artificial selection (by humans).  The question is, what is a most appropriate for selection?  What criteria does a  force have to meet in order to be considered to have acted selectively?

if a trait is beneficial to the host, then the chances are that it would be chosen by natural selection.

Related: What is the relationship between sexual and natural selection? and What does fitness really mean?

see wiki evolution page. its a nuanced question like "can it ever be right to kill?"

@comprehensible I am not sure I understand the relationship between "can it ever be right to kill?" and "How is “selection” best defined?". IMO (see my answer), Wikipedia does not offer a good short format definition of natural selection. NS is, mathematically speaking, very accurately defined. There is left to phrase it correctly. I don't think there's much nuance. I am not sure what you mean by nuance though as your example depends only upon ones set of values (philosophy > value theory).

@Remi.b So what is NS's accurate mathematical definition?

@sterid All the standard Fisher's equations of natural selection. Have a look at any intro book to population genetics (Books on population or evolutionary genetics?)

@Remi.b Would you please put into a response what NS's accurate mathematical definition is?  My understanding is that Fisher's fundamental theorem of natural selection has been subjected to some controversy as a result of Price.

I don't think the so called Fisher's fundamental principle of NS is questioned by Price equation (but I might be wrong). Consider for example this simple equation for haploid selection $$p(t+1) = \frac{W_Ap(t)}{W_Ap(t) + W_aq(t)}$$ For more equations and explanations, please just have a look at an intro book to population genetics.

@Remi.b What do those terms represent?  Also, would you provide a citation please?

It really is a very standard equation. You'll find it in any good intro book to population genetics. It was published by Fisher at the beginning of the 20th century. I am a bit lazy to find the original paper but in any case, I would rather recommend to read an intro book than Fisher papers (Fisher is not really an easy to read author)!

I have a couple of intro books and I haven't seen that equation.  What do those variables mean?

Re my comment about Fisher, I was referring to what he wrote in this paper (DOI:  10.1111/j.1469-1809.1972.tb00764.x), "Fisher's fundamental theorem of natural selection is mathematically correct but less important than he thought it to be."

Consult a dictionary to see the meaning of the word, and then apply it to the context of interest, which you is not defined in the question, although I don't think it has anything to do with who is playing in a sporting event.

My favourite definition

Selection is a fitness differential associated to a genetic variance among individuals in a population.

You might want to have a look at What does fitness really mean?.
What I like about this definition
I personally went with this definition because it is short and clear cut and directly highlight the importance of mathematical statistics in the evolutionary biology literature.
What I don't like about this definition
This definition has the issue that it may be hard to be fully understood to a layman reader. Also, I think my definition lack a mention of the phenotype as being causal to the fitness differential. While such mention is not necessary, I think it would clarify in most minds what selection is really about.

Now, let's consider the definitions that we typically get when we google the question
Wikipedia
Here

Natural selection is the differential survival and reproduction of individuals due to differences in phenotype

I am quite unhappy with this definition. While I like that it highlights the fact that fitness difference is caused via phenotypic difference, it completely lack the idea that for a change in allele frequency to happen, this variation must be correlated to genetic variation.
I would note that the rest of the introduction on the wikipedia article clarify my criticisms. I only attack the short version (one sentence) version of the  definition.
Dictionnary.com
Here

the process by which forms of life having traits that better enable them to adapt to specific environmental pressures, as predators, changes in climate, or competition for food or mates, will tend to survive and reproduce in greater numbers than others of their kind, thus ensuring the perpetuation of those favorable traits in succeeding generations.

There are a few things I don't like about this definition
..traits that better enable them to adapt..
It sounds like they are talking about evolvability. I would just say traits that are better adapted.
..too much emphasis on the role of the environment..
Also, I don't like that it is presented as if all selection pressures where environmental (predators, climate, competition for food, etc...) and completely ignore a very important source of selection which are simply related to the functioning of the body. A mutation that causes an individual to fail copying DNA anymore will obviously be lethal and under very strong purifying selection. Such the "outside-of-the-body environment" is important but it is definitely not the only thing.
It is kind of a common misconception about evolution that selection occurs when there is a climate change and not so necessarily in other case in most people's mind.
..ensuring the perpetuation of those favorable traits in succeeding generations..
Well.. it does not "ensure" that these traits will be kept. First because it only increases the probability of certains allele to be kept or to reach fixation, it does not ensure it. Also, because depending on the genetic framework, once the underlying QTL have reached a given frequency, depending on the actual genetic mechanism (epistasis, dominance and others), traits that are being express might differ quite a bit from those that have been selected for.
Overall, I think the definition lack any notion to genetics.
Biology-online
Here

A process in nature in which organisms possessing certain genotypic characteristics that make them better adjusted to an environment tend to survive, reproduce, increase in number or frequency, and therefore, are able to transmit and perpetuate their essential genotypic qualities to succeeding generations

I like this definition. The only issues in my opinion are very similar to my above opinions

too much emphasis on the environment as done before
it seems that they define more the consequence of natural selection than what it actually really is.

What Google gave me when I entered 'what is natural selection?'

the process whereby organisms better adapted to their environment tend to survive and produce more offspring.

Again there is IMO, too much emphasis on the environment and no mention of thee actual mechanism (fitness - genetics correlation).

Potential confusion
Some people might use the term "selection" to refer to the existence of phenotype - fitness correlation and the "response to selection" as being the effect of such correlation of the population genetics whenever there is a non-zero association between phenotype and genotype. This nomenclature would typically be inspired by the terminology used in the Breeder's equation (see How to interpret the breeders equation?).
However, none of the definitions I could find clearly suggested that selection was nothing but a phenotype - fitness correlation as all of them implied that selection has a long term impact on the population phenotype which such phenotype - fitness correlation would not have in absence of a phenotype - genotype correlation.

Lewontin recipe
I am not sure a recipe count as a definition but Lewontin recipe is a good way to understand the what is natural selection

Individuals in a population varies in terms of a given trait
This trait has some heritability.
The fitness varies (not necessarily linearly) as the trait varies.

The recipe hides the complexities behind the term heritability. You can learn about the math of heritability at Why is a heritability coefficient not an index of how “genetic” something is? .

I find your preferred definition (at the top) too inclusive. Why does selection have to lead to changes in allele frequency, in the general case? It has to for the selection to lead to evolution, but you can have natural selection without evolution (if the selected traits do not have a genetic basis/no narrow sense heritability). In definitions, there are however often some confusion about whether they are defining natural selection or evolution by natural selection.

I'm also wondering why you only cite website/dictionary definitions instead of books/papers from evolutionary biology and/or philosophy of biology.

Yes, NS can be a process of evolution, but so can other factors as well. That doesn't however mean that NS has to lead to evolution. And I don't get your second point; ofcourse you can find argument on NS i peer reviewed literature (papers and books). Online encyclopedias are hardly an authoratative source. My answer contains a couple. Its a somewhat tricky topic though that sometimes bordets on semantics and the philosophy of biology. And I agree that there are probably conflicting views out there.

I think you're right. NS refers to the fitness - genotype association and not to the resulting change in allele frequency. I got confused due to the post The falsifiability of natural selection, edited my definition wrongly. I've edited it back to the original definition. I've removed my comment too. Thank you!

I seem to be missing something with your favorite definition of selection. When I think of selection, I think of a verb, and with that definition, am not seeing a verb. What am I missing?

Selection is defined as a process. It is a noun. Note that outside of biology the term selection can also be both a noun and a verb.

@Remi.b I think I now understand. I was misinterpreting the differential part to be before selection instead of after. So, the differential decreases as unfavorable/deleterious genetic variants get removed.

To be fair the word "is" was missing in the definition before. I edited after reading your comment $\ddot \smile$ That probably created your confusion.

@Remi.b Say the frequency of an allele has gone from 0.5 to 0.6 within a generation.  If you are given only this information, you do not know whether this is attributable to genetic drift or selection.  However, the fact that there is a change in frequency means there’s a positive correlation between the allele and fitness.  This does not mean there was selection.  This positive correlation could be attributable to luck/chance.  That is, it could be a change in frequency due to drift.  From my vantage, in order for there to be selection, there has to be an influence toward directional change.

Directional change, such that the population becomes better at managing the force of selection.

How selection is "best defined" is clearly subjective. However, even though it is a key process in evolution, the exact delimitation of (natural) selection is not clearcut, or rather, authors have defined it in slightly different ways in relation to the evolutionary process (see below, especially quote at bottom from Wade & Kalisz). A paper worth reading as a starting point, if you really want to dig deeper into the definitions of evolution and natural selection is Godfrey-Smith (2007) "Conditions for Evolution by Natural Selection". There, he goes through several attempts of verbally defining "evolution by natural selection" (among them two version of Lewontin's recipe that Remi.b mentions in his answer).
Many of the definitions take a similar form as this modified version of Lewontin's recipe (the 1980 version, page 491 in paper):

A sufficient mechanism for evolution by natural selection is contained in
   three propositions:
(LI) There is variation in morphological, physiological, or behavioral
   traits among members of a species (the principle of variation).
(L2) The variation is in part heritable, so that individuals resemble their
   relations more than they resemble unrelated individuals and, in particular, offspring resemble their parents (the principle of heredity).
(L3) Different variants leave different numbers of offspring either
   in immediate or remote generations (the principle of differential fitness.

The aim in this paper is however not only to define "natural selection" but "evolution by natural selection" (which is a bigger question). So from the definition above (or others in the paper), the issue is on how to draw the line between "natural selection" (as a condition) and "evolution by natural selection" (as a process). If this is at all possible. To me, it is natural to draw the line between "selection of phenotypes" and "transmission of phenotypes to the next generation" (through genetic variance/heritability), which sort of mimics the breeders equation. So to me, it is natural to see "natural selection" as the result of a fitness-phenotype correlation. In some ways, this mimics an the 1970 version of Lewontin's recipe (page 490 in paper):

Different individuals in the population have different morphologies,
  physiologies, and behaviors (phenotypic variation).
Different phenotypes have different rates of survival and reproduction in different environments (differential fitness).
There is a correlation between parents and offspring in the contribution of each to future generations (fitness is heritable)

Here, point 1-2 corresponds to my view of "natural selection", while the 3rd point is necessary for "evolution by natural selection". Note however that this definition has other problems if taken on its own, mentioned in the paper.
A similar view is expressed in Haldane (1957):

Natural selection is a statement of the fact that the fictitious parental population differs significantly from the population from which it was drawn. For exemple, with regard to any specific metrical character it may differ as regards the mean, variance and other moments. A difference in means is called a selection differential (Lush,1954).
Selection may be genotypic or phenotypic. Phenotypic selection may or may not lead to genotypic selection.

Here, (natural) selection is clearly seperated from the possible subsequent effects of selection (evolution).
Even more clearly put (also highlighting that there are different views on this topic), from Wade & Kalisz (1990, Evolution):

When we measure phenotypic selection in natural populations, we compare the phenotypic distribution at one time with the phenotypic distribution at some later time(s) within the same generation. It is from this comparison that we drawn our inferences regarding the operation of viability and fecundity selection. We deliberately avoid examining changes across generations because, when the process of transmission changes the phenotypic distribution, we would confound selection and transmission. We consider the clear separation of these two processes to be conceptually and practically important to the study of selection although we acknowledge that other authors prefer to include inheritance as part of the definition of natural selection (e.g. Endler, 1986).


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What is the name of this plant with orange fruit clusters in india?
Location: South India.
Month: June
Season: Rainy Season.

I think it is some species of Duranta sp..

I didn't exhaustively check the species but if anongoodnurse's ID is right, D. erecta is toxic; its berries and leaves and it's only songbirds who are not affected by those (Source wiki).

The easiest way to find out the name of this tree is to realize that the flowers (and therefore the fruit) are in the form of a raceme.

Googling India bright orange fruit raceme in Images quickly brings up your specimen among others.

The name of that image leads to other sites discussing the plant.

Duranta erecta
  Scientific classification
  Kingdom:    Plantae
  (unranked):     Angiosperms
  (unranked):     Eudicots
  (unranked):     Asterids
  Order:  Lamiales
  Family:     Verbenaceae
  Genus:  Duranta
  Species:    D. erecta
  Binomial name
  Duranta erecta
Duranta erecta is a species of flowering shrub in the verbena family Verbenaceae, native from Mexico to South America and the Caribbean. It is widely cultivated as an ornamental plant in tropical and subtropical gardens throughout the world, and has become naturalized in many places. It is considered an invasive species in Australia, China, South Africa and on several Pacific Islands. Common names include golden dewdrop, pigeon berry, and skyflower.


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Figuring out an honest indicator in intrasexual selection
In the first picture, the parameter $r$ seems to compare the direction and strength of two variables. In the second picture, $R^2$ seems to describe the variation of proportion of independent and dependent variables.

With this being said, are honest indicators determined by $R^2$?
Why is it a positive number for both graphs if we refer to the second picture?

I don't understand your question. I don't know if it is a stat question or a biology question. You have t give it more thoughts and split down to the individuals elements that are unclear to you. The r values are wrong. While R^2 is always positive, R can be positive or negative. It is negative when the slope is negative, positive otherwise.

Maybe, you are trying to understand what hones signalling mean. You could have a look at signalling theory and handicap principle as a start.

It's a biology question from general bio II that includes statistics. I want to know how we can determine an honest indicator in intrasexual selection based on statistics. an honest indicator comes from Zahavis hypothesis. Its pretty clear what I'm asking....I know what it means in terms of definition i just don't know how to interpret it in graphs.

Those graphs seem to just be teaching you what r and R^2 mean; there is no relationship to honest signaling except for the headers, and the data are all synthetic.