text:
Heart rate and Metabolic rate relationship
Metabolic rate in humans can be approximated using the Penn State equation.
It can also be estimated using direct and indirect calorimetry.
According to Kleiber's law, metabolism scales across species proportionally to the mass by a power of 3/4 (also by 2/3 or the [2/3, 3/4] range for other models).
Now, despite the known relationship between temperature, mass and metabolism, the relationship between heart rate and metabolism is less clear. Heart rate also scales with body mass approximately by a power of -1/4.
Usually, as a human ages, both its metabolic rate and heart rate decrease. Also, there are many examples of animals with a very high metabolism that have a very fast heart rate, like the hummingbird or the etruscan shrew.
I want to know if metabolism, after controlling for mass, is related to heart rate. I find it suprising that nobody has studied this relationship. I guess more data is needed to generate a model (I found this site, which could be useful, beats-per-life).
Heart rate is related to the distribution of nutrients and oxygen to all organs in the body. I think a faster metabolism would require/imply a faster distribution. We know this is true at least within the same individual organism, for example, during the elevated metabolic demands of exercise. Despite all of this, I haven´t found examples of it being used in relation to metabolism.
Any ideas about why this might be the case? What's the relationship between metabolic rate after controlling for mass, and heart rate, if there is any?
What about cardiac output? Cardiac output is stroke volume times heart rate. A bigger body tends to have a bigger heart, a bigger heart likely implies a greater stroke volume. Maybe if you adjust stroke volume by weight, and combine it with heart rate, you get an even better indicator of metabolism.

I think this is correct, the relationship between heart rate and metabolism exists, and can be explained by oxygen consumption. This is given by the Fick principle. That is:
$$ VO_2 = CO (C_a-C_v)$$
Where $(C_a-C_v)$ is the arteriovenous oxygen difference. So:
$$ VO_2 = (HR·SV)(C_a-C_v)$$
$$ MR ∝ VO_2$$
$$ MR ∝ (HR·SV)$$
Given that:
$$ SV ∝ Weight$$
You could estimate Metabolic rate using a combination of Weight and Heart rate.  Let's assume the stroke volume follows an allometric power law given by the exponent $e_{SV}$. Then:
$$ SV≈ a_1+b_1M^{e_{SV}}$$
(I guess lean body mass is more related to organ size than just Mass, so you probably could use it instead of Weight to estimate the Stroke volume)
$$ MR ∝ a_1+b_1M^{e_{SV}}·HR$$
Alternatively:
$$ MR ∝ LBM·HR$$
So, to summarize, I think Heart rate, through its effect on cardiac output and oxygen consumption, gives information about the metabolic rate that goes beyond mass, and can be used in combination to estimate it. The specific model type (logarithmic, linear, exponential...) that uses $ a_1+b_1M^{e_{SV}}$ and $HR$ is unclear but It might still work.

Please make sure to readers where Fick's principle ends and your personal assumptions start. While your assumed correlations individually seem plausible, they are presented without any source whatsoever. Especially, the step from ∝2 to ∝(·) seems dubious. Sure, there is a correlation between cardiac output and metabolic rate, but what is the margin of error? The OP, based on their research, asked the question WHY the heart rate is NOT used in the literature to determine MR.


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Could there be some safe, hypothetical way of turning on and of thermoregulation?
This is something I thought of with the whole artificial gill concept.  Could a modification to the brain/nervous system allow a human to turn off their thermoregulation in air/water of the right temperature range, so they wouldn't have to expend as much oxygen?

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How does the bladder transition from releasing urine at night to being able to hold urine at night?
I wonder about this.  What's the biology of the transition from wetting the bed at night to holding urine at night?  Is there a chemical change with how the bladder muscles contract?

When I first read the question, I thought the question deals with the difference between bladder activity during the day and during the night.
A second read two days later makes me think you are actually asking about maturation of the bladder, or in other words, what is the process by which children "learn" to control the bladder during the night when they are off diapers. It seems the answer you accepted deals with the former interpretation, but your phrasing points to the latter. Can you please clarify your intention?

I'm not sure how much the bladder has a role in this. Mostly, the reduced frequency of urination during the night is the result of less urine production by the kidneys. This is in response to a hormone called ADH, antidiretic hormone (it has other names as well). ADH acts on the distal convoluted tubules of the nephrons in the kidney to fine-tune the reabsorbtion of water in the tubule bringing it back into the circulatory system. This hormone is released in reponse to a few factors including blood volume. But it's release is also cyclic over a 24 hour cycle. https://www.ncbi.nlm.nih.gov/pubmed/202988
It can happen that this daily cycle of ADH release intensity gets out of adjustment and you urinate more frequently at night, perhaps more than in the day. This has happened to me. Also, according to my GP, it is a frequent cause of bed wetting in children.

The bladder is controlled by both the autonomic and somatic nervous systems. This means that part of the bladder activity is voluntary and another part is involuntary - more precisely, the detrusor (which is the smooth muscle in the bladder wall) is controlled involuntarily, while the external sphincter (the muscle around the bladder neck) is controlled voluntarily (see picture, this is the female bladder).
I found all kinds of references that describe the maturation process of the bladder during infancy. This paper, from Pheonix Children's Hospital, is about voiding disorders in children. It notes in the first paragraph three conditions that make up the bladder's maturation process (the rest of the paper discusses voiding disorders):

The bladder capacity must increase.
The child must develop voluntary control over the sphincter muscle in order to start and stop voiding.
the child must develop voluntary control
over the infantile voiding reflex which allows the child to stop involuntary bladder contractions.

This article discusses the topic of bladder maturation in greater detail (see the first section titled: MATURATION OF BLADDER CONTINENCE). From the article: "As bladder urine increases, a critical volume is reached (functional bladder capacity), which initiates a spontaneous reflex contraction that is mediated by the sacrospinal ganglia. As the bladder contraction ensues, the increased bladder pressure overcomes the detrusor muscles at the bladder neck and spontaneous emptying occurs. As the infant grows and matures, control centres in the pons and medulla initiate inhibitory signals that slowly dampen this reflex over a period of years ... Nighttime continence is achieved in association with the abolition of spontaneous bladder contractions, mediated by the pons and medulla; a nocturnal bladder volume less than the nocturnal functional bladder capacity (NFBC), which is ADH-dependent; and the achievement of prolonged rapid eye movement (REM) sleep and attainment of sleep arousal."

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Meaning of 'forms of free energy'?
I was doing a practice exam paper and it asked for different 'forms of free energy'. I am a physicist rather then a biologist so 'free energy' to me means Gibb's Free Energy:
$$G=H-TS$$
But I cannot see how you would could have different forms of this. So is my interoperation of 'free energy' right and how can we have different forms of it?

Can you provide the exact context i.e. the complete question in the practice paper?

@WYSIWYG it was a biophysics paper and it simply said 'Give the main forms of free energy', which I guess is not very helpful, but the question came with no context apart from this.

AFAIK, there are two types of free energy: Gibbs free energy and Helmholtz free energy (A=U-TS). However, Helmholtz free energy is almost never used in biophysics or biochemistry. Energy minimization principle in biochemistry always assumes constant temperature and pressure of the closed system.   HFE is used when pressure can change. The other two thermodynamic potentials are Internal Energy and Enthalpy. Anyway, without the context it would be difficult to answer this question.


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Membrane conductance in phase 1 of the cardiac action potential
Correct me if I am wrong, but in phase 1 of the cardiac action potential (for ventricle cells) there is flow of potassium ions due to the opening of transdent potassium channels. To me this would correspond to an (sudden) increase in the conductance of the membrane to the potassium ions, $g_K$, however looking at graphs on the internet  do not seem to indicate such a change in conductance. Please can someone explain why such a change does not occur (sources would be helpful).


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Why must bacteria outrun diffusion?
In 'E.coil in Motion' Howard Berg says that

'If it [a cell] is to go far enough to find out whether life is
  getting better or worse, it must outrun diffusion.'

I am confused about the exact meaning of this expression and can't seem to find an explanation. What is meant by 'life is getting better or worse' and why can't a cell just wait for things to come to it by diffusion?

Because then it wouldn't be going anywhere, and the first part of the sentence is specifically about traveling.
Without more context that might make me wrong, I think the statement is intentionally tautological and is just meant to set up a problem to solve.
By "better or worse" I think the author means to generalize about conditions that an organism may prefer: nutrient concentrations, temperatures, etc.
Restated, I think the author is roughly saying "For cells to spend more time where conditions are best for them, they have to move on their own power."


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When performing mutagenesis for an assay, how do you decide on the sample size of individuals to be mutated such that all genes are covered?
If I want to study, say, gustatory response of salmons to a bile acid, I need to mutagenize a sample of salmon males. However, given that there are many genes involved in this response, what is minimum no. of salmons I should mutagenize, such that ALL the genes involved have some mutations?
I have searched quite a lot for some statistical method that tells me this, but to my surprise I haven't found any.

Don't think about mutagenized animals, think about mutagenized genomes. Depending on when the mutagenesis is carried out, and how efficient it is, a very small number of males could give rise to thousands of mutagenized F1 progeny, each carrying a uniquely mutagenized genome. That is the number to focus on. Typically, in fruit flies and soil nematodes the animals are hit "pretty hard" such that each F1 is carrying hundreds, if not thousands, of mutated sites, randomly throughout the genome. The trade-off is to not mutagenize them so much that they suffer a drastic decrease in fertility or viability, while at the same time minimizing the number of F2 homozygotes you have to screen for phenotypes.
In C. elegans exposed to 50 mM ethylmethane sulfonate for 4 hr, you might reasonably hope to recover 1 loss-of-function mutation after screening 2,000 mutagenized F1 genomes.
Are there good genetic markers along all of the salmon chromosomes?  If you are only interested in recovering dominant mutations then you can screen the F1 directly (however dominant alleles tend to be much rarer than recessive alleles, and interpretation of dominant phenotypes is challenging without lots of good genetic tools, like duplications and deficiencies). Otherwise you will have to mate the F1 to obtain male and female F2 and then set up brother-sister matings so that you can score the F3 for phenotypes of interest.
None of these numbers would apply to salmon because the genome is much larger, and unless someone has already done a dose-response curve on the optimal mutagenic dose for salmon, you would need to do that first.


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Role of microvilli in cell volume regulation
Does the presence of microvilli on a cell's surface ensure that it's more resistant to cell swelling or lysis in a hypotonic solution, as compared to a normal cell?

Microvilli, are cellular protrusions on the membrane and hence they increase the total surface area of the cell in context.
If we evaluate the characteristics of microvilli and the structural appearance, we know that; they have many small folds; strengthened and lined by the protein filament actin; bedded in a terminal web of alpha-actinin and keratin. All of these characteristics, work in harmony to support its ability, for it to do its function. That being, to allow greater diffusion whilst controlling the cells integrity. Evidently, the microvilli do help resist the hydrostatic pressure within a cell as a result to the distribution of pressure and the microfilaments present.
Most animal cells have microvilli so, there is a huge excess of factual evidence to support what happens to them in under specific conditions. Knowing this, it confuses me why you even asked this question. It just takes a simple comparison.
I'm presuming, a normal cell is a cuboidal cell, too. So, yes, if they were both placed in a variable hypotonic solutions, with gradual increases in concentrations for comparison, the cuboidal cell would rupture much earlier rather, the cell with the microvilli would be still standing at a further stage (concentration). However, the cell with the microvilli will nearly all of the time still lyse despite it's additions. Microvilli don't sorround the entire cell, if they did, the integrity of the cell in greater hypotonic solutions would be more applaudable vs a plant cell (cell wall containing pectin).
Yes
References:
**
http://www.histology.leeds.ac.uk/cell/cell_cytoskel.php ; 'keratin is a type intermediate filament in cells' [...] 'The nucleation of actin fibers occurs as a response to external stimuli, allowing a cell to alter its shape to suit a particular situation.'
**
http://www.westfield.ma.edu/personalpages/draker/edcom/final/webprojects/sp10/cell/Ross44.jpg; 'A hypotonic solution has decreased solute concentration, and a net movement of water inside the cell, causing swelling or breakage.'
**
http://www.histology.leeds.ac.uk/cell/cell_cytoskel.php ; 'Intermediate filaments are inserted into desmosomes at cell-cell junctions, and help to maintain cell-cell connectivity, as well as the structural integrity of the cell itself.'
P.s. Most of the answer was achieved by the application of knowledge so, direct references cannot be found!

Can you add few references to your answer ?

Yes! I will add some now (it was late).

Most animal cells have reservoirs of membrane, including microvilli (Sheetz et al, Annu. Rev. Biophys. Biomol. Struct. 2006. 35:417–34). This can help preventing lysis in hypotonic conditions, but has other functions as it allows the cell to take varied shapes without being constrained by its membrane area.
This is not volume regulation, by the way, but rather accomodation of volume changes. There is evidence that volume is regulated, but some osmotic challenges can be too great or to sudden for the volume response.

You can add example of insect photoreceptors where increase in surface area of membrane due to microvilli is needed to increase probability of hitting photon on rhodopsins.


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Trying to understand sleep
I don't understand sleep.
Before, I naively thought it was related to some kind of 'energy' or 'wakefulness' resource that gets depleted as time goes by without rest.
But that's not it, higher activity levels don't make you sleep sooner, they might make you more fatigued and it might correlate with sooner sleep onset but the relation is not 1:1, more activity doesn't equate to earlier sleep, in fact many times it might do the oposite.
Even plants follow some regular pattern of higher and lower activity levels, but seems more related to the environment and resources available.
Maybe we sleep because of the day-night cycle? we adapted to live in daylight, so by specializing we focus our biological resources, and during the night what we do is sleep to limit the consumption of those resources (metabolic rate slows down during sleep) because doing anything else is not useful, we are not adapted for being nocturnal.
So basically sleep is like some kind of instinctual behavior, sleep is induced by the body, the body actively makes us sleep. But then, why do perform so poorly if we don't sleep? a consequence of our adaptations to that day-night pattern? If sleep is only an induced physiological behavior, Why if we stay awake a lot we risk our health? is this dependence on sleep an accident then?
My question is this. If we consider sleep as a behavior actively induced by the body, akin to an instinct, rather than the depletion of a physiological resource (I think this is true), why does insufficient sleep result in adverse health effects, such as those observed in conditions like fatal familial insomnia?

Stack Exchange is for specific questions and specific answers; can you narrow your post to one specific question about sleep?

Why are the two options "depletion of a resource" and "learned behavior"? Clearly sleep is not learned.

Yes, I imagined someone might misunderstand that part. I never said sleep is learned, but seems similar, like an instinct, but probably doesn't fit the definition. I think the question is if a biological system requires intrinsically periods of less activity (not only regular sleep) to maintain proper functioning indefinitely. We have the confounding factor of the sun periodic effects, which caused even fruit flies to have an internal 24h clock, and this relates to the existence of sleep. If life evolved in a place with no periodic effects and constant resources, would sleep exist?

"Learned" and "instinct" are opposites, so yes it's quite weird to use one to describe the other.

Sure, maybe "like an instinct" is better than "like a learned behavior"

Do existing Q&A like https://biology.stackexchange.com/questions/324/why-did-the-process-of-sleep-evolve-in-many-animals-what-is-its-evolutionary-ad answer your question? If not, can you clarify why not and what your specific question is?

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Rough estimation of stroke volume
I wanted to know if you could use PWV in combination with PP to estimate SV (pulse wave velocity, pulse pressure and stroke volume).
My understanding is, the higher the arterial stiffness that is, the higher the pulse wave velocity the lower the arterial compliance and therefore for the same volume change in the arteries the observed blood pressure would be higher.
That means that PP would be roughly similar to the SV divided by C (arterial compliance).
If we rearrange this we can get an estimate of SV by multiplying arterial compliance with pulse pressure, or the other way around, dividing pulse pressure by PWV.
Is this estimate sound and will reflect a somewhat linear relationship in general with stroke volume? is it better than pulse pressure alone? I dont want the specific value of stroke volume i just want a rough somewhat linearly correlated estimate that is better than pulse pressure alone.
Edit
I would probably add the Liljestrand and Zander adjustment, so the equation would end up looking like this:
$$SV ≈ \frac{\text{PP}}{(\text{SBP} + \text{DBP}) \times \text{PWV}}
$$
Edit 2
This is actually interesting and reflects real world physics to some extent, the equation for the radial stress in a thin walled pressure vessel (like an artery) is the hoop stress equation:
$$σ = \frac{\text{P}r}{\text{t}}
$$
Given that we are interested in the  change in the artery radius which would be reflective of the stroke volume, and the arteries behave elastically we have to take into account this to get the strain:
$$σ = E · ϵ
$$
The strain is defined as this, in relation to radius:
$$ϵ =  \frac{Δr} {r_0}
$$
If we substitute everything we obtain:
$$Δr =  \frac{Pr^2} {Et}
$$
The unit $Et$ is the young modulus times the thickness which combined are basically a measure of the stiffness and resistance to deformation of the walls, and therefore conceptually very similar to PWV.
So I think using PWV here could add more information, given this analogy to real world physics.

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What is the very hard sphere inside the eye of many common fish made of and how is it called?
Inside the eye of many common fish, like tuna, scad, snapper, actually probably all fish I have eaten, is a small sphere made of some very tough substance. This sphere is even hard to crush with teeth, and seems to be made of homogeneous material. That is after the fish is cooked, not sure how it is uncooked. It is immersed inside a quite soft, almost liquid substance inside the eyeball.
Is that the lens, or is the whole soft semi-liquid tissue the lens?
What substance is the small tough sphere made of? I imagine some type of proteins, but what type of proteins exactly?

From what you describe, it seems the hard sphere is the lens and the semi-liquid substance is the vitreous humour. Like the lens of other vertebrates, the fish lens is made of lens fibres—cells rich in proteins called crystallins.
For more on the anatomy of fish eyes, you could read this page and watch this dissection video.


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Why most small organisms seem not to be interested in any organic matter which has all moisture removed?
On the first glance, it seems that most small organisms do not exhibit any interest in consuming any live or dead organic matter if it is completely dehydrated. Regardless if the food consists of protein, fats or carbohydrates, or any mixture of them, it appears to me that removing water makes bacteria, mould or even insects not consider it food.
Here I consider organic matter which can last for years without being subject to decay by small live organisms:

ghee, made from butter by boiling off all water, lasts for a year or more
freeze-dried food, which still can have 0.5% to 3% moisture, but can last 20 years
honey, supposedly can last forever

While the humble homo sapiens will happily put freeze dried milk in his mouth, most small organisms seem not to have any interest in organic matter with ultra-low moisture:

bacteria
mould
and to a certain extent even insects

For example I noticed ants will quickly gather around any drop of fat used in cooking, which has moisture and other impurities, but will ignore clean, dry ghee.
Why is moisture removal such an universal protection against small organisms and where exactly is the boundary between organisms which can't consume dry matter and the ones which can? Are there any known microorganisms which will consume completely dry organic matter?

Just a hypothesis: a lot of these small organisms who are not interested in completely dehydrated "food" would also be ones who don't explicitly drink water (at least, not enough). Pretty much all organisms need water to live, they also lose water to the environment via urination, perspiration, or other pathways. For organisms that don't explicitly drink water, their major source of water would come from the food. So if the food doesn't contain enough water, they don't bother.

For microorganisms, the lack of water in the food may inhibit their ability to even break down the food, mechanically (too hard) or chemically (lack of solvent to facilitate chemical reactions).

TL;DR
If it doesn't last forever this is some organisms consuming it. It is a matter of ecological niches, what are the requirements (humidity, temperature, etc.) to live and reproduce
I believe we should separate the discussion in two: small organisms and microrganises
Microorganisms
Microorganisms that consume our food need to get there, either they got there from the air or they are already there. Other vectors can be insects, animals, water and soil but since this discussion is about food and we tend to keep our food protected from those vectors I'm going to ignore them.
Most of the microorganisms of interest (Bacteria, Archaea, Fungi & Oomycetes) exist in air as spores. This are analog to seeds, they are alive but inactive and need to arrive to a good environment to sprout. Spores can survive for many years, even millions of years("Revival and identification of bacterial spores in 25- to 40-million-year-old Dominican amber". Science. 268 (5213): 1060–1064.). This survival mechanisme includes dehydration and therefore rehydration is necessary for sprouting.
In addition some of these (mainly oomycetes) need free-water to live & reproduce while others require some levels of moisture.
Dehydrated organic material tends to be hygroscopic. Thus if the non-spore form of the microorganism lands on it the organism will probably loose water and die.
Microorganisms, like every organism, have niches they occupy. One of the characteristics of these niches is the temperature. Freeze-drying includes freezing which lowers the temperature below the survival temperature of many microorganisms and preserves the food. Microorganisms that grow in low temperatures grow slower so it will take more time for us to notice their presence. They still require water so the combination of freezing and dehydration provides a good protection.
Honey has a antibacterial activity in it preventing growth of microorganisms. In addition honey contains a lot of sugar and other molecules making it hypertonic to most microorganisms causing them to loose water if they land on it. Also his high viscosity prevents the free movement of microorganisms.
Small organismes
Many small organismes still need water to live and reproduce (like nematodes)
Insects are highly specified to their environment and food intake. They might not be able to consume dehydrated food.
In addition, as mentioned in the comments by Kal

a lot of these small organisms who are not interested in completely dehydrated "food" would also be ones who
don't explicitly drink water (at least, not enough).[...] For organisms that
don't explicitly drink water, their major source of water would come
from the food. So if the food doesn't contain enough water, they don't
bother.

Ants and other insects do eat dehydrated organic material like seeds, but it still has around %10 moisture
Oil is not hydrated but liquid, since it is oil and not water


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How can a viral infection (like shingles) recur in a healthy individual?
I don't quite understand how a viral infection, like chicken pox (Herpes Zoster), can recur in a healthy individual. If the body has created an immune response, how can the virus just spontaneously reactivate in a healthy adult? Or is this just an unknown mystery?
I understand that in an older person, perhaps the immune system weakens, so there is a recurrence, but shingles does recur in ordinary adults. For example, apparently Justin Bieber has had shingles and he is 28 years old.

What have you learned from reading about shingles?

I once saw a 6 year old immunocompetent child with shingles. Herpesviruses are very interesting viruses. The herpesvirus responsible for infectious mononucleosis reactivates often and asymptomaticly. It makes for some interesting reading.

When I got shingles for the second time at the age of 28, a colleague who studies such things laid out a hypothesis that shingles (zoster) has gotten more among common younger adults, in part, because of more widespread use of the chickenpox vaccine. In a nutshell, the body's adaptive immune responses wane over time. Occasional re-exposure to similar antigens can help boost that response and help maintain it for longer. Now that most kids are vaccinated and never get chickenpox, there's a lot less natural re-exposure happening for those of us who were taken to chickenpox parties as kids.


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What is the word for a small (under 50 bp) structural variant?
What is the word for a small (under 50 bp) SV? Perhaps it is MNV (multi-nucleotide variant)? Something like microindel? I do not like SNV as "single nucleotide" is not really correct and I want a indel-specific term.
SV = structural variant
bp = base pairs
SNV = single nucleotide variant
indel = insertion or deletion

@JiminyCricket. Yes, done

One can clearly find instances of "microindel" in the literature. However it does not seem to be very common.
"Small indel" appears to be the preferred term, noted here:

Typically, small indels are termed for insertions/deletions of shorter than 50 bps while longer ones are considered as structural variants (SVs) [2, 3].

For example, DeepVariant uses this term.


text:
Is heritability just slope?
Is broad-sense heritability just the slope of the line that passes through the coordinates:

(1, The phenotypic correlation among monozygotic twins)
(0.5, The phenotypic correlation among dizygotic twins
[Optionally] (0, The phenotypic correlation among unrelated individuals)?

Here, the X axis is the relatedness (0 for unrelated, 0.5 for dizygotic, and 1 for monozygotic) and the Y axis is the correlation coefficient r. Is this the same as twin-based broad-sense heritability?
(This would also mean you can estimate heritability by taking the slope of the line through only dizygotic siblings, as they don't always share 50/50 of their DNA and there will be some spread in the X dimension.)

Context here is important, slope of what? Wht kind of plot are you looking at.

@John Slope of the line which passes through dizygotic twin correlation and monozygotic twin correlation, where the x-axis is relatedness (0 to 1) and the y-axis is correlation (0 to 1).

typo: bounty should not say "twin A," it should just say "A."

In a population without genetic variation, the slope would be 0 while the offsprings are essential clones. Wording a meaningful definition of what it is, that you are calculating is not so easy. Maybe it would be easier the other way round: You start with a definition of what you want to calculate.

The broad-sense heritability is the ratio of total genetic variance to total phenotypic variance. H2 = VG/VP (as defined here), so no, unless in a very limited sense of one trait with binary values for phenotype.

@bob1 the slope from the axes described in the question would correlate with twin-based heritability very well. This makes it seem to me that we can define heritability by modifying the situation I laid out somewhat.

@KaPy3141 By "relatedness," I mean "genetic relatedness," which is similar to the kinship coefficient.

@bob1 it turns out the original post is exactly what the Falconer's formula says heritability (including for continuous values) is. So heritability is just the slope.

I found this paper, where the "heritability value" was taken as the regression coefficient (slope) between offspring height and parental height. https://doi.org/10.1203/00006450-199810000-00016. However, they also express it as fold-SD (standard deviations) further characterize it by stating the the correlation coefficient (Pearson R).

@KaPy3141 Great! This is very interesting. I have seen a similar paper comparing siblings

The original question's guess happened to be exactly how heritability is defined in the Falconer's formula.
Given genetic relatedness (1 for mz identical twin, 0.5 for dz fraternal twin) on the $x$ axis and twin correlation for the phenotype on the $y$ axis, we can define these two points:
$$\begin{align}
(x_1, y_1) &= (0.5, r_{dz})\\
(x_2, y_2) &= (1, r_{mz})
\end{align}
$$
Then, we can write the line between them in the two-point form:
$$(y - y_1) = \frac{y_2 - y_1}{x_2 - x_1}  (x - x_1)$$
$$(y - r_{dz}) = \frac{r_{mz} - r_{dz}}{1 - 0.5} (x - 0.5)$$
Therefore, the slope is $\frac{r_{mz} - r_{dz}}{1 - 0.5} = 2(r_{mz}-r_{dz})$, which is equal to the broad-sense heritability.

See also the pages leading up to page 185 in INTRODUCTION TO QUANTITATIVE GENETICS by D. S. FALCONER, University of Edinburgh. It seems he arrived at this in a similar way (by looking at genetic relatedness), though he maybe didn't make an explicit connection to slope.


text:
Is there one second messenger molecule for each hormone?
I have learnt about a number of different types of second messenger molecules including cAMP, IP$_3$, Ca$^{2+}$ and DAGs. Hormones interact with signal proteins in the cell membrane which transduces a signal into second messenger molecules inside the cell. I haven't been able to find out how the hormones map onto these second messengers. For example, there could one second messenger for each hormone and so eg. maybe ADH and only ADH triggers cAMP. Then glucagon would have a different second messenger molecule etc.
I got the impression that this is not the case however and things are more complex. Maybe each second messenger molecule has its own function in the cell and different hormones trigger different amounts of second messengers? So like, maybe ADH triggers cAMP a little bit, and glucagon triggers it a lot, but LH never triggers cAMP. And then ADH triggers IP$_3$ a lot and glucagon leaves it unchanged, etc.
Anyway that's just two possible explanations that I came up with. So, how do hormones map onto second messenger molecules?

There are typically multiple different second messenger systems used by a given hormone, and multiple hormones use the same second messenger system.
Second messengers aren't really a property of the hormone/ligand, they are a property of the receptor, so you'll want to look for information about different receptors for a ligand to know what second messengers are involved.
Take ADH/vasopressin for example: https://en.m.wikipedia.org/wiki/Vasopressin
Vasopressin binding can result in both calcium release and cAMP increases.
Same with glucagon: https://en.m.wikipedia.org/wiki/Glucagon_receptor
Specificity comes from expression, co-expression, and localization. Only cells that express a receptor will be affected by a hormone. Only receptors for a second messenger that are expressed in that cell type will be affected by second messenger changes. And finally, second messenger signalling is often local, so it's not as if calcium for example increases in equal amounts throughout an entire cell, it increases and has effects locally and is sequestered by calcium binding proteins as it diffuses away.


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Cell culture contamination
I've been culturing my cells over 2 weeks and just yesterday these things popped up in my flask , I'm not sure if they're contamination or not.uesterday they looked white and today I found one of them in black .Any ideas on what these things are?

we would need a picture to in any way ID what you are seeing.

What kind of cells are those? My immediate first reaction when I saw the image was mycoplasma. Bleach them immediately and clean the incubator thoroughly.


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What's the fastest dinosaur? and what properties make it so fast?
I am a new user.
I was curious about the fastest dinosaur that existed during the Mezozoic era.
However as I researched, via Google, I was unable to find any precise information as few of them gave the title to, Troodon, other to Velociraptor, others refer to NanoTyrannosaurus. (According to my personal research, I find 3 dinos in the first place since the run at the same speed of approximately 80 kmph, Nano T-Rex, Troodon and Gallimimus as suggested in the comments, I don't think Velociraptor is classified as the fastest because they run at almost half the speed as the fastest ones. I was looking whether is there any better estimate of their speeds which keeps only 1 at the top)
So who is actually the fastest dino (including both  Saurischia and Ornithischia dinosaurs i.e regardless of hip structure. Also I want to know whether the fastest ones are generally bipedal or quadrupedal ,Probably Bipedal because the fastest dinos fall under the category of theropods?)?
Thanks!

On our current Earth, birds of prey stooping can reach up to 200 mph/320 Kph. We can measure that with scientific instruments as it happens. What kind of an answer are you looking for considering the time elapsed since any of these creatures were around? Also consider, estimates vary and experts disagree on what might have been possible.

@JiminyCricket. Thanks for telling me about that. I think that There should be some genes, that make a theropod so fast, like myostatin inhibits muscle growth, there must be some ancestor whose mutation caused the agility of theropods in the gene pool. I would like to know about that ancestor of current living dinosaurs a.k.a birds.

You should note that the earliest/oldest DNA we have been able to recover is about 2.4 million years old and is not from fossils, but frozen in permafrost. Dinosaurs became extinct 65 million years ago and all the remains we have are fossilized, which does not preserve DNA, not even promising amber samples (a la Jurassic Park) have been shown to contain DNA that is older than a few thousand years. This means no chance of working out genes!

@bob1 Thank you for telling me that. But I have a question: Would we able to study the fast dinosaurs by studying the fossils, maybe we have found, similar hip, leg structure for the fastest ones? Then perhaps we could trace the earliest dating source and compare living specimen, birds to find the gene?

Potentially yes, but it would take lots of modeling of locomotion of each species to work out speeds - paleontologists can't even agree on whether T-rex was an active hunter and speed or if it was a scavenger and slow walker, and that's one of the more studied species.

Ichnology, (study of dinosaur traces e.g. footprints) is one of the things being explored with technology, but some limitations are the few samples available compared with the totality of extinct life, and the uncertainty of CG models built on fuzzy data.

@bob1 So according to our current technological capabilities, we won't be able to figure out the speed of the fastest dinos? Will we able to estimate it in the near future?

We can refine the techniques we use to study the currently available data including comparisons to extant species, but unless we get a time machine to get first-hand data, we're still working with speculative (but informed) models based on a limited data set.

@JiminyCricket. Thank you for telling me that. So was ichology performed on theropods, and related species?

It's like detective work of a crime that happened hundreds of years ago and without any witnesses when the evidence has been trampled by elephants. We work with the traces available and it's the best educated guesses as to what creatures they belonged to. Footprints seem to match what we know of fossils - but it's not as if they conveniently own-up to who's footprint belongs to which species. That's why there's so much varying opinion between experts, the data is, as I said, fuzzy.

@JiminyCricket. Ok, Thanks for letting me know that. So, because of our technological capabilities we won't be able to find the neither the gene nor the ancestor who caused the mutation . Please don't mind my questions since I am a newbie in this field (I have just 1 last doubt), but can we estimate it using osteology, and skeletal analysis from their fossils just how we found for some theropods like troodon and Nano-TRex?

Let us continue this discussion in chat.

There's an interesting paper that might help you get an idea of the state of the art re genetic paleobiology: Ancient DNA and paleogenetics: risks and potentiality. It might help give you an idea of the limitations that are being worked with - notice that in the long-term, the DNA degrades by itself from thermal noise. Thermodynamics puts a limit on how long it survives, the length of fragments limits the ability of reassembly on a computer. This isn't the place for discussions (however interesting), but so dig into the topic.

question for a paleontology forum. gallimimus was allegedly about 80kph.

@JiminyCricket. Thanks. The paper is quite interesting, I will read it to get to know more about it

With many competing ways of reconstructing and estimating speed, combined with how many dinosaurs just have not been studied in this way this is unanswerable.


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Is there any research on episodic-like memory in reptiles?
I've been studying the area of episodic-like memory in non-human animals and our old reptile cousins seem to be really underrepresented (or not represented at all). Is there any research that I am missing? Anything that would point to reptiles remembering what, where and when of an event? The only papers I could find were related to spatial memory (what & where), like this:
Rapid learning of a spatial memory task in a lacertid lizard (Podarcis liolepis) - by Enrique Font
Also here: @ https://doi.org/10.1016/j.beproc.2019.103963

Have you tried google scholar? if you go trough the papers that cited the one you mention you will get some related research.


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Why are Anisakiasis infections relatively rare in Japan?
In Japan raw fish are routinely eaten in the form of sushi and sashimi, and frequently no freezing or other preservative treatments have been applied. Even so, incidence of illness due to the common parasite Anisakiasis is reportedly only about 1000 cases per year. Given that very high concentrations of Anisakiasis and other nematodes are found in many types of food fishes, like mackerel, why would parasitical illness be so low?

Can you edit your question to include a source for the "1000 cases per year" figure? In fact, a source I found states that Japan accounts for 90% of global cases, which would suggest that such infections are relatively common in Japan.

When a question includes the word reportedly, the question that follows is “reported by who?” It is expected that askers include sources for their claims, especially those as specific as a number of cases. Concerning your assertion that cases are relatively rare in Japan, relatively is the operative word, there. I took that to mean “relative to other countries”, hence my comment.

Regardless, the crux of your question is essentially “Why are cases in Japan lower than expected?” I believe the answer is “it isn’t”. What is the base rate of Anisakis-containing fish consumption in Japan and other countries? What is the per-capita incidence of Anisakiasis in Japan and other countries? What is the likelihood of Anisakiasis given parasite ingestion? Each of these questions needs to be answered before you can assert that Anisakiasis is “rare” in a given population.

What do you consider rare? Japan accounts for more than 90% cases of Anisakiasis globally. The rest 10% coming from other countries like Netherlands, Spain etc. So, you need to consider those countries.

I read the freely available article:
“Anisakidosis: perils of the deep”.
It mentions that Japanese chefs are skilled at detecting Anisakis, hence infection is less likely.


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How do viruses attacking the outside of the body invade if the upper strata of the epithelial layer is metabolically inactive?
The top two layers of the epithelia, the layer of skin on the outside of the body, are the stratum corneum and the stratum lucidum. Both of these layers are metabolically inactive, in other words they are dead cells that do not manufacture anything. Since viruses rely on the manufacturing apparatus of their host cell to proliferate, how do viruses infect and penetrate these two layers?
This question pertains only to viruses that infect the body of the host through the epidermis. So, that would include viruses that cause warts, herpes viruses and viruses that infect the respiratory epithelia like cold viruses. If these different kinds of viruses penetrate epidermal defenses in different ways then that would be relevant to the answer.

This article might provide you some answers.

Viruses generally can't penetrate the stratum corneum and stratum lucidum - that's (partially) why we evolved tough skin. I could hold some virus in my hand and wouldn't get infected unless I had some sort of break in my skin like a scratch. Our skin is extraordinarily good at protecting us from the huge numbers of potentially pathogenic microbes we encounter on a daily basis.

The viruses cited are typically transmitted directly to blood, e.g., via microcracks during sexual intercourse. In general, viruses cannot infect through the skin, but rather through the mucous membranes in respiratory tract, digestive system or sexual organs.

Since viruses rely on the manufacturing apparatus of their host cell to proliferate, how do viruses infect and penetrate these two layers  [stratum corneum and the stratum lucidum] ?

Who says they do penetrate them?

So, that would include viruses that cause warts, herpes viruses and viruses that infect the respiratory epithelia like cold viruses.

The respiratory epithelium doesn't have a stratum corneum nor a stratum lucidum. There are no "dead cells on top" of that epithelium.
If you're curious how the respiratory epithelium is protected (to some extent) on its outer surface, there are antibodies "lurking" in the mucus that covers the ciliated cells. These antibodies bind their target pathogens sometimes to each other in larger clusters, which in turn enables them to be trapped in the mucus mesh network. (https://erj.ersjournals.com/content/49/1/1601709)


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Why does the body not develop immunity to rabies during the period of incubation?
Rabies typically has an incubation period of 20 to 60 days and most cases develop only after at least a month after the bite from the infected animal.
Nevertheless, rabies is nearly always fatal and the host seems to consistently fail to develop an effective immune response to the virus, even though it has been exposed to the virus for weeks or even months.
It generally is supposed that an immune response takes about 10-14 days to develop. In other words, if the body is presented with a novel viral pathogen, it takes 10-14 for the body to recognize the pathogen and begin making antibodies to defend against it. However, this does not seem to hold true in the case of rabies, which can be present and motive in the body for many weeks before causing fatal infection, yet the body still fails to mount an immune defense. Why is this?

I hate to ask, but what did you find on searching for an answer? There's a very simple reason that it's not like a lot of other viruses in terms of exposure and development of immunity. Incidentally, there are people in areas of high incidence of rabies who have developed antibodies without known exposure. The mechanism for this is unclear.

@anongoodnurse My research was to read the chapter on Rhabdoviruses and specifically the Lyssaviridae in Field's Virology. I didn't find any explanation there of why immune response does not develop.

Gosh, then I think you should read better sources... It's a really interesting virus, one I've spent a considerable amount of time reading about, and have had several personal encounters with. It's fascinating, really. There is suggestion in the literature that the longest incubation time recorded for the virus is 18 years! Can you imagine how well it hides from the body's immune system? I'd try Google if I didn't know.


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How can viruses have an incubation period of only 3 days?
Cold viruses seem to typically have incubation periods of 3 days, but from a mechanical point of view, I wonder how this is possible?
For example, if we read this viral assay protocol document: https://www.virapur.com/protocols/Virus%20Plaque%20Assay%20Protocol.pdf we can see that when a viral plaque is grown, then the plaque becomes visible in "5-7 days". So, since viruses have reproductive cycle of 6 hours, then that would be about 24 generations. Presumably each generation can only infect cells immediately adjacent to the infected cells since viruses cannot move on their own. So, the virus spreads in rings emanating outwards from the initial innoculation site.
If the visible plaque is 4mm in diameter, then we presume each generation is growing by 4mm/24 = 0.17mm which in itself is kind of suprising because a cell is only about 0.005mm in diameter, so the virions would seem to be simultaneously spreading by 0.17/0.005 = 34 layers of cells per generation. It is hard to see how they could do that without moving in some way. Maybe diffusion of some kind is occurring?
In any case, from geometrical standpoint I don't understand how a viral plaque in the wild could spread fast enough in only 3 days given what we see in the lab.

Viruses could easily be carried by the circulatory system, even if they actively infect only certain kinds of cells.

A viral plaque assay is an artificial system which limits the physical dispersion of newly released virions. It is designed to count the number of infectious virions (plaque forming units) in a given sample, not to measure the rate of reproduction or spread. Since each plaque begins with a single infected cell, the number of new cells infected with each cell burst is going to be limited by the physical proximity of cells to the infected cell, not by the number of infectious virions released.
In a living system, a single cell burst from a viral infection can release anywhere from a few hundred to up to several tens of thousands of new virions which will then be carried in all manner of different bodily fluids to infect new cells, dramatically increasing the potential number of new cells infected after each replication cycle, compared to a plaque assay.
Another consideration is that some of the symptoms of the common cold are generally similar to those common in the prodrome phase of most viral infections, so it is probably difficult to distinguish its true incubation period from the onset of any acute viral infection.


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Cell viability assay: Problems with MTT assay in the solubilization step
I am testing two compounds against 3 cell lines to determine cell viability. Two lines grow in Eagle media, one in DMEM (+10 Percent bovine serum) which contain phenyl red indicator.
I prepared 3 plates to let the compounds take effect for up to 96h. For each time point I treat the plate with MTT for 4 h, then remove the media, than add DMSO and incubate for 15 min. On the first plate it appeared to be a positive correlation between increasing concentration and decreasing cell viability. However on the second plate the trend is not as obvious. I would also assume that cell viability is reduced more than at the first time point which is not the case in a clear way or I can't see it from the data until mow. You find an image of the first plate here

On the plate columns 1-4 are cell line 1 (with increasing compound concentration), 5-8 cell line 2 and 9-12 is cell line 3. Rows A-C are triplicates of compound 1, rows D-F are triplicates of compound 2, and G+H and is just media as negative control.
For me the plate does not look good with bare eye: The first row is off completely and from column 1-4 the intensity should either decrease or at least stay steady.
I am assuming the problem could be related to multiple factors:

During media removal always some crystals will be sucked in by the pipette. I tried to avoid this by centrifuging the crystals to create a more stiff layer but this did not work well. Also tilting the plates a little bit did not work nicely.

When you're too careful not to suck any crystals in on the other hand media will remain in the well which will change concentration and also show some absorbance  due to the indicator.

I am wondering how your experiences are with with these issues with the MTT assay? I personally find it to be a huge design flaw, that you need to remove the media, witch will lead to possible problems with the quantification.
The alternative works with 10 Percent SDS in 0.01 HCl overnight to dissolve the formazan. I am also wondering if you can share experiences on this modification as well. I am likely to do this for the 3rd plate to see if the overall structure of the data is more consistent.
Alternatively, should I switch to XTT, WSF-1, MSF etc.?

The easy answer is to use acidified SDS 10 Percent in 0,01 N HCl. I added this directly, to my media and did not have any problems with crystal removal anymore. The acid will remove the coloring of the indicator. The triplet accuracy increased enormously in comparison to the DMSO approach. I would not recommend the DMSO technique at all, because you might ruin all your work. At least if media removal is involved. But you need to incubate overnight as stated in various protocols if using SDS.Also additional mixing with a pipette or a plate shaker might help if you have a gradient of color in your wells. On the other hand maybe it would be possible to add acidified DMSO, or DMF or an alkohol in acidified Form without the need to remove media.
See this publication for an overview of MTT, MTS, XTT, WSF-1, WSF-8 and different advantages and cons of each variant: https://onlinelibrary.wiley.com/doi/10.1002/fft2.44
Edit: If you have air bubbles, use gently a heat gun. The bubbles will disappear instantly.


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What makes a cancer contagious?
Most human cancers are not (very?) contagious (perhaps besides a couple of incidents). But the Tasmanian devil seems to have a form of cancer which is contagious. Now what makes the difference between a contagious cancer and a non contagious cancer in the DNA mutations of a cell?

There are two relatively common contagious cancers: Tasmanian Devil Facial Tumor, and Canine Transmissible Venereal Tumor.  Both are truly contagious cancers, in that the cancer cells themselves are transmitted from one host to the next, and expand and cause disease in each successive host.  (There was also a contagious cancer of hamsters, which has long since gone extinct, and there are some transmissible tumors in clams and oysters; the latter don't have immune systems that are remotely similar to dogs, Devils, or humans.)
It's believed that one key aspect of the Devil Facial Tumor is that Tasmanian Devils are immunologically closely related.  Normally, cancer cells from one host would be a tissue graft in a different individual and would be rapidly rejected as with any allograft.  However, immunologically closely related individuals can tolerate each others' grafts, and it's believed that this is part of what allows the Devil tumor to spread -- a lack of genetic diversity among Tasmanian Devils.

Major histocompatibility complex class I and class II genes have extremely low levels of sequence divergence in the devil population from the Tasmanian east coast (Siddle et al., 2007a, 2007b). ... The lack of diversity at MHC loci, coupled with weak responses of east coast devils to allogeneic mixed lymphocyte culture, has led to the suggestion that this population may be functionally identical at MHC loci, thus permitting the spread of DFTD as an allograft.

--Clonally transmissible cancers in dogs and Tasmanian devils
The genetic diversity explanation is widely accepted, but it hasn't been formally proven and there are a number of points that suggest that it isn't the whole story.  There are several other molecular features of the tumor that probably make it less immunogenic (see the review The role of MHC genes in contagious cancer: the story of Tasmanian devils) and the full story probably involves a combination of these things.
CTVT is different.  It's astonishingly ancient (it apparently arose in a dog, or a wolf, 11,000 years ago and has been passed from dog to dog continuously since), so it's obviously very successful at what it does, but it's not at all understood how it does it. Dogs are genetically pretty diverse and definitely don't tolerate arbitrary grafts from each other, so that's not the explanation. Lots of other possible explanations have been put forward, most of which point to various immunological features of the tumor; however, while that's clearly an important point, none of the things people have implicated are unique to CTVT -- tumors invariably have immune suppressive abilities and don't have the same ability to spread. (Going back to the Devil tumors, the low expression of MHC molecules on the cancer cells is probably a factor there too, but it's important to understand that low MHC expression is almost universal among tumors, including the vast, vast majority that can't transmit.)
Summary:

There do exist a very small number of truly contagious cancers.
The reasons for their transmissibility are not fully understood.
Genetic diversity and immune evasion are probably two of the causes.

Thanks a lot. The reading is quite diverse and very informative (read abstracts, will read the rest slowly.)

Very nice answer.

Joined just to upvote, very elaborate and interesting answer.


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Is there a kind of 'rule' which decides whether the male of female is bigger?
In human race usually males are larger than females, and probably is this for all primates. But some animals there are the females bigger, but what determines whether the male or female should be bigger. Is this just random with no logical system as evolution can be or are there some marks which indicates that it is better that the female should be bigger?

I seem to recall that some primates show dimorphism in which females are larger than males.

See Sexual dimorphism

In short, there is not a rule of thumb whether a given species will have bigger males or females. In some cases females are larger (often insects, invertebrates or fish), in other cases males are larger (often mammals and birds) but even these generalizations have exceptions (Ralls (1976)).
When a males and females of a species have morphological differences other than differences in reproductive organs, this is called sexual dimorphism. These dimorphisms can be thought of as adaptations which have evolved due to a specific evolutionary pressure.
In males, larger sizes can evolve from sexual selection on males in competition with other males for mates. Simplified, the bigger males are better competitors. In females however, larger sizes can evolve from a number of different pressures, but rarely due to competition for mates. More common pressures resulting in larger females are rearing success, competition for resources other than mates.
Whether males or females of a species are bigger is certainly not random, but rather a precise outcome of numerous trade-offs and benefits of being bigger.


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Why are mammals not very often (never?) toxic?
Often reptiles or insects have poison to defend themselves or to offend their prey. But I don't know any mammals which are toxic. So are there any mammals using poison and why aren't there so less/any?

The platypus has a venom, there's that.

A list of venomous mammals is available at https://en.wikipedia.org/wiki/List_of_venomous_animals#Mammals. It could be worth noting that, although there are nine venomous mammal species listed amongst the ~5500 species of mammals, there are no venomous birds amongst the ~10000 species of birds, which makes avians an even more extreme group in this regard.

Note that "toxic" and "venomous" are not the same.  E.g. a rattlesnake is venomous but not toxic (you can eat it), while a puffer fish is toxic (you die if you eat it) but AFAIK not venomous.

Answering the first part of your question: The cuban solenodon has venomous saliva. It's a mammal -- rather shrewlike in appearance. But yes, venomous mammals are rare!


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What causes us to see white light?
Humans have three cones of color light, red, green and blue. If the region of the green cone is hit by his photons we will see green light. Now we don't really receive green light but our eyes and brains are 'making' it to look green. But if all the different cones are hit by their photons we will see white. Now the question is why is that white? Why isn't our brain just keeping these different colors, is this a kind of black out of our brain or an overwhelming of input making us blind etc?

Our brain doesn't really use cones to detect green light, and detect red light, and detect blue light. Each cone can be excited by many wavelengths; they're just most excited by green, red and blue wavelengths respectively. The brain then uses the different information it receives from all three cones to infer the wavelengths of the light it receives. It doesn't look at the absolute excitation of a cone so much as the relative amounts of excitation different cones get.
So for example, if the brain sees the green cones are very excited and neither the red or blue cones are, the light is green. If the green cones and red cones are equally excited but the blue ones aren't, then the wavelength may correspond to yellow (a wavelength that excites both red and green cones in the same middling way, and blue cones not much at all), or there could be a combination of green and red wavelengths; and in fact both are seen as the same thing by the brain. That's why colors can combine to make other colors.
This is OK insofar as the point isn't to calculate the exact wavelength of incoming light, but to tell the difference between certain wavelength compositions because that provides more information about the world.
So the reason we see white when hit with all wavelengths is the same reason we see any color when hit with any combination of wavelengths.
As for why "color" feels like a single unified perception and not a combination of three numbers, that's a general aspect of perception in general. We don't sense the raw data our brain gathers; we sense how the world is (as guessed at by the brain from the raw data it gathered).
As such, the colors we see aren't even strictly determined by the wavelengths of photons hitting the cones; because colors are a proxy for what the things we see are like, the brain will not only look at the light it receives, but also use its own assumptions about the world (is this thing in shadow, in bright light, mottled light, colored light, near, far...) to guess at what the color "really" is given the wavelengths it has received. This gives us a sense that color is inherent to objects and doesn't depend on lighting conditions, which is generally accurate (an apple's redness is a feature of the chemicals at the surface of its skin, and those don't change with the lighting conditions).
That's where illusions like that of the blue-black or white-gold dress come from: sometimes you get ambiguous stimuli, where the wavelengths hitting the eye could correspond to a black and blue dress in bright light, or they could correspond to a white and gold dress in shadow, and in that case the brain picks one, and you see the dress as the color your brain decided it must be. Except because the stimuli were ambiguous, different brains (or the same brain at different times) will make different guesses, resulting in very different perceptions. But the guessing is actually what happens all the time, it's just that usually the stimuli aren't as ambiguous so all brains agree on their guess, and the guess does correspond to reality, and so the illusion that we perceive the world directly with no filter remains unbroken.


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Is tunneling of a proton in our DNA a cause of mutations?
Our DNA strands are tight together by hydrogen bonds. Can the proton of Hydrogen tunnel to the other complementary strand, and by this during the replication bind to a different/wrong nucleotide, causing a point mutation?

Perhaps of interest, though not specifically about complementary strand: Florian et al. 1996 (a highly cited paper) http://pubs.acs.org/doi/abs/10.1021/ja951983g

Keto-enol tautomerism involving proton transfer within a single DNA base can lead to mispairing and mutation during replication.  This is touched on in the previous citation provided by tsttst as well as this section from An Introduction to Genetic Analysis. 7th edition: https://www.ncbi.nlm.nih.gov/books/NBK21897/  I have not found a clear statement of whether the proton transfer is over sufficient distance to constitute "tunneling".


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Do ants also use the Earth magnetic field?
A lot of animals, specially birds use the Earth magnetic field to orientate on their flight across the Earth. Now some scientist suggest that ants has on their antenna a kind of magnetite crystals by which they also can use the magnetic field. But for what would and could an ant use this huge magnetic field, while they just walk for only meters a day?

Hard to say, but for at least one ant species (see below) it seems to be an orientation cue for (relatively short-distance) migration (even if you're only going a few meters, it can be important to walk in a straight line!). At present it seems we know something about the proximal mechanisms of magnetoreception, and a little bit about the observed behavioural patterns, but don't have much more than informed speculation about the ecological/evolutionary advantages of this form of spatial orientation.
Searching "ant magnetotaxis" gets to this article on magnetotaxis in the migratory ant Pachycondyla marginata:

The influence of geomagnetic field changes on the behavior of ants has been studied in the species Solenopsis invicta (Anderson and Vander Meer, 1993), Formica rufa (Çamlitepe and Stradling, 1995), and Oecophylla smaragdina (Jander and Jander, 1998) ... Another migratory insect species is the ant Pachycondyla marginata, which has very peculiar habits: a diet of living termites and migration in a preferential direction (Leal and Oliveira, 1995). These habits make such a migratory ant very attractive for the study of biomineralized magnetic materials.

From Leal and Oliveira 1995 ref above:

Migration by P. marginata colonies lasted over 2 days and covered distances of
  2-97 m (n=48).

Selections from Acosta-Avalos et al. 2001 Naturwissenschaften:

abstract: Migrations during the dry/cold season are significantly oriented 13 degrees with the magnetic North-South axis, while rainy/hot migrations do not exhibit a preferred direction. This result is discussed considering the hypothesis that P. marginata ants may use the geomagnetic field as an orientation cue for migrations in the dry/cold season.
Given that colonies resume nest relocation late
  in the afternoon of the second day, most of the migratory
  process takes place under darkness conditions.
On  the  other  hand,  nest  relocations  in  the  dry/cold
  season can be considered as typical migrations.
The  use  of  geomagnetic  cues  is  more  commonly  associated with darkness conditions, as reported for mole rats
  (Marhold et al. 1997) and also proposed for bumblebees
  (Chittka  et  al.  1999).  As
  P.  marginata
  ants  start  the
  migratory  process  in  the  afternoon,  they  can  use  any  of
  those  cues  in  their  orientation  during  the  migratory
  journey. However, it is intriguing that they prefer an axis
  around the North–South axis to migrate. The only possible
  cue  to  give  this  information  under  all  conditions  is  the
  one  provided  by  the  geomagnetic  field.


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How do special NK cells get to the uterus?
When an embryo is creating a placenta in the uterus, some special kinds of Natural killers cell of the mother will move and gather towards this placenta (for exmaple for growth components increasing blood of the placenta). But how do these NK cells know where to go....do they kind of 'smell' the uterus?

They are attracted via chemokines, which are molecules that NK cells sense and move towards the increased chemical gradient.


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Does cheese contain cells of animal stomachs?
When cheese is made with calf rennet, is it possible that the cheese contains cells of this calf (stomach)?
Dried and cleaned stomachs of young calves are sliced into small pieces and then put into salt water or whey, together with some vinegar or wine to lower the pH of the solution. After some time (overnight or several days), the solution is filtered. The crude rennet that remains in the filtered solution can then be used to coagulate milk.
Does this filtering exclude all stomach cells of the calf?

Somehow I doubt any whole cells exist after the process, the whole thing seems designed to break living tissues down and to denature protein. That being said calf stomach cells may be tough so +1.

@Duckisaduckisaduck - One would hope it doesn't denature protein. the whole puropse for the sacrifice is to obtain a complex set of enzymes. Denatured enzymes would be useless.

@anongoodnurse My error, I read too much into the adding vinegar part.

I’m voting to close this question because it relates to food analysis rather than a biological problem.

95% of cheese does not use animal rennet.
Many cheeses use no rennet.
Of the cheese that do use rennet the vast majority use rennet derived from bacteria, fungi, or plants. often because it is cheaper, easier, and more humane.
Of cheeses that do use rennet 5-10% of it makes it into the final product, so yes if your cheese uses calf rennet the cheese likely contains calf enzymes.
https://www.vrg.org/journal/vj2008issue3/2008_issue3_update_renet.php

Yes it is possible, filtering is unlikely to be fine enough to remove all cells (though the presence of intact cells based off of the culturing methods is unlikely), note though that modern methods of rennet extraction from stomachs are different than what you described. There are also non-calf rennet made with everything from fungi and bacteria to vegetables. Source

It all depends on the filter. Standard filters for preparations of this sort will be 0.45 micrometers (um), which is definitely smaller than a mammalian cell at 100-300 um, and even smaller than most bacterial cells at 0.5-10 um.

Please post references (ideally to primary literature) that support the part of your answer that is actually relevant to the OPs question. Without that support, your answer is indistinguishable from opinion and thus not a good fit for this site. Thanks.


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Why are human immune systems comparatively weaker than other animal immune systems?
Humans get sick on such a regular basis and animals will hardly ever get sick. Animals are typically exposed to the same pathogens as humans, yet a dog won't have a cold or the flu twice a year, with other miner health issues occurring regularly in between. I understand that humans are very structurally flawed due to some evolutionary processes, and I'm just wondering why our immune systems seemed to have taken a pretty big hit as well.

Sorry, but this is opinion based nonsense. Animals get sick as well and our immune system actually works pretty well in protecting us from the world.

Your pet dog likely isn't exposed to the hundreds/thousands of people a day that you are as you commute, perform your job, run errands, and just live your life. Your claim that humans are "very structurally flawed" is silly: compared to what? In what way? Do you have a citation for that statement? Do you have any evidence to support your claim that our immune systems are weak?

If animals could complain loudly in human languages, you'd probably hear a lot more about the illnesses they get.

@Chris that was very harsh.

The question probably has a mistaken premise.  Human immune systems are pretty similar to other species, at least in major structural elements. Our differences in adaptive niche have led to differences in some aspects; humans don't fare well with rotting meat, for example, while a scavenger can eat it without a problem.  Many scavengers have unique adaptations for dealing with this.  Dogs do not, however. Humans too have a unique niche, which is highly social, and thus have a well-developed social immunity (sometimes called a behavioral immune system).
Many animal populations have endemic diseases at fairly high levels.  Koalas, for example, famously have a very high level of chlamydia.  Sea lions rookeries often have infections, bats can have high levels of rabies, and so forth.  Lots of animals do get lots of infections.
However your question specifically on dogs is interesting, and probably gets to a risk factor which is very human.  Humans come into contact with far more other humans (and thus, likely more infected humans) than dogs encounter other dogs.  Diseases which spread through close proximity, such as airborn upper respiratory viruses, spread more readily in humans than these relatively isolated animal populations.  Combine that with a concerted effort to wipe out in animals any diseases which can transmit to humans, and pet infections are indeed relatively rare.  This is not due to the immune system per se, but the social factors associated with each organisms' niche.

+1 - I agree with most of this, but not the last paragraph. (My vet bills speak volumes; only $240 says "anaplasmosis.") Pet infections aren't rare; house pets are vaccinated against many illnesses, and aren't exactly vocal about the rest (just as the koalas don't complain about chlamydia.) The feral population are a pretty mangy, parasite infected, ill (esp. cats) bunch. Dogs are interesting because of their close association with man for most of their existence.


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What's this aquatic bug?
I have a small freshwater aquarium at home with only some aquatic plants at the moment. In the summer, I put some mud and sand from a local pond into the tank. At some point, I noticed a strange moving "segment" of plant:

Here is a video of it moving right under the surface of the water:
https://www.youtube.com/shorts/QbXv4QFDJpE
If you look closely, you can see that the "segment" is actually made from several smaller segments of a stem of an aquatic plant. In other words, this little creature chopped up the plant, then assembled this little "tube" for itself to hide.
Few weeks later, it apparently disassembled the little house and created a larger one from leaves:

Here is a video of it:
https://www.youtube.com/shorts/sraLS-XHfrM
It basically this little leafy house everywhere and can move up and down the water column. I think it feeds on different plants because I can see some visible damage in the tank.
Can you identify this creature? The location is northern Europe.

Those videos are great! It's some sort of caddisfly larva, known for the cases they create, but as there are ~14,000 species, I can't begin to say which one. Maybe someone else will know. :)

@anongoodnurse I would be quite content with just knowing the order or family! And yes, I think you are exactly right after reading the wikipedia page :)

in norwegian we call them vårfluelarver(spring fly larvae),one way to identify them is from the materials they use in their "house"different types use different materials,some use grains of sand other ones use dead leaves or as in your picture green parts of plants.


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Spider ID: What is this?
This crawled on my husband. It didn’t bite him, he was able to swat it away so that’s why it looks a little messed up. I honestly just want to know if this is poisonous. We live in AZ, Goodyear area and there’s usually only regular house spiders running around. There were no marking on the abdomen or thorax, the legs seem 2 toned but I couldn’t get a good look. It wasn’t more than an inch big but it has a thicker build.
enter image description here

This looks to me like a female of the common and harmless Southern House Spider, Kukulcania hibernalis (see below).
https://bugguide.net/node/view/508965

Yes, nice match.


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How to correctly assess the impact of invasive species on a community using the diversity index?
How can the impact of invasive species on a community be correctly assessed using the diversity index if the abundance of the target species, i.e. the invasive species, is not used to calculate the index?
We investigated the impact of two invasive alien plant species (goldenrod S. canadensis and S. gigantea) on plant diversity in semi-natural grasslands. Plant diversity is expressed in terms of Hill diversities (Hill species richness, Hill-Shannon diversity and Hill-Simpson diversity). We wanted to investigate whether the invasion of the perennial goldenrod species affects the species diversity of three plant guilds - herbs, graminoids and bryophytes. Therefore, we calculated Hill diversity indices separately for each guild. We excluded Solidago species from the species richness estimates for forbs (Solidago is a forb), as we wanted to assess the impact of invaders on the number of remaining species. However, for the Hill-Shannon and Hill-Simpson indices of herb diversity, Solidago was included because it would be meaningless to calculate these two indices without considering the abundance of Solidago in the invaded plots. The Hill-Shannon and Hill-Simpson diversity indices of graminoids and bryophytes do not "take into account" the abundance of Solidago, but an effect of Solidago invasion on the diversity of graminoids and bryophytes can be expected.
We found that invasion by Solidago spp. had the most pronounced negative effect on forb species richness and diversity. On the other hand, graminoid species richness and diversity were not affected by Solidago invasion; a similar pattern was observed for bryophytes.
While the Hill-Shannon and Hill-Simpson diversity indices of graminoids and bryophytes are mathematically sound, I think they are not (bio/eco)logically sound because they do not "take into account" the abundance of Solidago. (Or am I wrong and this approach is OK?)
What is your opinion?
How can the effect of Solidago on the Hill-Shannon and Hill-Simpson diversity indices of graminoids and bryophytes be assessed in a logical way? Or is it just a matter of interpretation?
I was thinking of something like taking Solidago into account when calculating diversity indices in the same way as covariates are used in a statistical model. But I don't know how to implement this...

My best recommendation would be to consider what each measure is actually telling you, and only using that measure for an appropriate question. Abundance and diversity are different things. As you recognize, a diversity index can tell you, for example, how the mix of grasses changes, but not whether grasses overall increase or decrease. If the question of grass abundance is important, then just measure that directly.
When faced with analytical decisions, I would go back and consider the core question of your research and what is motivating your analytical decisions. Why not calculate overall species diversity? What would it mean to include or exclude Solidago from that calculation? Does it make sense to include the invasive as part of diversity? What about the other non-native species in your plots?
You will likely need multiple observations to describe the important aspects of your results. You might describe the outcome by saying, "Invasion by Solidago had little effect on the mixture of grasses present, but reduced overall grass abundance by X%." You would then use the index statistic and the abundance statistic to support that claim.


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Does the brain always think of an appropriate response when reacting to a stimulus?
Does the brain always think of an appropriate response when reacting to a stimulus?
For example, when seeing things, does the brain have to think of an appropriate response to the eyes?

From the two answers seems this really unclear question.

This question seems sort of oddly upvoted and answered - it is pretty low-quality and unclear what you are asking compared to the normal standards for Biology.SE. What does "appropriate" mean?

Well, not always but most of the time; reacting to stimuli is what defines the nervous system and the part of the nervous system that includes the brain is called the 'central nervous system' or CNS. Reactions to stimuli (nerve impulses) don't always have to pass through the brain as the CNS consists of the brain and the spinal cord. This means that in the case of thinking, if what you see (or sense) is something harmful (a man with a knife, feel extreme heat) then you will react without the nerve impulse having to pass through your brain (instead it will simply pass through your spinal cord). This is because the body does not need nor want to waste time thinking about an obvious and protective response. This reaction that requires no conscious thinking is called a 'reflex reaction' or an 'automatic reaction'. If you want to know more about this you should probably look into the nervous system.

If you take the stimuli as light entering the eye, then this answer is a bit misleading, since even basic object recognition (e.g. to identify dangerous objects) is going to be performed by visual cortex in the brain. Yes other parts of the response may not be in the brain, and even if in the brain, it is not too clear what the OP means by "think".

@NeilSlater: The contraction of the iris when the stimulus is bright light entering the eye is an interesting one. It does involve the midbrain, so it's not like the knee-jerk reflex that involves only the spinal cord. But it might serve as an example which the question doesn't consider under the heading "the brain thinking of a response", if "thinking" is intended to refer to activity of the cerebral cortex (including image-recognition). I do agree with you though: this answer says that the reaction to seeing a man with a knife involves only the spinal cord, not the brain, which is false.

... in fact I think arguably the retinae could be considered part of the brain. In any case they connect to the brain via the optic nerves, and the spinal cord isn't in that path at all.

@Steve Jessop: Not only is it false, there's still the whole question of whether the response the brain comes up with is actually appropriate.  Present the same "man with knife" stimulus to a random sample of people, and I think you're likely to get a wide range of responses.

@jamesqf of course it goes without saying that each individual's reaction will vary due to several factors: situation, environment raised in, personality, self-confidence, etc. However, it I no question that every single person WILL react and upon impulse too; since not a single person will do nothing at all (obviously)

@Lucas Dyson-Diaz: I don't know about that.  Seems like the reaction of many people to that sort of situation is simply to freeze, or "run in circles, scream and shout".

@jamesqf or fight back or call for help or team up on him or throw stuff at him from a safe distance or call the police or don't call the police or accept your death or try to reason with the man. There are more responses to any situation than just stand there or don't (I just named 8).

@jamesqf: I don't put too much weight on the word "appropriate" in the question: surely the question here is not intended to be, "are humans always right about everything?". If so it belongs on Philosophy. If you see someone with a knife and shoot them, then I think for the purpose of this question that was the "appropriate" response, that is to say the response the organism makes to a particular stimulus, regardless of whether the jury eventually decides it was "appropriate" or "inappropriate".

@Steve Jessop: But the OP is specifically asking about "appropriate response", no?  Certainly we could go into philosophical/legal discussions about what reaction is appropriate to any given circumstance, but I think it's pretty obvious that there are some reactions that are inappropriate by any reasonable standard.

@jamesqf . Whether it is appropriate is not a decision for any one or two people to decide. Especially in such a desperate and life-threatening situation, there is little you could call inappropriate (other than killing the man, possibly, however that could philosophically be argued as appropriate too).

@jamesqf: I would say "no", the questioner is not intentionally asking specifically about the "appropriate" response in the wider sense that you refer to when you describe "scream" as an inappropriate response. I think they just mean "appriopriate response" in a sense something like, "the neural response necessary to make the organism do whatever it is that it does in response to the stimulus". So if the organism screams in response to knife-wielders, then the "appropriate response" is to signal the lungs, throat, face, etc. Even if screaming is a dumb idea by any reasonable standard.

No:

Optical illusions trick your brain and elicit an inappropriate response. Of course optical illusions don’t need to be engineered, they abound in reality (remember The Dress that went viral two years ago)?
In addition to optical illusions, other senses can be tricked. There are auditory illusions, an illusory sense of touch, etc.

I can barely look at that. What's actually going on in it? It's like it's moving. Wow! It's weird. Now it's sliding. It's worse if you focus your eyes, if you unfocus your eyes it's easier to look at. I still can't figure it out. What's it doing?

@DanielCann It’s really just straight, equidistant, parallel lines with black/white coloured square boxes between them. The sequences of boxes in each row are offset at different distances from the left side. That’s all there is to it.

How do you know? We're both human, and it's an optical illusion which is designed to deceive humans.

@DanielCann Well I mean you can simply check with a straightedge and a set square/triangle/compass …

@DanielCann: or assuming you trust your PC not to conspire with Konrad to trick you, zoom in on the image in any image-editing program. The illusion doesn't work on a small enough section. Then you'll see that nothing's moving and everything in any given small section of the image is straight and square. Pan around the image until you're convinced it's true everywhere.

The answer to the question is if thinking is always a response to some external stimuli depends if we consider the memory. Thinking about the event in the past is surely possible many years after the stimuli is long gone. Continuous stimuli from the environment may not be required for the thinking process itself as spontaneous brain activity exists as well.


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Do most plants need long photperiods in order to germinate.
For a plant to perform photosynthesis, it needs long photoperiods, right?
But what about for germination, do MOST seeds need long photoperiods for germination?
Thanks


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Diffusion to center of the cell
I have been researching about the ratio between cell membrane surface area and volume.
Obviously, when the volume increases faster than the surface area, and up to a certain point, there is comparatively less membrane for substances to diffuse through and comparatively more organelles that need these substances.
http://scienceline.ucsb.edu/getkey.php?key=5203
The resource above says that "These nutrients then need to get to the center of the cell."
My question is: why do the resources get depleted before they reach the center of the cell? Aren't all the important organelles in the center anyway? For example, wouldn't the glucose go to the center of the cell, and not be used up "on the way"?
And just to be clear, the "center of the cell" refers to organelles like the mitochondria, nucleus etc?

The center of the cell in this case is a way to say "the nutrients arrive to every part of the cell", and should not really be taken literally as "the center". If the cell is modeled as a sphere, with the nutrients diffusing in from the outside, the whole sphere would be filled with nutrients when the nutrients "arrive to the center". Figure 1 shows how the nutrients would diffuse from the outside layer further in. It is like saying the whole glass would be filled when the water "arrives to the top". It does not particularly mean that the vital organelles are in the center, but is just used to illustrate the fact that nutrients diffuse into and can reach all parts of the cell.

Figure 1: an illustration to show how nutrients would diffuse from the outside to the center of the cell, filling the cell with nutrients. This image is trying to model a cross-section of a circular cell. The nutrients would for example enter from around the green layer, and gradually get to the middle/center dark blue area.
Resources may get depleted before they reach the "center" of the cell because of the rate of diffusion, and also because metabolic processes may convert the resources into other molecules (e.g. converting glucose into ATP; glycolysis happens in the cytoplasm, and can happen in any part of the cell. If that particular glucose molecule is used up, then it will not be able to travel to the center).
Moreover, the "important organelles" are not in the center in particular. If you have seen an image of a typical plant cell for example, most organelles are around the walls of the cell (Figure 2).

Figure 2: a typical plant cell electron micrograph.
Also, you must remember that the Surface Area to Volume ratio is also a restriction for the effective diffusion of waste substances out of the cell. The small volume / big surface area is not only because nutrients have to diffuse in, but also because waste products (like CO2) must be able to diffuse out of the cell, through the membrane.


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Where does the energy required to turn ADP into ATP come from?
My teacher states that in order to convert ADP into ATP, energy from respiration is required.
However, I watched a video which states that energy from the son is used to turn ADP into ATP.
Which is correct?

Both are technically correct, and both of these claims are happening in different organisms

This is a site for "biology researchers, academics, and students" where questions are expected to be accompanied by demonstration of one's own efforts to solve a problem. This is the sort of very basic question that is best addressed to your school teacher. @SonicSplasher  hinted at the answer, but you should flesh that out for yourself, and in future consider that two apparently different statements might both be correct in different contexts. So you will need to  ask yourself what contexts they were made in.

@SonicSplasher actually both can be true in the same organism...

@theforestecologist yup in the case of photorespiration

This is a common problem when asking about the explanations for things that happen in a biological context.  When you ask for why something happens in biology, the answer to that question depends on what, specifically, you want to know.  For example, the same question, "Why can humans see more colors than dogs?" can be answered using a physiological mechanism (Humans can see more colors than dogs because we have an additional cone type in our eyes), or an evolutionary explanation (Humans can see more colors than dogs because our ancestors were under selective pressure to be able to identify ripe fruit).  Both of these responses would be correct but they are answering from different perspectives.
The question of where the energy comes from to phosphorylate ADP is another one of these questions that can be answered in a couple of different ways.  The immediate mechanism for providing this energy is the proton gradient between the intermembrane space of the mitochondria and the mitochondrial matrix in the case of Cellular Respiration and the proton gradient between the Thylakoid Lumen and the Stroma in the case of Photosynthesis.  But where did the energy ultimately come from?  The sun.  In the case of Photosynthesis, it is energy from the sun that drives the photosystems that generate that proton gradient in the first place.  In the case of your own body, you either eat a plant or eat an animal that ate a plant that got its energy from the sun in the same way, and then use the chemical energy contained in that food to sustain your own proton gradient.  Either way, the energy ultimately came from the sun.  It's just that the proximate (immediate) explanation is a chemical one driven by a chemiosmotic gradient maintained either by sunlight and water in the case of photosynthesis or sugar and oxygen in the case of cellular respiration.


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Is the reason why lipid-soluble molecules can pass through membrane because
I have been studying about cell membranes and how water molecules are able to pass through it. (https://www.wiley.com/college/boyer/0470003790/animations/membrane_transport/membrane_transport.htm)
It is clear that the water molecules can squeeze through openings in the bilayer. My questions are:
1) Do small, non-polar molecules also enter through these gaps?
2) It states that the whole structure moves when vibrating. Does that mean the hydrophobic tails also move? If so, how do the non-polar molecules dissolve?
3) The top of the membrane is hydrophilic. How do non-polar molecules get past these hydrophilic heads into the hydrophobic interior core where they can be dissolved?
Thanks a lot!


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Why is this small fly trying to live in my speakers?
While having the window open today, I discovered a small insect repeatedly flying into my room. It had seemingly discovered that a small hole for the power LED to shine through was the perfect size for it's Torso and it couldn't help but repeatedly fly into there.

The location is Germany, this happened around noon. I'd estimate it's length to be around 5-10mm. The hole is plugged at the end and the insect could fit most, but not all of it's body inside.
After I taped the hole shut, it still kept returning for hours. It really really wanted to get in that hole it seems. All of the other perfectly adequate holes in my room wouldn't do.
I realize that the picture is probably too bad to positively identify the exact species. However, I'm much more interested in an explanation of this type of behavior more generally:

What general type of thing might this be? A friend thought male mosquito, I thought it looked more like a tiny wasp. However neither of those seem like they would have much use for the hole. Fungus gnats also seem to mostly just lay eggs in moist soil, which my speaker is not.
What might it have been trying to do? Why did it love that hole so much.
How did it keep knowing where it's favorite hole was hours after I taped it shut?

I don't know what the insect is, but it was probably doing something like making a nest/home in there or laying eggs. Sheltered, warm...

@bob1 I figured it was something like that, but I was struggling to find any examples of wasp-like creatures that built nests like that. They mostly seem to just shoot their eggs into their host of choice and fly off.


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How does fat produce more energy than glucose while the amount of energy released by glucose is more than that of fat?
According to my book Concise Biology Revised edition of Selina Publication for Class IX, "1 mole of glucose releases 686 kilocalories of energy". It's also mentioned there that " They produce more energy than carbohydrates do - one mole of fat releases 9.45 kcal of energy".
I think that the measure of the amount of released energy has been messed up. Some sites say that "1 gram of fat releases 9.45 kcal of energy."
But, I would highly appreciate it if anyone could explain it in a detailed manner (probably through mathematical calculations) and help me to know the correct value along with unit.

Check that you have your units correct.

Yes, that's what written in my book.

Welcome to SE Biology. Please read the Help on asking good questions. There are two points I would make. 1. You should give full details of your book, and verbatim quotations of the sentences containing the points at issue. We need to be sure you are not misinterpreting what is written, and may even be able to check the context. I personally would be suspicious of a book that talked about compounds “releasing energy”, or referring to “fat” rather than a specific triglyceride, for example. 2. We expect posters to try to answer their own questions. Have you done an Internet search on this?

I have edited my question...is it okay now?

A triglyceride can produce 450 ATP compared to glucose's 32. Triglycerides win in energy production.
TL;DR
One pyruvate molecule ultimately produces 15 ATP. Glucose produces 32 pyruvate for a total of
15 X2 ATP + 2 ATP = 30 +2 =32 ATP
per molecule of glucose including the 2 ATP generated by anaerobic respiration.
Triglycerides are a glycerol molecule linking 3 fatty acids. Each fatty acid has 16, 18, or 20 carbons in its composition, which is convenient, because pyruvate is a 2 carbon molecule.  fatty acids can produce 8, 9, or 10 pyruvate molecules. So fatty acids can produce 15x 8 ATP = 120 ATP. A glyceride, having 1,2,or 3 Fatty acids can produce up to  30 pyruvate molecules.
15 X30 ATP = 450 ATP
One triglyceride> 450 ATP
One glucose molecule> 32 ATP
Fatty acids have the potential to produce  more ATP than glucose  could hope to produce.

To answer the first question a little better: glucose gives quick energy. It is broken down to create 2 ATP for a muscle, say, or the brain, for example.


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What kind of very tiny bugs are these? Please help to identify!
The are very very tiny, finding number of them in my bathroom and bedroom, Difficult to see on non- white surface. Difficult to click pictures, This is best I can come up with.
Location - MD, USA

Are these bird mites?

That's a good guess based on coloration, etc., but it's hard to imagine why a bird mite would be walking around on its own... I've only ever seen them after handling a bird-in-the-wild.

We had a bird nest just below our bedroom window, I never paid attention, till I found these in my bedroom and started panicking. They must have entered through he cervices' of the window.

If the birds recently fledged, they are probably mites left behind in the empty nest, now looking for a new host. The invasion should disappear soon.