text:
Why do guard cells open stomata when they are swelling?
As the concentration of potassium inside guard cells increases, water enters the cell by osmosis.
But why does the swollen causes the stoma to open?
Does it relate to the thickness of the cell wall?
If so, how?

Welcome to Biology.SE! We encourage you to do some research on your own and then, informed by what you have learned, ask any questions you still have (ideally with references to reliable sources). For this question, you can find answers easily from reliable sources and so this question fits the criteria for "homework". We also expect you to search for answers on this site before posting! ——— Please take the [tour] and then go through the help pages starting with [Ask] questions effectively on this site. Thanks!

@tyersome, thank you for telling me that. However I have tried to do some research on it and I know how the concentration of potassium ions affects the cell's water potential which makes them swell or shrink.But my question is how swollen change the shape of cells and therefore open the stomata---why don't cells come more closely when swelling as they have larger volumes? ( and unfortunately I can't find the answers on the internet.)

Sorry I should have looked at that page closer, you are correct it doesn't actually answer your question. This site seems to have a reasonably clear explanation, though it doesn't address all types of stomata. Does that help?

The link that @tyersome mentioned in the comment does a great job of answering your question. In the event that you read it and still have some confusion, here is a metaphor: imagine guard cells as two modeling balloons (the long kind that clowns use to make figurines) that are slightly inflated and attached together at both ends. Since they are only slightly inflated, they are able to sit flush next to each other. Now let's say you inflate the balloons. Since they are still attached to each other at both ends inflating them will cause them to bow outward and away from each other. The expansion will cause there to be space between the two balloons.
This is not a perfect analogy since guard cells have a varied amount of rigidity in their cell walls contributing to the shape when water enters. But maybe this can help you visualize the concepts introduced in the link above intuitively.


text:
the blue whale calf gains 200 pounds per day- amazing biotransformation
MY main research topic is TIME in relation to biology the blue whale calf CONVERTING mothers milk to fuctional bio-mass(up to 200 pounds/day) IS amazing-if this secret could be uncovered and used in relation to crops/livestock it woud be a game changer QUESTION does anyone have knowledge of ANY research pertaining to this  (delta time-biomass accumulation/growth genetics)?

MY main research topic is TIME in relation to biology the blue whale calf CONVERTING mothers milk to fuctional bio-mass(up to 200 pounds/day) IS amazing-if this secret could be uncovered

Wikipedia says they weigh 40,000 lbs when they finish nursing, so I think the "secret" is to be really, really large.  Relative to body mass, gaining 200 pounds a day is actually very slow for a mammal.  Human babies grow faster than that.

It’s the “relative” bit that is important here.

you need to slow down a bit and REALLY think  about this as a biologist (are you one?)the mothers milk goes into the calf gets  broken down then absorbed the calf is taking in "raw material"and digesting it and gaining weight of 200 lbs  per day(BIOTRANSFORMATION  from mixed protiens+sugars [lactose)per day the "raw material"  is transformed to bio active physiological cells YOU DON'T think this is amazing in a big picture stem cell world? how much does a human leg weigh?(axolotl/starfish/worms/lizard tails)20  lbs?  TAKE the PROOF of the blue whale calf and a human leg could be re-grown 1DAY

@hyperchronos12 Asking people's opinions is offtopic here.  Stick to biology questions.

your community lacks scientific imagination and fails to project into the future---which is in some way good i will be the one going to sweden and stand on the carpet

i am not "asking for opinions" i am attempting to make clear the original question of  TIME vs-BIOMASS  accumulation, i used the blue whale calf as a proof of the possible   hopefully the readers have an understanding of genetic engineering/pluripotent stem cells/axolotl(ability to regrow severed limbs THE genetics that enable the blue whale calf is my interest-and the transfer  of such we must have an imagination quality in science FIND proofs first axolotl  CAN REGROW LIMBS(concept proof)   blue whale calf gains 200 lbs/day(concept proof) genetic engineering to regrow limbs  NOT PROVEN/YET

@hyperchronos12 The developmental genetics of mammals is an active area of research.  If that is what you're interested in knowing about, narrow down your inquiry to some specific questions and then post them.

master question  # 1 have the blue whale    "growth genes been isolated and cloned" ?-QUESTION #1(a)--  have the genes for the stomach/intestines/liver been elucidated that enable these systems to up-take massive amounts of proteins/fats/sugars in a short period of time-? Q #1(b)[bio physics]  is this massive conversion of raw food to bio active cells, exothermic-for which a water borne creature could only withstand?

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text:
If massive animals live longer, why do humans with gigantism die younger?
What I mean is humans suffering from gigantism (type 1 neurofibromatosis, Marfan syndrome, X-linked dominant acro-gigantism, et cetera) rarely live more than 5 decades (50 years).
The same can be said to wolves: wild ones rarely live more than 9 years, and domesticated wolves (dogs) can live up to 20 years if they are small like chihuahuas, beagles, and toy poodles, and no more than 7 years if they are massive like great Danes, mastiffs, and Rottweilers.
But, at the same time, horses can live 3 decades (30 years), but hamsters only live 4 years.

You are mixing gigantism, which is an anomaly, and the normal animal size. Wolves arenot chihuahuas with gigantism, but a different species.

In short many things determine life expectancy and the interplay between different factors will determine an individuals life expectancy and a species' average life expectancy.
How life expectancy links to size:

Among mammals there is an inverse relation between heart rate and life expectancy (mammals tend to average 7.3+/15.6 x10^8 beats per lifetime which appears to be a symptom of the fact that heart rate is a marker of metabolic rate and so there is a fixed 'metabolic lifetime' for animals (source). This is somewhat substantiate by metabolism variants in C. elegans and the link between metabolism and free radicals and DNA damage (source).
Larger animals are thought to have a slower metabolic rate by weight (not overall) due to scaling laws (see Kleiber's law) and how surface area and volume relate and change temperature regulation metabollic requirements.

Other factors that change life expectancy:

In breeding: a reduction in genetic variation caused by inbreeding (e.g. many dog species though the extent to which they are inbred will depend on the species) can lead to lots of underlying health issues that may reduce the lifespan independent of metabolic rate
Stress: Higher stress will reduce life expectancy
Nutritional abundance: reducing caloric intake may reduce metabolic rate and extend lifespan, though starvation will decrease lifespan

Gigantism:

Whilst the life expectancy for a species may be higher in general people with gigantism may live shorter lives than possible because of non-metabolic related reasons. For example many forms of gigantism are linked to hormones which promote cell division and growth which are also linked to forms of cancer.

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text:
Why are almost all inborn errors of metabolism autosomal recessive?
Technically, the only inborn error of metabolism I know that is autosomal dominant is acute intermittent porphyria. Also, the only inborn of metabolism I know that is X-linked recessive is Lesch-Nyhan syndrome.

Have you considered what the effect would be if the error of metabolism was autosomal dominant?  How likely would it be that the affected individual would live long enough to reproduce and pass it on (etc., etc.)

i would suggest doing more research into mechanisms of the various inborn errors and seeing what you find.

Most deleterious mutations are partial or complete loss-of-function (LOF) mutations; most of those can be functionally compensated for by the presence of a wild-type (normal) copy on the other chromosome and so are recessive. Genes on the non-pseudoautosomal parts of X or Y are effectively hemizygous in males and thus LOF mutations there will likely be dominant.  Such LOF mutations in females may also be dominant, depending on whether mosaic expression (due to X-inactivation) results in the phenotype.

From How do I write a good answer? in the [help], Answer well-asked questions. Not all questions can or should be answered here.


text:
Blood and plucked-feather sample storage
This next field season I will be collecting both blood and feather samples and I wondered how best to store the samples. The blood samples will be used for microsatellite and/or SNP analysis. The feather samples will be used for genetic sexing and/or microsatellite analysis.
Feathers: can these be stored in envelopes at "room" temperature? I've seen mixed answers in the literature. They are plucked feathers and so may have a bit of blood or tissue at the tip. If they are used for microsatellite analysis, I want to ensure this DNA is not degraded. I will be storing them frozen at my field site, but our partners at other sites may not have access to freezers.
Blood: we will be collecting blood into capillary tubes. I have a few Whatman FTA cards, but not enough. So I'm planning to freeze the blood in the capillary tubes. Are there better options than this? I'm planning to use non-heparinized tubes. Out of curiosity, has anyone used blood from FTA cards for microsatellite or SNP analysis? Can I expect sufficient DNA quantity and quality? Bird DNA is nucleated, so I should get more bang for my buck (volume-wise).
I appreciate your help!

I've always used pure ethanol to store samples in the field before extraction. Is this possible with feathers?

I'm not sure, it seems possible and I can see if there is anything published. Unfortunately we are dealing with international shipping, so that may be difficult (that's a question for my advisor!). So far, for feathers it seems that people freeze them or store them dry. I have seen ethanol recommended for blood samples.


text:
Estimate sex-specific survival from mark-recapture data using multi-site, sex-specific cormack-jolly-seber model?
I am interested in identifying sex-specific survival rates. I have a long-term dataset of individually marked birds from one breeding colony. Of these, I am able to genetically sex a subset. Additionally, I have access to mark-recapture data on nearby breeding colonies and so can estimate emigration from my target breeding colony. However, I am only able to sex individuals from my focal breeding colony.
My research project addresses both survival and dispersal (permanent emigration). So I'd like to disentangle these as much as possible and look at effects of sex. One approach is to only model the subset of birds I'm able to sex. Another approach would be to model all individuals, including unknown sex, and apply the techniques in Nichols et al. (2004) to apply probabilities of "male or female" to unknown-sex birds (I may be summarizing that poorly).
Can I use a multi-site model if I only include individuals marked on one colony, but do have data for permanent emigration to other colonies? Would it make sense to use a multi-site model with all individuals from all colonies but only have sex information from one colony?
Thanks in advance!
Nichols, J.D., Kendall, W.L., Hines, J.E. and Spendelow, J.A. 2004. Estimation of sex‐specific survival from capture–recapture data when sex is not always known. Ecology 85(12):3192-3201.


text:
Wounded Pigeon in my balcony
There is a, probably wounded, pigeon (common rock pigeon) in my balcony. It is dark right now and thus, I have very little idea about its condition. But it seems it is finding it difficult to fly/move its wings because when I approached the balcony door, it 'walked' towards the farther end of the balcony while flapping its wings very slowly.
What is the right way to handle the bird and what is the best thing I can do for him/her?

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Call the RSPCA or whatever animal rescue is active in your country and neighborhood.

More likely to be suffering from disease, old age, or poison. Providing food and water would probably be appreciated.

If you have a cat carrier then trying to intice it inside with some food would be a good idea. Try to contact your local wildlife vet for information on whether they would be willing to treat the animal. If you think it may be injured then I wouldn't reccomened handling the bird as you may hurt it further, but if you do need to then handle it by placing both hands over the wings in order to pick it up (https://www.rspb.org.uk/birds-and-wildlife/advice/how-you-can-help-birds/injured-and-baby-birds/if-you-find-an-injured-bird/) . In addition the bird could have gotten used to its injury and learned to live with it so you could monitor it for a bit and see how it's getting on. Hope it turns out alright.
If you live in the UK here is some advice from the RSPB: https://www.rspb.org.uk/birds-and-wildlife/advice/how-you-can-help-birds/injured-and-baby-birds/sick-and-injured-birds-faqs/#:~:text=For%20most%20injured%20birds%2C%20place,how%20you%20can%20help%20it.

Well, I don't have a cat carrier. Will it be wise to let it remain there till the morning?

It'd be a good idea to wait until the morning to see how the bird is doing. If it's still in bad condition then I'd advise calling a wildlife vet, otherwise the animal will likely get used to its injury or, unfortunately, pass away

When I checked in the morning, it had already flown away. Thank you for your help:)

I hope it'll be alright. No problem!


text:
Inheritance of FEVR (Genetic Disease)
If a woman has FEVR and is affected by the disease, what are the chances of her passing the disease to future generations. I read somewhere from a credible source like NIH(I couldn't find the link again, I am attaching another https://rarediseases.info.nih.gov/diseases/1613/familial-exudative-vitreoretinopathy#:~:text=Familial%20exudative%20vitreoretinopathy%20(FEVR)%20is,the%20blood%20supply%20to%20retina.), that the babies that the woman conceives could be affected by or carrying the FEVR causing genes, or may neither be carrying nor affected by them. Depending on the type of inheritance, which are autosomal dominant, autosomal recessive, or X-linked recessive, the chances of having a normal baby vary. The chances of having a healthy kid for autosomal dominant and autosomal recessive are 50% and 25%, respectively ( I am intentionally excluding the possibility of X-linked recession).
Therefore, if the inheritance is autosomal dominant, then, there is a 50% chance that the baby is healthy and not carrying the genes. And the successive generations created by the baby will not have the gene causing FEVR. Is my understanding correct?

Are you asking about the mendelian inheritance calculations?

The answer depends on (at least):

whether the woman is affected by the condition
whether the allele is autosomal dominant or autosomal recessive (excluding X-linked recession)
the frequency of the diseased alleles in the population
the presence or not of inbreeding

Below I assume no inbreeding.

The woman is affected and the inheritance is autosomal recessive. This means that the woman carries two disieased alleles and with certainty passes one of them to her children (i.e., with probability $1$). Whether the children will be affected by the condition depends on whether they get a second diseased allele from the other parent. Assuming that the frequency of the diseased allele in the population is $p$, this means that the probability of a child inheriting the disease is $p$.
The woman is not affected and the inheritance is autosomal recessive. The woman carries only one diseased allele, and passes it with probability $1/2$ to her child. The probability that a child is affected, i.e. that s/he has two diseased alleles is $p/2$.
The woman is not affected and the inheritance is autosomal dominant. In this case the woman carries no diseased allele, so the children are not affected.
The woman is affected and the inheritance is autosomal dominant. The woman carries at least one diseased allele, and could be carrying the second with probability $p$. In the former case she passes it to her child with probability $1/2$, in the latter with probability $1$, so the probability that the child inherits the diseased allele is $1/2 + p$. This is also the probability that the child is affected by the condition, since they will be affected regardless of the allele passed by the other parent.

Assuming very small probability $p$, case 4 gives us the probability $50%$, whereas the probabily in cases 1 and 2 is much lower. The numbers given in the question are calculated assuming Mendelian experiments, which are a heavy case of inbreeding (and even then not quite correct).
John H.Gellespie, Population genetics
Matthew Hamilton, Population genetics

The above assumes complete penetrance; many disease show only partial penetrance, where some individuals who carry the disease allele(s) show no sign of disease. That greatly complicates calculations, significantly changing cases 2 and 3 above.


text:
Why are probionts not considered cellular life?
I am currently studying Prescott's Microbiology, 10th edition, by Willey, Sherwood, and Woolverton. Chapter 1.2 Microbes Have Evolved and Diversified for Billions of Years presents the following figure:

The authors then ask the question: Why are the probionts pictures above not considered cellular life?
I'm unsure of why the probionts are not considered to be cellular life. If I'm not mistaken, the probionts contained ribozymes, no? This means that they have the capacity to catalyse their own reproduction. And, according to the figure, later probionts also consisted of proteins, so I'm presuming that catalysis and reproduction were not issues here.
I would greatly appreciate it if people would please take the time to clarify this.

Welcome to Biology.SE! Please take the [tour] and then go through the help pages starting with [Ask] questions effectively on this site and [edit] your question accordingly. In particular, please check out the help on "homework" questions. ——— Also note that whether you consider something "cellular life" depends entirely on how you decide to define "cellular life". Consequently this seems to be more a matter of definition and opinion rather than a fundamentally biological question. Thanks!

This https://biology.stackexchange.com/a/9455/57068 answered my question.


text:
Relationship between bacteria size and temperature?
I'm, doing a research in a TOC (total organic carbon) degradation in a BAC (biologically active carbon) filter for the grey-water treatment. Recently, I started to wonder if there is a relation between bacteria size and temperature. If anyone know any research paper or did a research by himself/herself where such relation has been checked, it would be of a great help.
Thanks in advance.

There is a negative correlation between growth temperature and genome size for prokaryotes, which may be driven by selection for smaller cell size overall in warmer environments. Sabath et al., 2013 provide a good discussion:

Smaller cells tend to have smaller genomes in both prokaryotes and unicellular eukaryotes (Shuter et al. 1983; Lynch 2007), for reasons that are not fully understood (but see Dill et al. 2011). This correlation suggests that cell and genome size are functionally related, such that an evolutionary change in one would induce an evolutionary change in the other. Previous studies have hypothesized that reduction in cell size could be advantageous, either to optimize surface-to-volume ratio for uptake of scarce nutrients (Dufresne et al. 2005; Giovannoni et al. 2005; Moya et al. 2009), or to decrease predation by bacterivores or bacteriophages (Yooseph et al. 2010). Similarly, we speculate that bacteria adapted to high temperature could be subject to selection favoring smaller cell size, which also requires smaller genome size—regardless of gene content.


text:
In enzyme kinetics, Can the Kp be greater than K1 in any way?

Enzyme reacts with substrate to produce a complex. And finally the products in a catalysis reaction.

To answer this question, we need to delve into the world of
dimensional analysis
and to consider when and how rate constants may be compared.
The OP considers the following simple kinetic mechanism, (which, after defining kinetic constants such as
$K_m$
and
$k_{cat}$
in terms of rate constants,
gives rise to the
Michaelis-Menten
equation):
$$
E + S \xrightleftharpoons[{k_{-1}}]{k_1}
ES
\xrightarrow{k_p}
E + P
\tag{1}
$$
First and Second Order Rate Constants
As written, $k_1$ is a second-order rate constant and  $k_p$ is a first-order rate constant.
Therefore $k_1$ will have units of  $concentration^{-1}\text{. }time^{-1}$, and $k_p$ will have units of $time^{-1}$ (as will $k_{-1}$).
For example, $k_1$ may be spoken of as having a value of
$10^9 \text{ M}^{-1}\text{ s}^{-1}$ (
here
and
here),
or as having a value of
$10^9 \text{ L mol}^{-1}\text{s}^{-1}$, and $k_p$ may be spoken of as having a value of $10^6 \text{ s}^{-1}$.
By the laws of
dimensional analysis,
it is meaningless to compare quantities of different units.
It is absurd, for example, it ask if pH 7 is greater than (or less than) $10^\text{o}\text{C}$,
or if 2 mol is greater than (or less than) 5 seconds.
So too with rate constants: it is meaningless to ask if a second-order rate constant is greater than or less than (or is equal to) a first-order rate constant.
The application of dimensional analysis to situations often encountered in enzyme kinetics is well described in
Fundamentals of Enzyme Kinetics
(Cornish-Bowden, 2013, 4th Ed, Section 1.3) and the relevant section seems to be freely accessible via
Google Books.
For example, we can multiply and divide quantities of different dimensions, but we
cannot add or subtract them.
Thus, inspection of the numerator of the following equation shows that it is CLEARLY WRONG:
$$
K_m
=
\frac{k_p + k_{1}}{k_{-1}}
\tag{2}
$$
The CORRECT expression for $K_m$ for the mechanism shown in Eqn (1) is
the sum of the two first-order rate constants, divided by the second-order rate constant:
$$
K_m
=
\frac{k_p + k_{-1}}{k_{1}}
\tag{3}
$$
We can also infer from Eqn (3) that ${K_m}$ has dimensions of molarity,
even if we have no idea as to what the symbol ${K_m}$ refers.
$$
  \frac{\text{s}^{-1}}{\text{M}^{-1}\text{ s}^{-1}} = \text{M}
  \tag{4}
$$
Application of the rules of dimensional analysis is often useful in 'scanning' the
equations encountered in enzyme kinetics.
$$
Y=
\frac
{1}
 {1 + \frac{[A]}{K_m^A} + \frac{[B]}{K_m^B} + X}
 \tag{5}
$$
For example, without any prior knowledge as to what $X$, $Y$, $K_m^A$ and $K_m^B$ refer to,
inspection of Eqn (5) allows the following conclusions to be drawn:

$X$ is dimensionless
The quantities $\frac{[A]}{K_m^A}$ and $\frac{[B]}{K_m^B}$ are dimensionless
$Y$ is dimensionless

Pseudo First-Order Rate Constants
Although $k_1$ and  $k_2$ have different dimensions,
$k_1 \text{[A]}$
has dimensions of a first-order rate constant $(time^{-1})$ and can be directly compared
with $k_p$ and $k_{-1}$.
The quantity
$k_1 \text{[A]}$
is often referred to as a pseudo first-order rate constant. (Personally,
I don't like the term)
Thus, to argue that $k_1 \text{[A]}$ >> $k_p$ is perfectly OK from a dimensional
analysis perspective.
Perhaps more importantly, a pseudo first-order rate constant may be added to or
subtracted from a first-order rate constant.
Thus, an equation such as the following presents no problems (again from a dimensionless
analysis point of view):
$$
Y=
\frac{k_1}
{{k_1} [A]  + k_{-1} + {k_p}}
 \tag{6}
$$
Common Confusion Concerning Rate Constants: An Example
It is surprising how often the laws of dimensional analysis are misapplied in
the world of enzyme kinetics.
For example, in a paper published in J. Chem. Educ. in 2011, it is stated "For the classic Michaelis-Menten enzyme,
$k{_1} > k_{-1} >>  k{_2}$" where "... $k_1$ is the forward rate constant for the first step, the
fast binding of substrate $(S)$ to enzyme $(E)$ to make the non-
covalent enzyme-substrate complex $(ES)$,  $k_{-1}$ is the reverse
rate constant for the dissociation of $ES$ back into $E + S$; and $k_2$
is the rate constant for the subsequent slow catalytic step converting $S$ to product".
Let's state it bluntly: $k_1$ cannot be greater than $k_{-1}$, as $k_1$ is a
second-order rate constant and $k_{-1}$ is a first-order rate constant.
Furthermore (and very surprisingly), J. Chem. Educ. has not corrected the error.
(In my opinion, the paper is otherwise good).
Reference
Cornish-Bowden, Athel (2013)
Fundamentals of Enzyme Kinetics
4th Ed,   Wiley-Blackwell
[ google books ]


text:
How much sunlight is required for photosynthesis to peak?
I've read that photosynthesis peaks at some point over light intensities https://en.wikipedia.org/wiki/PI_curve According to https://www.bbc.co.uk/bitesize/guides/z9pjrwx/revision/5 suggests

At very high light intensities, photosynthesis is slowed and then inhibited, but these light intensities do not occur in nature.

But https://en.wikipedia.org/wiki/Photosynthetic_efficiency seems to suggest otherwise

most plants can only use ~10% of full mid-day sunlight intensity

If plants can only use ~10% of mid-day sunlight, then the intensity of mid-day sunlight would have been too high for the rate of photosynthesis to plateau.
Are the two incompatible or am I missing something?

Varies by plant

^this. Also I would be cautious to assume that 10% of mid-day sunlight energy utilized by a plant translates into 100% energy utilization at a tenth of mid-day lighting conditions.


text:
Why the total phosphorylation of certain neuronal proteins decrease during development?
Looking at the effects of RIM1a which is a protein involved in neurotransmitter release. Any ideas as to why its total phosphorylation decreases as the rats develop?
Many thanks
Image; https://i.gyazo.com/16170fd79bd1f96517e028dfa2e70fbf.png
Paper; http://www.cell.com/cell/pdf/S0092-8674(03)00727-X.pdf

Here are a couple Wikipedia articles that might help out:
Critical period - Critical period: the idea that certain types of plasticity in the nervous system occur only at certain "critical" times.
Long-term potentiation - LTP, talked a lot about in the paper you linked: it's a mechanism for strengthening of synaptic connections.
Synaptic pruning - # synapses/strength of synapses tend to decrease from adolescence to adulthood
The paper you linked talks a lot about the role of phosphorylated RIM1a in LTP. Without knowing more specifically about this protein, and from just a glance at the paper you linked, I'd suspect that RIM1a is phosphorylated during periods of increased LTP, particularly earlier in development, and as animals age and their brains go into the synaptic pruning phase, LTP is downregulated overall, and one of mechanisms could be the lack of phoshporylated RIM1a.

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text:
Does somebody knows this european bird that i saw close to a river in an open grasland?
I saw today afternoon (10. June) this bird and would like to know the species name. It was on a sunny day in the middle of the Netherlands (central Europe) in an wet meadow close to a big river. I took several picture from the same individual, but they were two birds of the same species passing quite fast close to the ground of the meadow.

I'm no expert or from europe , but I think common linnet, based on a very brief google image search for "finch europe". Maturing reddish head and breast, gray neck,brown wings with dark tips.

thanks for your input. I was also considering this the marks are not that clear. sure the quality of the picture is also not great. but anyway.

I think marks aren't clear because juvenile heading into adult, but as I said, no expertise on this at all, other than some search skills.


text:
What does it mean for a species to be ancient?
When we say that a species like cockroaches is ancient, what does it mean exactly?
Does that mean that cockroaches haven't evolved for a long time? But isn't evolution always occurring? So is that because they haven't evolved as much and are very similar to their ancestors, ie they had a "very slow rate of evolution"?

It depends on the context.
first "cockroaches are ancient" is different than a species being ancient, cockroaches are not a species but a group of species with a similar morphology and ancestry (similar to a clade).

It can mean they are mrophologically similar to their ancestors. Which is very different than saying they have not evolved. It means the pressures on the linage have not favored much in the way of morphological change. Some shapes just work well,(or reach equilibrium) and once you reach it the morphology don't change much even when other things are changing.
It often means that the split between the lineage in question and other groups is old. example, you could say mammals are ancient for instance because the mammal lineage split off the rest of the amniotes 275 millions years ago. They have changed a great deal since then but the groups as a whole goes back a long time. the issue here is these splits are minor when they occurred, like any other specialization event, but look big due to human constructed categories.
But it can also mean that the lineage has not undergone a specification event for a long time, It has changed but has not left behind any offshoots, this is the rarest case but can happen.

Note however this is a phrase the media like to throw around when it doesn't have a solid scientific definition, it is a qualitative contextual statement. They often have little understanding of its meanings. They also often fail to clarify which they mean, and often fail to properly define the "thing" being ancient.


text:
Overcoming palmitic acid intolerance
What can stop the body from being able to process or break down palmitic acid?  The acid stays in the stomach and burns causing a similar reaction as heart burn when the volume is high.  Heart burn medication makes the issue worse. In smaller doses it causes the esophagus to swell causing a asthma type reaction and wheezing when breathing through the mouth but leaves the nasal passages unaffected.  The symptoms appear several hours after consumption.  The reactions have been noted in any food containing the acid natural or additive usually in the form of palm or peanut oil.  Once such natural example is a Pizza with Mushrooms, several hours after eating nausea will occur along with the burning sensation.  Expelling of the contents reveals acidic liquid and the mushrooms only.
Is there any recourse for neutralizing the acid safely or supplementing the body with the missing function to process the acid.

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text:
What defines a single organism?
I suppose what prompts me to ask this question is my wondering if it is possible to have a multicellular prokaryotic organism. For instance, can a biofilm be considered a single organism? Why or why not?
Why is it that multicellular prokaryotes do not exist (if they do not)?
At what point can a collection of cells be considered one whole -- do they need to all share identical DNA?
Fire away.

What defines a single organism is ongoing debate in biology. It will probably never be answered because it is a human attempt to create discreet categorizes for something that exists in a continuous spectrum.  Because there is a lot of gray area, generally when dealing with an edge case an author will say what definition they are using.

I agree with John. See here for an example of a discussion of issues and proposed definitions. I don't necessarily agree with the proposed definitions, but I think the article does an ok job of pointing to some literature for further discussion.


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Does inactivated COVID vaccine also contain mRNA that is active in human body?
Inactivated vaccine primarily relies on proteins to elicit immune responses. My question is, does inactivated COVID vaccine also contain mRNA that could be actively transcribed into new proteins in human body, similar to those mRNA vaccine?
To my knowledge, the mRNA in mRNA vaccine is slightly modified such that it can be transcribed. Without those modifications, can mRNA in inactivated vaccines still be transcribed? If the answer is yes, then, is the concentration of active mRNA high enough that the transcription activities can be detected?

Short answer: no. Basically all the inactivated vaccines use cross-linking agents that will cross-link or damage the RNA (e.g. aldehydes, Beta-propriolactone or ethylene imine) through a chemical reaction. Many of these sorts of vaccines are then formed into subunit vaccines which undergo extensive purification to get the antigenic protein of interest.
A reasonable reference for this is (also the second link above):
Iris Delrue, Dieter Verzele, Annemieke Madder & Hans J Nauwynck (2012) Inactivated virus vaccines from chemistry to prophylaxis: merits, risks and challenges, Expert Review of Vaccines, 11:6, 695-719, DOI: https://doi.org/10.1586/erv.12.38


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Glycemic Index and two-hour blood glucose response curve (AUC)? Where are the AUC charts?
I understand the "Glycemic Index" (GI) of foods is calculated using the area under a 2-hour glucose/blood response curve (AUC) after a 24 hour fast and consuming carbohydrates. Therefore a higher GI indicates there is more glucose available in the blood stream during this 2 hours.
It seems the GI is a general indicator and glucose/blood levels over 2 hours and has little information on when the spike of carbohydrate to glucose conversion occurs or when carbohydrates are first converted to glucose. Is this a true statement?
I searched for the AUC charts online but found little information. I suspect the AUC charts would show when the glucose/blood levels first increase and how they are effected over time. Does anyone know where to find these charts for foods?
Also, is the correct forum to be asking this in? Unsure if Beta Medical Sciences StackExchance is appropriate.

You could search something like:
https://scholar.google.com/scholar?hl=en&q=glycemic+index+AUC+glucose
and your results will include papers that calculate glycemic index for some food based on glucose measurements. For example this one:
Robert, S. D., Ismail, A. A. S., Winn, T., & Wolever, T. (2008). Glycemic index of common Malaysian fruits. Asia Pacific Journal of Clinical Nutrition, 17(1).
has this figure:

You can expect that the conversion of carbohydrates to glucose begins immediately after eating, so it's mostly the rate that varies by food, producing different curves.

This paper is available from https://pubmed.ncbi.nlm.nih.gov/18364324/

I added another question on performing the GI calculation using integral calculus here: https://biology.stackexchange.com/questions/110854/calculating-the-glycemic-index-using-an-auc-glucose-blood-curve


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Calculating the Glycemic Index using an AUC Glucose/Blood curve?
Does anyone know the mathematics to calculate the Glycemic Index using a AUC Glucose/Blood curve?  Is there an article documenting the process?  I understand that algebra and integral calculus is involved.
For instance, here is an AUC Glucose/Blood graph of foods against a Glucose reference:

I know the definition of the Glycemic Index is the relative rise in blood glucose level two hours after consuming food.  It is the area under a 2 hours glucose/blood response curve, following a 12 hour fast and 50 g ingestion of a carbohydrate.
I know Glucose has a Glycemic Index of 100 and I'm unsure how this relates to the integral of (area under) the Glucose curve in the above graph.  Also, the Glycemic Index appears to be unit-less, which is further confusing.
I try a rough calculation as follows and the results appear off.  I draw a rectangle where the glucose curve is pictured here between 0-60 min, it comes out to 10 mmol/L - 6 mmol/L = 4 mmol/L y-axis, 60 min - 0 min = 60 min x-axis.  The resulting area of the GI is 4 mmol/L * 60 min = 220 mmol/L * min and when the GI for Glucose should be 100.
Appreciate guidance here.

Glycemic index is the ratio of blood glucose AUC for some carbohydrate source to a reference source, usually either glucose or white bread.
It's unitless because it's a ratio of numbers with the same units:
(concentration/time) / (concentration/time)
Glucose is defined as having a glycemic index of 100. This is an entirely arbitrary choice. It could have been 1, it could have been 42. 100 is convenient, because it will tend to make most foods have numbers in an easy range, basically the same reason that proportions are often expressed as percentages ("20%" rather than ".20").
To calculate area under  the curve from a set of discrete measurements like in the graph above, typically one would use the trapezoid rule though any other integration approximation would give similar results.
An example from the methods section in one paper:

The incremental area under the blood glucose response curves (IAUCG) to test and reference foods were calculated geometrically using the trapezoid rule, ignoring the area below the fasting baseline

So, for the above curve, the first step would be to subtract the fasting baseline which appears to be around 5.8 mmol/L, then use the trapezoid rule to get the AUC in units of mmol/L * time for glucose and each fruit, and express the glycemic index for each as 100 * fruit/glucose.

For above graph using the glucose curve with two sides, Baseline: 10 mmol/L - 6 mmol/L = 4 mmol/L.  Trap Rules: 30 min -0 min * .5(0 mmol/L + 4 mmol/L) = 60 min * mmol/L,  120 min - 30 min * .5(0 mmol/L + 4 mmol/L) = 180 min * mmol/L,  60 min * mmol/L + 180 min * mmol/L = 250 min * mmol / L, then GI for glucose is 100 * (250 min * mmol / L) fruit / (250 min * mmol / L) glucose = 100.  Does this calculation appear correct?

Another question, if the Glycemic Index of a fruit is 50, the fruit/glucose ratio is 1/2.  Does this imply the fruit has less glucose over time than the reference glucose?  Or perhaps the integral of the fruit extends past the 2 hour window?

If you go to the paper they report the AUC for glucose to be 259+/-15 mmol x min/L from the actual data, so yes it seems like your 250 is a pretty good estimate from the figure but I'm not going to bother auditing your math in this format.

Glycemic index is a measure of how much a food affects blood glucose. That's it. If you want to know how much total energy a food contributes, better to look at calories. Glycemic index doesn't measure anything else about metabolism, just blood glucose.

@Nick Importantly, blood glucose is under homeostatic control, so it's not as if every molecule of glucose in the diet causes a proportional change to blood glucose. GI is just a simple measure based on something easily measurable by a lab (blood/plasma glucose), it's not an attempt to create a full metabolic model.

Thanks. I’m still confused how same 50 grams of carbohydrates can yield different AUC curve areas, unless like you say the the carbs may be equal but they effect glucose/blood levels differently. As glucose is energy I would expect the area the curves to be the same for the same carb content, unless the curve extended beyond 2 hours.

@Nick Yeah, it's just not that simple.

do you know of any other resources I can read to reconcile this question?  Specifically, why glucose level area does not correlate to carbohydrate intake of the food?  Are different food carbohydrates either being converted to something else other then glucose, or the glucose / blood level remains high beyond the 2 hour measurement window, which would lead to a lower glycemic index and area under 2-hour curve?  Thanks

in another post regarding glucose, someone stated "glucose levels will change depending on the type of carbohydrate, and some form of carbohydrates are even impossible for the body to digest and are either digested by bacteria in the gut or simply excreted in the feces."  So this may suggest the perhaps only some mass of carbohydrates may be converted into glucose, which would suggest the low AUC integral and Glycemic index for some foods.  Does that sound right?


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Research surrounding visualisation (inner eye)

Aphantasia is the suggested name for a condition where one does not
possess a functioning mind's eye and cannot visualize imagery.

I have self-diagnosed aphantasia, so I might be asking a question that is obvious to everyone, but completely alien to me. In that event, I am asking for a 2-3% minority of the population that have aphantasia.
I cannot visualise faces or people at all. When I close my eyes and try to visualise the rubics cube on my desk, at my worst, I don't see anything at all and at my best, I see something like each of the two images on the right (and that's really pushing it):

How are other people able to visualise a rubics cube, in how much detail? Is there research surrounding this?
Some people state, they are able to vividly visualise faces, people, their clothing etc. If they can visualise a face, with all it's details and complexities, how are they completely unable to visualise a simple string of numbers? Because if they could, they would be able to do complex arithmetic calculations inside of their head.
Since I am not (or barely) able to visualise I would like to comprehend how other people are able to visualise anything. For example, I can easily calculate something like this in my head:

If I was able to visualise things, what's stopping me from doing this in my head, and a lot more?:

Other people can't even do "5727:3". The article on wikipedia suggests that people with aphantasia often become mathematicians or engineers, which seems counter intuitive to me, as being able to visualise would give me a great advantage in either field. I cannot wrap my mind around how someone can visualise an entire face but fail to visualise a few numbers in a grid and failing basic arithmetics.

You might not get anything here, but our sister-stack [psychology.se] might be able to help. Be sure to take their tour, read their help centre etc, and be sure to include some instances of prior research to satisfy their standard requirement for it.

The question indeed is better suited for Psych & Neurosci. However, before migrating, I need a clear question from you. I cannot make up what you want to know. Literature on aphantasia? If yes, about what aspect? Or do you need a diagnosis of some kind? If yes, please seek professional help (self-help questions are offtopic here and on Psych&Neurosci). One way to bring focus to a question is by adding prior research efforts on your side. That can help to crystallize a focused question.


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How does the social structure of lion prides prevent incest?
I assume that lions don't have a concept of incest and they will just mate with any adult lioness in heat, daughter or not.
If so, is incest inevitable as the female cubs will grow up and remain in the pride? Their brothers will be kicked out as they reach mating age. But the females stay, so what is the mechanism that will prevent their fathers from mating with them?
I suppose that their fathers will be driven out of the pride by incoming males sooner or later. But if it doesn't happen soon enough, then what prevents them from mating with their daughters?

It is true that African lions have recently become more prone to inbreeding, largely due to human actions (reasons include limited dispersal and at least temporarily reduced pride sizes). see here
Generally though, lions likely avoid mating with close relatives innately as most animal species do. see e.g. here
A few things about the social structures of lions (ref.):

First, many prides are not controlled by a single male. Although the males might often be related to one another.

A single male might often not be in control for long enough to mate with his grown daughters.

Females do not only mate with the leader of their pride, but mate sometimes with males from outside of the pride.


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num_tol_term in PeptideProphet result
What is the meaning of the num_tol_term attribute in a PeptideProphet (pep.xml) search_hit?
<search_hit hit_rank="1" peptide="DATDDFEDVGHSTTAR" peptide_prev_aa="K" peptide_next_aa="A" protein="Traes_5AL_64120ED6B.1"
    num_tot_proteins="4" num_matched_ions="9" tot_num_ions="30" calc_neutral_pep_mass="1735.7364" massdiff="-0.0269"
    num_tol_term="2" num_missed_cleavages="0" is_rejected="0" protein_descr="| AT2G32720.1 | member of Cytochromes b5">

Found the answer in the PeptideProphet paper: number of tryptic
termini (NTT)

This number, which can be 0, 1, or 2, measures how
  many of the peptide termini, on the basis of amino acid sequence,
  are consistent with cleavage by trypsin.

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


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Bootstrap question

I have a question about bootstrapping:
The way that I understand it is that each number represents how well a given node is supported. So in the diagram presented, we can see that the "Seal-Bear-Cat" clade is fairly well supported with a bootstrap value of 87. From that, the "Seal-Bear" clade has a bootstrap value of 95, making it quite well supported within the larger clade.
My question is this: Does that 95 for the "Seal-Bear" clade refer to the idea that that given relationship is a true 95, and therefore very well supported, or is it a value of 95 within 87, making it a true value of somewhere closer to 83 for the overall tree?

Welcome to Biology.SE. Your title could more accurate (and then attract more users). It is typically pointless to use the word "question" in the title given that obviously the post contains a question.

The term bootstrapping is a concept of statistics that is much broader than its particular application to phylogenetics. Bootstrapping refers to the process of sampling iteratively your own sample in order to approximate the sampling distribution and calculate confidence intervals.

Bootstrap support is merely the percent of bootstrap iterations that support the clade, it doesn't account for tree hierarchy.

where is this slide from? Could you give us some references? Bootstrapping can be used in many contexts as @Remi.b pointed out.

I've voted to close the question unless more contexts can be given.

I don't have any references on me, but the answer is the "95". You may be pretty confident that seals and bears are each other's closest relataive, but you might be less sure about the placement of the cat (maybe it's more closely related to pigs? It's not, but you get the point)

If the values on the branches indeed represent bootstrap supports, they indicate the percentage of times a clade has been obtained in a set of trees computed from resamplings of a starting data matrix. This is irrespective of the topology within the clade or outside it, because this is merely a count of bipartitions (a branch corresponds to a bipartition of the taxa in the tree).
I think there is no real sense in multiplying bootstrap percentages along a tree, contrary to what the end of your question suggests.


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Human Eye Diagram: question about some dimensions
Does anyone know any of the answers to these questions about this human eye diagram:

What points should be the center of the circle for the radius numbers (Rn) in the following diagram?
The difference between the two values R1 and R2?

My suspicions: From what I can tell, Cornea R1 refers to the left side (front) of the Cornea measured from the right side (rear) of the Lens at its apex.  I'm not sure why R1 differs from R2.  Lens R1 values represent the lens between its changing diameter when it focuses (due to muscles) and is measured from the center of the largest circle of the eye in this picture.  Again, not sure how R1 differs from R1.  Retina is measured from the center of the largest circle of the eye in this picture.

ref: reference


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Vision System: neural activity is modulated using FSK?
I’m learning about the human vision system and signaling. Does anyone know if the signaling used by the vision system is modulated at the neuron using amplitude frequency shift keying?
I present my understanding of this below.
It’s my understanding that the rods and cones of the retina have a mechanism involving opsin and a geometry change which ultimately causes neurotransmitters to signal. This signal is an action potential over an axon ion channel.  The neurotransmitters in the vision signal path excite, inhibit or neither. This results in three frequencies of signal over the ion channel corresponding to the retina receiving light (20 Hz), no light (1.7 Hz) or unknown/baseline (.19 Hz). The light intensity changes the amplitude or voltage of the signal.

I think this is a case where you're much better off learning about how neurons work first, and then much later trying to relate this to other things you already know about, say, technological radio communication. It'll be way less confusing that way. There are definitely not only 3 possible firing frequencies, though; neurons can fire at any frequency from never up to a maximum governed by the kinetics of their ion channels (100 Hz would be a reasonable expected maximum for a typical neuron).

A good place to start might be understanding the individual figures in your links.


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Neurons: how does the brain reduce electromagnetic interference?
I read that the frequency of signal over neural ion channels in the brain can range from .19 Hz - 30 Hz at low voltage. For an interference example, AC electricity is 60 Hz at high voltage and generates an electrical field. From cited research below, it appears neural activity is impacted by EMR/RFI. Question: does the brain have some process it uses to reduce this interference? Forward error correction?
It seems that if there is an electrical field, force will be placed on these charges traveling over the ion channels and as a result lots of interference.
Research:
Electromagnetic waves, particularly RF-EMFs emitted by mobile phones are absorbed into the brain to such an extent that it can affect the activity of neurons (Kleinlogel et al., 2008; Hinrikus et al., 2018). Also, in 2011 World Health Organization’s designated mobile phone RF-EMFs as Group 2B, that is, possibly carcinogenic to humans. Recent studies show that RF-EMFs emitted by cellular phones are absorbed into the brain, to a degree, that can affect neuronal activity (Kleinlogel et al., 2008; Jeong et al., 2015; Jiang et al., 2016). physiological changes in cell membranes and ion channels at cellular levels have been reported (Pall, 2013; Buckner et al., 2015). Changes in cell membranes and ion channels induce alterations in the electrical activity of neurons, and these changes stimulate or inhibit neuronal activity through interaction with voltage-gated ion channels (Nanou and Catterall, 2018).

Take the easy data. Check the thickness of a neuron's cell membrane, and the voltage across it. Calculate the Volts per metre. Compare this with any external influences.

There is an extensive Q&A about the difference between brain waves and EM waves over on our sister site Psychology & Neuroscience: https://psychology.stackexchange.com/q/15222/14382 (though some of the answerers beyond the first two are a bit confused)
In summary, the brain doesn't care about EM in that range at all.
Light travels about 300,000,000 meters per second, so a 30 Hz electrical signal has a wavelength of about 10,000,000 meters. Nothing in a brain is long enough to resolve that length of wave. All electricity in the brain is via potential differences over membranes; a wave that long is almost exactly the same amplitude on both sides of the membrane so there is no consequence.
Yes, 30 Hz is a common neuronal firing frequency, but that has little to do with EM waves. Neurons don't communicate with each other through EM waves, but through release of neurotransmitter and opening/closing of ion channels. It becomes a problem for recording neuronal activity, but that's it.

I'm still confused why a 60 Hz signal has no impact on the potential voltage difference of the ION channel.  Even if the wave is long, it is still oscillating at 30 or 60 Hz, which would induce current on the ION channel due to the Lorentz Force.  Why would the length of the wave have anything to do with this?  It's the time of rise and fall of the EMF that is located along the ION channel isn't it?  The neurotransmitters (glutamate, dopamine, GABA, norepinephrine, etc) are released at the terminals of the ION channels, so would be effected by the ION channels and induced EMF.

I also read another article from NIH https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6025786/.  It states that "several studies have reported that exposure to EMF results in oxidative stress in many tissues of the body. Exposure to EMF is known to increase free radical concentrations and traceability and can affect the radical couple recombination."

@Nick That's an NIH site that indexes journals. Saying it's from NIH is like saying that Google said something because you found it on a Google search. Try out what Polypipe suggested in a comment.

There are two aspects to this question.  The first, dealing with EMR associated with AC generated in the usual range is already properly answered.  However, in the case of mobile phone radio and wifi frequencies of the order of 2 to 4 Ghz for example, the wavelengths are precisely in the range of the internal dimensions of the human calvarium: e.g. at 2 Ghz, the wavelength is ~15 cm.
Now whether this correspondence implies any physiological effect in the brain -- if you can imagine microwaves of that frequency rattling around the brain, being variously reflected and refracted by the calcific structures of the skull -- is another question, possibly worthy of specific research.
However, in the instance in which such microwaves might be slightly refracted or reflected within the calvarium, there will certainly arise a beat frequency deriving in any interference effect between those refracted or reflected components which is conceivably of the order of the so-called frequency of 'brain waves', which as noted are not really 'waves' in the ordinary sense -- rather an integrated effect deriving in the more-or-less synchronised signaling or 'firing' of myriad neurons.
Again, whether wave interference resultants arising with these comparable frequencies imply any actual physical effect which is directly dependent on those hypothetical beat frequencies is a further question.  Perhaps the brain becomes confused about the origin of these 'beats'.
To address your central question, perhaps the brain even learns to interpret not only this interference effect, but given the correspondence mentioned between radio and microwave wavelengths and the dimensions of the brain, perhaps it is in fact learning through the endless and inexorable processes of adaptation how to decode the information transmitted through such EMR.  All the more wondrous then, all the more tantalising and seductive that one should then hear and see this data in full flower slightly delayed in the devices themselves, on screens and in speakers.  Perhaps somebody will devise an appropriate experiment (if the whole thing isn't already an experiment).


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Studying the epigenetic variability, can I use SNPs?
So, I'm trying to study the effects of epigenetic variability on the brain structure. Can I use SNPs associated with a gene's higher expression to compute the likelihood of that gene being expressed in the brain region? I don't have environmental data, just the SNP information.
Since epigenetics refers to the variations in the gene expression without changing the DNA sequence, I don't really understand if there could be a connection.
Any help would be appreciated, thank you!

Welcome to StackExchange! If I got this right your main interest are epigenetics and brain structure, I'm not sure how SNPs play into this since they are only loosely connected to either. I think you could improve your question by making clearer: 1) what kind of data you will/can work with (data types & internal/public resources), 2) What your approach to studying this is (project time frame, dry lab / wet lab, expected readout).

Thank you for your response! :) The SNPs are basically used to compute the probability of a gene being expressed in a brain region (thalamus for example) and then correlate that with the brain structure for patients with psychosis, in my case. The data is from public databases like BrainEAC that have information about the gene's SNPs. The title of my project suggests that I'm studying epigenetic variability of psychosis but I will be using SNPs associated to gene expression to determine the expression of a gene. My adviser is not available and I needed this to proceed with my lit. review.

Starting from what appears to be your main question:

Can I use SNPs associated with a gene's higher expression to compute the likelihood of that gene being expressed in the brain region?

I would strongly advise against using SNPs determine if genes are expressed (at all) in a given tissue.For one thing SNPs that affect expression (then often called eQTLs) will usually only have small +- effects on expression instead of switching it on/off and also have that effect in many/all cell types. Unless an (individual) SNP has clearly described /and validated effects on gene expression in a specific tissue/brain region, you should assume it has global effects.
Now, luckily for you gene expression in different cell types, tissues etc is a relatively well studied area and there are resources for gene expression in the brain available (brain atlas is probably closest to what you might look for).
You can uses these resources to determine which genes are expressed in your regions of interest and from there on check if SNPs associated with these genes correlate with certain structural brain features you are interest in.
One more thing you note:
The title of your questions (as well es comments) mention that you are interested in epigenetics. Neither gene expression nor SNPs/eQTLS are diretcly linked to epigenetics, so if this is your actual focus you should also look for availbale ChIP-seq data or similar and also include this into your analysis (correlation of SNPs with epigenetic marks is difficult but not impossible)

I agree with Nicolai. Epigenetic variation is usually studied as DNA methylation (usually via bisulfite sequencing) and histone modification (via chip-seq). The study of gene expression is another topic. What is your research question?


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Easy Hardy Weinberg Equilibrium

Hi
My friend and I get 2 different answers to this question. I would like to know how to calculate the value of q. My friend says that 500/1500=q because there are 500 recessive alleles in the population and there are 1500 alleles in total. I say that p2= 500/1500 and P is the square root of that value and  q+p=1 but we both get different answers.  Please let me know which way is correct. Thank you guys in advance

P=(250 × 2 + 500)/1500 = 0.66
Q=500/1500 = 0.33
Your friend was right, you miscalculated P because forgot to add the alleles coming from the heterozygotes.


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Have humans evolved to live longer?
Do people live longer only because of better hygiene, medicine, society etc or also because they're slowly evolving to live longer under same circumstances?

There's going to be mostly opinion in answering this.  Technically, the title and body are asking slightly different questions; the latter probably can probably be answered (medicine/vaccines more important) but, again, is likely going to be just opinion-based (as is this comment).

There is an article about it here: https://www.abroadintheyard.com/ancient-teeth-reveal-30-made-you-old-aged-30000-years-ago/ it hints at cultural changes based on teeth.

Yes and no.
According to this paper, great apes and our ancestors had a life expectancy at birth of about 13 years (chimpanzees). Over a few million years of evolution, human life expectancy rose to >30 years in the 18th century. Industrialization and improved nutrition, hygiene and medicine resulted in a jump to >60 and now around 80 years in developed countries in just 200 years. The paper compares data from Sweden, but if you look at the data from gapminder.org, you see that this trend holds true for all nations (especially developing countries like India and China, who doubled their life expectancy in just 50 years).
So, while humans have evolved to live longer (as you asked in the title), due to a lower mortality and resulting increase in the age of maturity as well as the likely benefit of "grandmothers" (older, infertile females helping to feed their grandchildren) (discussed in this source), the recent increase in life expectancy in just a few generations is unlikely due to evolution.
While humans are still evolving, we have reduced the selective pressure. There is no benefit to the survival of the offspring when we live past 80-100 years. And comparing countries with lower standards in hygiene and medicine (I totally recommend playing with the gapminder tools), their life expectancy was still pretty low in recent years, only increasing with access to clean water, food and medicine. Comments on extending the lifespan usually refer to medical interventions to cope with the effects of aging.

There's no evidence that any of the changes in life expectancy you've cited are due to evolution.  Reducing infant and young-child mortality is the major cause of increased life expectancy.

@Amory: The recent changes in life expectancy are due to improvements hygiene, nutrition and medicine and not evolution, as I have stated in my answer. Nevertheless, without these improvements human life expectancy is longer than for our ape ancestors, which is one of many things that changed in human evolution.

I would say that humans have not developed to live longer. There have been many harmful changes. One is that humans have lost the ability to produce their own Vitamin C.
Vitamin C
Hygeine has been a huge factor in humans living longer, especially drinking water being clean. For instance the American Public Health Association campaigned since the 1870's for antibiotics, clean water separate from potable water, immunisation and other health measures to be freely available. Their positive effects are discussed at causes of longer life

This is just an opinion and not really an answer. Please provide an explanation suitable to the main point of the question and include appropriate references.

Humans didn't lose the ability to synthesize Vitamin C; that change happened long before, in an ancestor of the group which includes monkeys and marmosets as well as apes.

Yes. My answer is opinion. But the OP is very broad opinion and 2 questions. Unlike some other people I don't downvote.


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What are internal and external osmotic pressures when referring to a cell?
I've seen the term used but cannot find a clear answer:
What are internal and external osmotic pressures when referring to a cell?

The internal osmotic pressure is the osmotic pressure inside the cell. The external osmotic pressure is the osmotic pressure outside the cell. Osmotic pressure is proportional to the concentration of solutes.
Wikipedia has a perfectly reasonable page about this.


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Why are interneurons needed in the spinal cord for polysynaptic reflexes and somatosensory tracts to the brain?
The single explanation I found for the polysynaptic reflex is that the interneuron diverges into more pathways, such as the efferent motor neuron, the inhibitory neuron to the opposite extensor muscle, and a ramification that goes to the brain. But why couldn't the afferent neuron axon solve for these ramifications? Furthermore, it is counterintuitive for a nociceptive reflex, that must save the damaging tissue as fast as possible, to be slowed down by an additional synapse.


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Do I need primers if ordering from a DNA synthesis provider
Do I need to design / synthesize primers for PCR if I am ordering from a DNA synthesis company and they are providing free cloning into my preferred vector backbone? Any good reason to order primers as well?

It really depend on what you need to do with the plasmid you are ordering. Can you specify it?

Only if you intend to subsequently amplify the DNA you've ordered. I tend to never fully trust anything I don't confirm myself so primers to sequence the insert in the construct they give you might not be a bad idea either.


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How to read a floral diagram?

The above image is a floral diagram of the family Solanaceae
So I was hoping someone could explain how to read this floral diagram
The Centre suggestion axial placentation to me
The ameboid like structures suggest  that it's bisexual
And the aestivation of the petals suggest Valvate aestivation
But how do I read the green part and the bumps at the edge of the diagram?

Edited to add: Floral diagrams have an interesting history, having been developed in 1875. Per Wikipedia, a floral diagram

is a graphic representation of the structure of a flower. It shows the number of floral organs, their arrangement and fusion. Different parts of the flower are represented by their respective symbols. Floral diagrams are useful for flower identification or can help in understanding angiosperm evolution. They were introduced in the late 19th century and are generally attributed to A. W. Eichler.

As you can see from my (very dry) answer, a simple diagram gives a lot of information, and can introduce a way to observe a flower more thoughtfully*. If wildflower identification is an interest, a simple drawn diagram in the field - no words required - helps to later identify those that were difficult to identify in the field. It also shows how it's related to hundreds of other flowers that might not be intuitive. It's just a fun little tool to most, but a serious one to botanists seeking classification, etc. In 2017, scientists found a fossil pushing back the appearance of the Solanaceae family (which includes potatoes, tomatoes, petunias and belladona) back to 52 million years ago. Potatoes may have been on the menu millions of years before we thought. (Cool! But maybe only to plant nerds like me.)

If this flower diagram is of the family Solanaceae, the green things are sepals. I assume the "bumps" for both the petals and the sepals represent the fact that they are fused (so the petals are gamopetalous, and the sepals are gamosepalous.) And yes, the placentation is axile, and the aestivation is valvate .
This is a link to the Solanaceae flower diagram. N.B. the floral formula. (In this case, it's for the potato, but that doesn't matter.):

Where ⊕ = Actinomorphic (radial symmetry), ⚥ = Bisexual, K(5) = Calyx: 5 sepals, gamosepalous, C(5) = Corolla – 5 petals, gamopetalous A5 = Androecium – 5 stamens, polyandrous (free), epipetalous (attached to petals),and G(2) = Gynoecium – bicarpellary, syncarpous (united), superior ovary.
Which is more than you asked for, sorry. Here's an image of Jimson Weed (Datura wrightii); you can easity see the fusion of the petals and the sepals. (From Southwest Colorado Wildflowers, non-copyrighted.)

*There is more information in that diagram than in my answer.

thanks! How did you determine that the ovary is superior based on the diagram?

@mathandphysicsforever - I can't tell from that diagram if the ovary is superior; that information is found in the flower formula, which is true of all Solanaceae. :) If triangles had been included near the ovary, it would show the position of the ovary. Cool question, btw!


text:
Can you find the mass of drug X remaining in the body after an oral dose with only bioavailability and half-life?
I'm reviewing this question and think you can't find the answer with the information given.

A patient receives 1g of drug X as a single oral dose. Drug X has a
half-life of 12 hours and an oral bioavailability of 40%. What mass
(in milligrams) of drug X will still be present in the body 24 hours
after a 1g dose?

I think the fact that it is an oral dose means the question is more complicated, involving absorption and distribution of the drug, meaning more factors are needed which are provided in the question.
Is it as easy as:
$1000mg \times 0.4 \times 0.5 \times 0.5 = 100mg$
Or there is is more it than that as I suspect? Many thanks!

I'm no pharmacist at all, but I think you have given yourself a red-herring. The bioavailability surely means that this is the proportion absorbed?

@bob1 It does but it doesn't tell you over what time-scale the drug is absorbed. You could answer what mass of drug in total will make it into and out of the body (400mg) but not how much at a specific time point (24 hours).

Unfortunately, it is not so easy, the easy calculation you suggested might be a good approximation if the drug was administered intravenously via bolus, but for oral administration, as you say in the comment, we need to know something about the dynamics of absorption from the gastrointestinal tract, such as Time to Peak Concentration (how long it takes for Drug X to be fully absorbed and reach peak concentration in the bloodstream.), and Absorption Rate (the rate at which drug is absorbed, as this influences the concentration profile in the initial hours after administration.

Well $40\% \times 1 g = 400 \space mg$ That's how much drug is in your body's fluid compartments.
If the drug's half-life is $12$ hrs, the amount of drug in your body (after $24$ hrs) = $\frac{1}{2} \times \frac{1}{2} \times 400 = 100 \space mg$.
If dose = $d$ and bioavailability = $b\%$ and half-life = $h$ hours ...
The amount of drug left in your body after $t$ hrs = $\left(\frac{1}{2}\right)^{\frac{t}{h}} \times b\% \times d$

EDIT 1 START
This fancy geometric/mixed (?) series might be of interest ...
$1 - \left(1 \times \left(\frac{1}{2}\right)^1 + \frac{3}{2} \times \left(\frac{1}{2}\right)^2 + ... \right) = 0$ where $1$ = bioavailability, the exponent is $\frac{t}{h}$ and the rate of drug absorption = $1$/hr.
EDIT 1 END

No, that's not how it works. Bioavailability is how much of the drug ends up in the body ever; your answer is making an unstated assumption that it all enters immediately at time 0. Robert's answer explains already why this is a problem. You're just restating the attempt OP mentioned ("is it as easy as") without acknowledging this is what you did. Do you understand the question?

Ah, a simple error. You mean to say that at no point in time (after drug ingestion) is there around $40%$ of the drug in the body? We must then discuss concentration of the drug in the body as a time function $f(t)$ so that by integration we get the average concentration which we can then use to find bioavailability which is exactly what cogito is $40%$. What's bioavailability then if it isn't that simple. Why calculate it if it serves no purpose? Also, the $40%$ may be the maximum amount of the drug in the body which will be important for toxicity assessment I suppose.

No, that is not what bioavailability is. Bioavailability is the amount that ever gets into the body. If it takes time to be absorbed and is eliminated at any rate, it will never all be in the body at the same time. That doesn't mean it's not a useful concept, it just means it's not sufficient information to answer the question.

Indeed, but $40%$ is the grand total amount of the drug that can exert a therapeutic effect. What do you make of, $1 \times \left(\frac{1}{2}\right)^1 + \frac{3}{2} \cdot \left(\frac{1}{2}\right)^2..$

@BryanKrause, much obliged for the feedback. I edited my answer.


text:
What type of epithelium are the pancreatic Islets of Langerhans?
The human pancreas contains exocrine acinus cells (simple cuboidal epithelium) and Islets of Langerhans. Despite looking online I cannot identify what type of epithelium the Islets of Langerhans conform to (e.g., cuboidal, columnar, squamous). I'm confident it is not squamous due to the shape of the cells, but the distinction between cuboidal and columnar seems equivocal here.

I think the image you've attached lacks clarity. If you see the image below, you could say that the epithelium is cuboidal with central rounded nucleus.

Unlike the oval nuclei of columnar epithelium, rounded nucleus suggests that they are cuboidal in shape.
The image is from https://webpath.med.utah.edu/HISTHTML/NORMAL/NORM010.html

Welcome. Can you add sources to your claim and mention where the image was extracted from?

It is a fact that cellular morphology as well as the shape of nucleus will be taken into account when describing a cell as columnar or cuboidal. Due to the lack of clarity in the OPs image, I am showing this image as it is clearer to understand.


text:
modify PCR steps to include a ligation
Imagine a multiplex PCR in which after the extension step, the dsDNA is nicked and requires a ligation reaction to repair the nick before the next denaturation step. So the steps would be:

Denature
Anneal
Extend
Ligate
steps 1-4 X 30

There are thermostable DNA ligase enzymes available (best activity at 65C), which don't get heat-inactivated by the high temp at the denaturation step.
It seems like this should work, but I can't find any info on anyone trying this. Any ideas?

I don't get this. Why would you nick the dsDNA?

@Chris it's a multiplex PCR with 3 primers. Two flanking and one mutagenic in the middle. Assuming all 3 primers anneal, the polymerase will "bump into" the dsDNA in places where the other primers are hybridized (and either continue polymerizing or not depending on whether it's a non-displacing enzyme), but not covalently link the two ends. So before the next denaturation step those two pieces need to be ligated together. So the nick is an unfortunate byproduct of the PCR design that necessitates ligation. Now I'm doing in it separate rxns. I'd like to do it all in the same iterative reaction

Ah, thanks. There are two problems I could imagine: First: The reaction may be hard to optimize in terms of the needed temperatures for annealing and the enzymes to avoid by-products. Second: Buffers needed for the different enzymes are incompatible. Or it is simply much easier to simply take the whole PCR reaction in the end, add some ligase and incubate it for an appropriate amount of time, so nobody ever bothered.

yes, the buffer compatibility was my main concern. My guess is that the ligation should be fine in the presence of pcr buffer, since as you mention, people just add dna ligase to their pcr rxns, post-pcr. But whether pcr is inhibited by ligation buffer I don't know. Looking at the buffer compositions it at least seems like it's worth a shot. Do you agree? Temperature I'm not so worried about, as there are ligases available with high optimum temps, i.e. right around my target annealing temp. They don't have inactivation temps, so my guess'd be that they won't mind high denaturation temp steps

If the buffers are compatible (especially for the magnesium content), you could give it a shot. The Taq shouldn't have much activity at these "low" temperatures, so at least you shouldn't have to expect some unexpected here :-)

In case this helps anyone, I found a technique called Gap Ligase Chain Reaction which includes both a thermostable ligase and a DNA polymerase enzyme in the same reaction:
Ligase Chain Reaction (LCR) --Overview and Applications (Wiedmann et al.) PCR Methods and Applications
Amplification of Chlamydia trachomatis DNA by Ligase Chain Reaction
Preliminary Evaluation of the Ligase Chain Reaction for Specific Detection of Neisseria gonorrhoeae
Detection of point mutations with a modified ligase chain reaction (Gap-LCR)


text:
metabolism preference by the body
What I know about metabolism is that,during exercise body uses carbohydrate first then fats and then protein,so my question is why does body prefer glucose first as fuel for energy and what makes glucose biochemically preferred molecule to be metabolized first

None of them can be directly use for energy. We all talk about aerobic oxidation, which is the major process for metabolism.
They all need to go into the tricarboxylic acid cycle (TCA cycle) and oxidation phosphorylation to produce ATP, which is the energy used in organism.
For glucose, they can break down into two pyruvate and enter the TCA cycle. That is the fastest pathway organism use to produce energy.
For fat, since they have long carbon skeleton chain, they cut off 2 carbon compounds from the fatty acid every time. And under a series of process, it become pyruvate and go into the TCA cycle. So it really takes long time and complicated pathway to oxidate the whole fatty acid molecules.
For protein, it is much more complicated. Since protein is not energy store form, it need to become a energy store form first. First it need to be degraded into amino acid, and different amino acids takes different procedure to go into the TCA cycle. Here is the picture I found on the book  by John L. Tymoczko, Jeremy M. Berg and Lubert Stryer.

In sum, glucose is the fastest energy form that body can use to take metabolism, oxidate fatty acid or proteins take much more complicated pathway.

I already forget all of the structure of carbohydrate, fat and also protein. But I still remember the reason for body using order of these compounds is related to the structure.
None all of carbohydrate can be directly used, only simple carbohydrate, like glucose, can be directly used.
For fat, it can be turn by carbohydrate for storage, and of course they are storage form, then they won't be easy for using. Even fat need to be used, they will turn to be carbohydrate again then using.
For proteins are another story, they aren't storage form, but they have some ability to form carbohydrate. So if the body is very starving and there is no other resource, the body will begin turn the protein to carbohydrate for using.


text:
How to Download the broadpeak files from the encode chip-seq experiment matrix?
I have tried the SqlDatabase of Encode opened it trough R ,i have tried other packages in R, i have tried the ENCODExplorer package but none of them seems to do what i want. I have an app that asks the user which cell type and which antibody factor wants to choose in Shiny. These cell types and antibody targets are drawn from chip-seq matrix here https://genome.ucsc.edu/ENCODE/dataMatrix/encodeChipMatrixHuman.html. I want to download the .broadpeak file from the experiment that was made using the two selections of the user . I cant find where the data from this matrix are stored and for sure they are not stored in the new website database of ENCODE.
Does anyone has an idea ??
These are some notes not all  from a what i searched

1)https://www.bioconductor.org/packages/3.3/bioc/vignettes/ENCODExplorer/inst/doc/ENCODExplorer.html
New portal of ENCODE https://www.encodeproject.org/
#Load the ENCODExplorer
suppressMessages(library(ENCODExplorer))
#Find all the files from the experiment with biosample from A549 human cell using H2AFZ as antibody target
query_results <- searchEncode("a549 chip-seq homo sapiens h2afz") or
search_results <- searchEncode(searchTerm = "a549 chip-seq h2afz", limit = "all")
//downloadEncode(resultSet = search_results, resultOrigin = "searchEncode", format = "bed_broadPeak")
cant find any broadpeak files

2)Connect to an Oracle database(Encode sql Database) using R
http://rprogramming.net/connect-to-database-in-r/
channel <- odbcConnect("genome-mysql.cse.ucsc.edu", uid="genomep", pwd="password", believeNRows=FALSE)
http://stackoverflow.com/questions/15420999/rodbc-odbcdriverconnect-connection-error
#Database schema
install.packages("RMySQL")
library(RMySQL)
drv = dbDriver("MySQL")
con = dbConnect(drv,host="genome-mysql.cse.ucsc.edu",user="genomep",pass="password")
album = dbGetQuery(con,statement="show tables")
Tables_in_hgcentral
1          blatServers
2                clade
3                 dbDb
4             dbDbArch
5            defaultDb
6               gbNode
7          genomeClade
8            geoIpNode
9            hubPublic
10           jorgetest
11       liftOverChain
12       liftOver_bkup
13           sessionDb
14   tableDescriptions
15            targetDb
16              userDb
17           wikiTrack
3)Not working-->https://www.simple-talk.com/sql/reporting-services/making-data-analytics-simpler-sql-server-and-r/

There is an FTP link from where you can download the data (I had downloaded it from there). In any case this question is off-topic because it is not at all about the bioinformatics aspect of the data.

http://hgdownload.cse.ucsc.edu/goldenPath/hg19/encodeDCC/wgEncodeRegTfbsClustered/

I'm putting this question on hold because it is not about biological or bioinformatics principles.


text:
How do humans know what goes on in optical illusions?
Optical illusions are designed to deceive humans, I think.

That thing is moving! It really is! It's moving!
However, user Konrad Rudolph just told me what went on in a different optical illusions through a comment on a separate answer. I believe he is a human, as stack exchange has a box you have to tick to prove you're not a robot. Considering Konrad Rudolph is a human, how did he know what was happening?
Loads of people have told me 'what's happening in the illusion' but I just can't see it. How does everyone know?

How can people know what is going on in an optical illusion?

Or maybe... You're all robots?

We know what's going on in optical illusions because we have a great deal of knowledge about how sight and visual perception work. That should be pretty obvious. I really don't understand what your question is.

Furthermore, if you look at the actual pixels in that image or just a small segment it is clear that it isn't actually moving. And a person created that image, and it is a still image.

Of course it's not moving. It's merely a bunch of pixels. Please refine the question and get rid of the robot fluff.

"Optical Illusions" or sometimes referred to as "Geometrical Illusions" aren't illusions in the sense that we are seeing something that isn't there. It's an illusion in the sense that the interpretation of what is there is wrong.
Typically this involves seeing movement where there is none as in the picture you provided. A scientific way of describing them could be:

When subjects are instructed to carry out a task to which the visual system is not adapted.[1]

Which in layman's terms means our brains cannot handle the way the information is being presented to us. It is presented in such a way that our brains force us to interpret something that is not happening physically, even though what we see is actually present.
Interestingly this doesn't just happen with optics but audio as well. [2] This gives credence to us being able to detect what is actually going on versus what is being interpreted as going on by our brains. As noted in the study:

Listeners were presented with a sequence of sinusoidal tones, each tone 250 msec in duration and with no gap between adjacent tones. All tones were either 400 or 800 Hz, and these frequencies were presented in strict alternation. This sequence of alternating tones presented at equal amplitude to both ears simultaneously for 20 sec. However, when one ear received 800 Hz, the other received 400 Hz and vice versa.

It's important to note that this study found that no listeners interpreted the stimulus properly. We know this because the researchers only used 400Hz & 800Hz frequencies and controlled exactly which ear was receiving it. People either heard something that was not there or something contradictory to what was being played. This shows we can measure what actually happened in the illusions since we created it and are able to quantify it.
This can similarly be done with your image.
1) A human created that image thus we can create a similar image and know exactly if we created a moving image or not, then compare to what people interpret to see if illusions occur.
2) You can track any pixel on that image using software to see if it moves and compare to what subjects interpret.
There are also other interesting studies such as the optical illusion of a baseball being in motion. [3] This is particularly useful as this can be described with physics which can tell us what is actually going on versus what we are thinking is going on.
Another interesting study is that autism may change the way the brain interprets optical illusions. [4] Leading more to the idea that our brains are flat out wrong about what is happening because even though the information has not changed it has been interpreted differently. Sometimes resulting it people being less susceptible to an illusion.
The answer to "How does everyone know?" is that people can know because we can use tested methods of interpreting data correctly and observe the difference between that and what our brains alone interpret. Our brains are evolved for specific types of environments and sensory illusions are things that are often too unfamiliar to our brains to deal with properly.


text:
What is the most-stable gene identifier?
I've struggled in the past with designing data(bases) around gene-identifiers that evolve over time.  For example, UniProt and Ensembl change their identifiers for certain proteins/genes and the IDs go stale after a while (years).  HGNC seems possibly better for this?  What I'd like is to have a single unique identifier for each human gene that will remain stable for many years.  I know genes get re-classified occasionally, but you shouldn't end-up with a new identifier for the same locus.
Suggestions?
Thanks

We use HGNC. But there's certainly no guarantee the symbol will stay the same for years.

Maintaining IDs consistency is a common problem. I've never seen any reasonable solutions for it and don't believe that there are any. However, there are a few shortcuts.

You can create an extra table with aliases for later renamings and refer them to original ids. Pros - it is flexible. Cons - maintaining is exhausting and you need to figure a way to explain to users why they input one id and receive other.
The solution is pretty obvious - if you'd like to have "a single unique identifier for each human gene that will remain stable for many years" you can just take a snapshot of current state of any database you like and don't touch it for many years. You can release version-specific releases of your database and specify versions of reference database you use. E.g. "Glioblastoma_drug_perturbation_2016_(GRCh38_ENS87)".


text:
NADH generated by glycolysis must be oxidized back to NAD+ in order for glycolysis to continue. What three positive pathways exist for this to occur?
I know where NAD+ is reduced to NADH but don't have the slightest clue as to three pathways where NADH is oxidized to NAD+.
If you could give me some guidance that would be great!


text:
Staying underwater: would mutual rebreathing help?
If two people want to stay underwater for as long as possible, could they last longer if they exchange breaths in turns (ie: through a simple tube or mouth-to-mouth) than if they simply hold their breaths alone?
Would there be any dangers in doing this somewhat regularly?

Theoretically:
I'm going to assume that in your scenario, both individuals took a deep breath of regular air before submerging themselves, as this changes quite a lot (you'll see why in a second). Regular air on Earth as you probably know is made up of 78% Nitrogen, 21% Oxygen, and other trace elements like CO2 and ArgonColumbia University. What we care about is oxygen, as this is what our body can't function without.
The air we exhale is approximately 14-16% oxygen [2], which is a significant decrease, but is still very breathable. If we choose 15% as the exhaled percentage and 21% as the inhaled percentage, the percentage decrease is approximately 29%. Thus, with each breath taken by the other individual the amount of oxygen in the shared air decreases drastically. Another problem is the dilemma of CO2, which is exhaled at a 5% percentage increase. I would imagine the two people wouldn't make it more than a minute before the oxygen level in the shared air is too little to be absorbed and the CO2 makes them both lightheaded to the point where they faint and forget about the tube altogether.
If both individuals had breathed in pure 100% oxygen it would delay their impending deaths but it wouldn't prevent it. I love doing this sort of stuff and could calculate the difference in time between both before the air is unbreathable but...
Practically:
It wouldn't work. It may sound like something that would work but think about it this way: the very first breath one of them takes it literally sucking the air out of the other's lungs. No matter how much one tries to synchronize breathing in and out with the other -  based on lung size, lung volume, diaphragm surface area and many other factors - one's breathing in simply cannot equal the other's breathing out. One of them would eventually breathe in too much, leaving the other choking and gasping for air, leading to a tug-of-war of air, that unless they resurface will lead to both of them drowning.
[2]:
P.S.Dhami; G.Chopra; H.N. Shrivastava (2015). A Textbook of Biology. Jalandhar, Punjab: Pradeep Publications. pp. V/101.

Another method: Since CO2 production rates are higher when breathing from a tube (compared to both people holding their breaths), both people would run out of air faster.


text:
What are the evolutionary reasons behind men being taller than women?
Human men and women are sexually dimorphic: there are some phenotypic differences between men and women.
Men being taller than women is an accurate stereotype. Overall, men are on average 13 centimeters taller than women. The most extreme example is Macedonia, where the average man is 18.5 cm taller than the average woman.
When you look at animals, I think it's pretty intuitive to think that females are often larger than males from the same species. Spiders, fish, insects, some birds, there's an endless list of examples of bigger females than males. This is explained by a variety of different reasons depending on the species, from mate competition to the ability to bear children. So why would human males be so much bigger than women?
We all know that there are a lot of factors behind the height - and, on a related subject, strength - differences between the sexes. There are some genetic factors, as pointed out in this interesting Quora post about the topic. We also know that nutrition has a large impact in growth. In a word, we know what causes the height difference between men and women. There is a great post about it here. But I couldn't find any conclusive evidence as to why men are taller than women.
Is this because women naturally like tall men? Did prehistoric men have to be taller than women in order to thrive? Or is it just genetic drifting that, more or less randomly, led to this height difference?

The motivation behind my curiosity is feelings-driven. A while ago, my dad said during a conversation that he once "saw a documentary in which they explained that early men stole all the good proteins from the women, so they could grow taller and stronger unlike the poor females." As much as I love and respect my dad, I have a hard time believing that men are natural culprits and thieves. I am by no way making this post just to "prove him wrong" - I am absolutely interested by the topic and would love to know more. Also, if anyone knows the documentary he was talking about, I would be glad to give it a watch.
All apologies for any bad English you might find. Please tell me if I make recurring grammar mistakes.

In many mammalian species, the male is larger than the female. It is not a special case in humans.

For some reason taller men are preferably chosen for leadership positions. This happens today and so probably happened in past ages. Those in leadership positions historically have had more access to mating opportunities.

I assume by asking why, you are asking about the distal evolutionary causes, and not the molecular mechanisms that account for these things.
(Important disclaimer: these causes are difficult to be certain about; they require a fair amount of informed speculation.)
With that said: it is widely agreed upon in evolutionary biology that human males, as in other mammals, are thought to be larger mostly due to sexual selection. In other words, size is sexy, and sexy individuals fare better with respect to mate choice, on average. Sexual selection can also work via male-male competition. There may be other causes that are relatively minor contributors compared to this one.
Notice, however, that in humans, females evidently do not remain tiny with respect to males, but they get 'dragged along' in terms of their height, so that males are not drastically different in height (unlike, for instance, in elephant seals). This too may be a result of sexual selection, quirks of physiology across the sexes (e.g. genetics of dimorphism), or even natural selection. Think hip size and the size of human skulls.
Additionally, differences in development time (e.g. length and onset of puberty) can skew body size. Humans certainly exhibit dimorphism with respect to development.

Thank you for this very interesting answer. Indeed, my question was about distal evolutionary causes, and not molecular things. The example of the elephant seal is great, I was not familiar with this.
I can't vote on your answer due to low rep but I greatly appreciate it.

Women do not get dragged along, more extreme sexual dimorphism exists in other great apes. Differences in sexual dimorphism is well predicted by levels of competition and cooperation.

Sexual selection isn't an arbitrary process, it's generally based on objective evolutionary qualities. So shouldn't it rather be: Size is better, so size is sexy. But then this answer is really missing the point?

Certainly sexual selection can be a completely arbitrary process and in many (in many clades, most) species it is completely arbitrary and devoid of any real hallmark of signal of fitness. Sometimes, things just become sexy and this drives traits for that sexiness to be selected, and it often also sometimes drives species to extinction due to the trait rendering individuals unfit for competition in their habitats. Beetle weaponry and bird coloration and generally all sorts of ornamentations come to mind.

Sexual selection would explain tall people. But it doesn't explain taller MEN. Because the same tall men would produce both sons and daughters. Unless the argument is that tall men would produce more sons (e.g. the children of Presidents of the United States), while short men produce more daughters.

More details to support @SPr's answer, from the abstract of Plavcan (2012): "Sexual Size Dimorphism, Canine Dimorphism, and Male-Male Competition in Primates: Where Do Humans Fit In?"

While dimorphism in primates is associated with agonistic male mate competition, a variety of factors can affect male and female size, and thereby dimorphism. The causes of human sexual size dimorphism are uncertain, and could involve several non-mutually-exclusive mechanisms, such as mate competition, resource competition, intergroup violence, and female choice. A phylogenetic reconstruction of the evolution of dimorphism, including fossil hominins, indicates that the modern human condition is derived. This suggests that at least some behavioral similarities with Pan associated with dimorphism may have arisen independently, and not directly from a common ancestor.

mate competition: bigger males can beat up smaller males to gain access to females
resource competition: bigger males can beat up smaller males to gain access to resources (and hence survive better/gain access to females/have their offspring survive better/etc.)
intergroup violence: bigger males are more likely to survive & win when fighting with smaller males in other groups
female choice: as @SPr says: "size is sexy, and sexy individuals fare better with respect to mate choice, on average"

And "the modern human condition is derived": that means that our best guess is that human dimorphism and behaviour have evolved since we split off from the rest of the primates; this makes it slightly harder to use non-human primates as a model.


text:
Identifying a bone I found in Central France
I found this bone in Auvergne as a child. This specific area is apparently well-known to paleontologists and I found the bone in a field very close to scientific excavations (literally meters away from the area that was delimited by ropes). I picked it up and brought it to a local museum but back then they simply told me something like "lucky find, it might be a prehistoric animal! You can keep it, we only do mammoths here."
Years passed and I've kept this bone (probably a vertebra, coccyx or sacrum) on a shelf. Now, my curiosity is having the best of me and I would really like to identify it.
I spent some time looking at "bone identification" forums, databases and charts online, but they were quite disappointing. However, I am almost sure the bone belongs to the spine of a mammal.
Here are pictures (mug for scale):

Definitely spine, pretty certain on sacrum too, which most likely makes it mammalian (given location...), but have no idea on species. Might not be identifiable as lots of it is missing.