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What happens when someone is stung by a jellyfish?
What happens in the human body when someone is stung by a jellyfish; namely a box jelly. Judging by what I have heard about the stings I'm guessing that they involve a neurotoxin.

But what is actually happening? What are the symptoms and what happens after the sting (treatments and survivability)?

Someone else should pee on it

The problem is that box jellyfish doesn't specify one jellyfish but a group of different jellyfish. Some of these are highly venomous - I pick here Chironex fleckeri, as this is often called "the most venomous jellyfish in the world".
Chironex fleckeri has long tentacles which are covered with millions of explosive cells called Cnidocytes which inject a dart with the very powerful toxin upon touch. It is therefore very dangerous to touch the tentacles with bare hands to remove them.
The toxin is a mix of different bioactive proteins which have cytolytic, cytotoxic, inflammatory or hemolytic activity. Case reports (you can find information in reference 3 about it) show that the tentacles "burn" though all skin layers causing immediate strong pain and lasting scars (if the victims survive) which tend to show signs of necrosis. The toxins itself paralyze the muscles of the heart and the respiration and also causes hypokalemia by hemolyzing red blood cells (one of the toxin acts as a membrane pore in the blood cells). This causes further problems and often a cardiac arrest. See reference 1 and 2 for details on the toxins. Especially 2 is interesting, as this is a PhD-Thesis on this topic with a lot of references.
Treatment depends on how severe the injury is - in severe cases an antivenom can be used. Besides this typical measures are CPR, giving oxygen and removing the tentacles (with appropriate protection). See reference 3 (good overview) to 5 for details on this topic.
References:

Chironex fleckeri (Box Jellyfish) Venom Proteins: Expansion of a
Cnidarian Toxin Family that Elicits Variable Cytolytic and
Cardiovascular Effects
The molecular and biochemical characterisation of venom proteins
from the box jellyfish, Chironex fleckeri
Chironex fleckeri (Multi-tentacled Box Jellyfish)
Jellyfish stings and their management: a review.
Cytotoxic and cytolytic cnidarian venoms. A review on health
implications and possible therapeutic applications.

Oh, I didn't know that there are different types of box jellyfish XD

You've misspelt venomous twice here, once as "venomenous" and the second as "venemous".. SE's silly 6 char minimum won't let me change it.

@FaheemMitha Ups, thanks for the notification.


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How does aspirin "thin" blood?
As we all know, aspirin doesn't actually thin the blood, as it has been explained to me, it makes it "slippery". Slippery blood doesn't stick to itself hence this helps prevent internal blood clots (or allows blood to pass more easily around an existing clot). I also understand that having your blood too "slippery" can lead to the body attempting to counteract that and making it too "sticky".
Anyhow, my question regarding that is this, how does aspirin work? How does it make the blood "slippery"? (If there is a more medically correct term for "slippery" and "sticky", I'm all ears).
P.S. I paid the Mayo Clinic's website a visit before coming here, the information about aspirin's mechanism wasn't particularly helpful to me.

Aspirin doesn't make blood slippery (like lubricant's might allow machinery to work.) Blood clots require thrombocytes (aka platelets) and blood proteins to form. Too many platelets and clotting is more likely; not enough (or inactivation of some of the platelets) and clots don't form as easily. Anything that activates platelets (as described below) can result in a clot. Aspirin inhibits that.

Aspirine irreversibly inhibits the enzyme cyclooxygenase. This enzyme facilitates the reaction from arachidonic acid to prostaglandin G2/H2. The further reaction leads to the generation of Thromboxane A2 which is important for the activation and aggregation of platelets. See the figure (from here) for an overview:

Thromboxane A2 usually stimulates the activation of new platelets and increases their aggregation, with a shortage of this compound these activations are not possible and the coagulation of blood is reduced.

Aspirin  inhibits COX in the endothelium which is required for prostacyclin (PGI2) production. PGI2 is an anti aggregant and vasodilator  . Aspirin also inhibits thromboxaneA2 ( TXA2) production in the platelets. TXA2 is a platelets aggregant and vasoconstrictor hence antagonist of PGI2.
So aspirin decrease both PGI2 and TXA2 production but endothelium cells  can reproduce new COX inside them hence can quickly come over the inhibition of aspirin while platelets can't reproduce new COX so once they are inhibited then they can come over this inhibition only when new platelets are produced in the bone marrow so it takes too much time .
So what aspirin does it that it shifts the PGI2-TXA2 equilibria towards PGI2 so reduce platelets aggregation. Hemostasis , Harper 31st edition.
https://www.webofpharma.com/2021/02/harpers-illustrated-biochemistry-31st.html?m=1

Can you add sources to this answer as well to allow others to background read on your material?

Yupp now I added my resource: hemostasis chapter  form Harper 31st edition

Please do not upload book pages. This is a copyright violation and not tolerable.

Ohhk ,,I apologise

Thanks for all your efforts ro improve your post. Kudos. Can you please add a weblink to the book you cite?

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Book-recommendation: plant biophysics
I'm a physicist by training am looking to learn more about the biophysics of plants.
Can you give me your recommendation of good resources on plant biophysics? Books are preferred.

Seeing that someone voted to close this post, I completely rewrote your post (incl. title and tags). Don't hesitate to switch back if you don't like my edits. Disclaimer: I know nothing about plant biophysics!

Book recommendation questions are considered 'opinion-based' if specific details are not provided. Please edit your question to add details.

@WYSIWYG can you please expand on what specific details are missing? To me, the question seems on-topic. 'Plant biophysics' doe snot seem too broad as a subject but I might be mistaken.

IMO it contains insufficient detail on the users background in bio, the level of book required (high school, undergrad, post grad), and what specific topics need to be covered

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Is evolution a predictive theory?
My feeling is that almost any observation can be explained by current evolutionary theory. Is there any example of someone developing a rigorous framework or mathematical model of how evolution works?

I edited your question to remove the "primarily opinion based" part. Feel free to roll back if you don't like the edit.

While I agree the OP might be opinion-based (see its activity on the site so far), with the edit the question is not anymore. I agree it is impossible to draw a full picture of mathematical models used in evolutionary biology (would be too broad), it is still possible to answer to the question whether or not such mathematical modelling exist in biology. I think this question should remain open especially that it may help future users.

I have removed "useless as" from the title. If you want to know whether the theory of evolution has or does not have predictive power, the shortened title does this perfectly well. Including "useless as" is an unsubtle and unscientific way of indicating that you are expressing an opinion rather than asking a question.

It's still useless

Evolutionary biology is a highly quantitative science and offers a fair amount of predictive power. However, at the same time, there are plenty of things that we are completely unable to predict.
What are we good at predicting?
There are plenty of things and it is impossible to list them all. Here are a few examples of things we can predict.

Number of pairwise differences (or other measures of molecular differentiation) do we expect between two lineages that recently split in a given number of years.
Number of pairwise differences between individuals coming from the same population.
Number of mutations of given fitness effects (whether beneficial or deleterious) do we expect to accumulate over a given period of time in a population. We can predict the age of a lineage.
Predictions about the evolution of multicellularity, sociality, etc. in lineages that are limit-cases (relating again to our ability at a short time only).
Speed of evolutionary change as measured in Haldanes or in Darwins (these are units) (from knowledge about the genetic variance).
Predictions about the heterozygosity of a population and the loss of heterozygosity through time.
predictions about the gene flow, migration rate or strength of selection.
Predictions of the consequences on fitness that a change in population size may cause.

Generally speaking, we have good predictive abilities at short time scale OR for neutral sequences OR for conserved sequences (strong purifying selection).
In short, we can predict a lot of things but by far not everything yet.
Main complications in doing predictions in evolutionary biology
I would suggest decomposing the reasons why predictions can be hard into the following categories. However, I might well forget something and one could argue that my semantic is less helpful some other semantic.

Environment

One issue related to making predictions at long time scale is that the environment changes through time in a way that we are not able to predict accurately enough yet.

Noise (incl. genetic drift)

I am not here talking about measurement error or sampling error (these are statistical concepts you may want to check if you don't know them), I am talking about the stochastic process that is inherent to biological systems such as the randomness of mutation processes and genetic drift.

Genotype-phenotype map

We have too little understanding of molecular genetics in order to be able to predict how different specific mutations would affect the phenotype. As a consequence, today we still have very little predictive power about the evolution of a phenotypic trait that is currently totally inexistent.

Complex systems

For example: demography affects evolution which affects the social environments, which affects demography which affects the pattern of species competitions which affects the evolution of another species which affects its demography which affects the evolution of a third species which affects the demography of our first species, etc... These kind of complex systems are often mathematically not tractable.

Parameters

We often don't know the exact parameters of the lineage we are interested in. There is a lot of measures to take to be able to make predictions and we often don't have the money (or the time) to make all these measurements (assuming we are able to accurately measure them). For this reason, we are often relatively good to make predictions for a few model organisms but pretty bad for the vast majority of species.

Applications of evolutionary biology
There are not a lot of applications of evolutionary biology for the moment but still, there are some proving its predictive power. These applications include

medicine and epidemiology (incl. evolution of resistance)
artificial selection and other techniques mainly to improve crops (e.g. nuts)
Various search algorithms such as the genetic algorithm

Note, my answer was partially recycled from this other answer of mine
Answering directly in your text

It seems like almost any observation can be explained by current evolutionary theory

This is wrong. You should learn more about evolutionary biology (starting with Understanding Evolution by UC Berkeley for example) and you will understand why it is wrong. I can't make a whole introduction to evolutionary biology in a single post.

Is there any example of someone developing a rigorous framework or model of how evolution works?

Yes, there are thousands of such models depending on the exact evolutionary process of interest. Just to give you a feeling of it, you could have a look at any book recommended on the post Book recommendation on population/evolutionary genetics?. If your knowledge in math is a little weak, then you might want to have a look at the introductory book A Biologist's guide to mathematical modelling in evolution and ecology (Otto and Day). While this book is quite introductory, I would still recommend starting with an even more introductory course as suggested above.
Standard mathematics methods used in evolutionary biology include branching processes, birth-death processes and other Markov Models, mathematical statistics and probability theory, diffusion equations, approximation theory, ...
On a side note, you would note that the development of statistics is very much related to evolutionary biology. This is true historically but is still true for the development of modern statistics. Just to cite one person, Ronald Fisher was an evolutionary geneticist (one of the fathers of the modern evolutionary synthesis) and he invented some of the most used statistical tests (t-test, anova-F-test, Fisher's tests).

So in other words the useful evolutionary biology ("complex systems") doesn't exist

Can you reformulate your question in the comment, I don't understand it. What do you call "the useful evolutionary biology"?

If your comment asked "is there any usefulness to evolutionary biology", I redirect you to the application section in my answer. Yes, to medicine, to designing better crops (resistant to drought or to the warming climate), to predict the yield that can be achieve by fly farming and to know what population size should be used for fly farming, etc...

That's agronomy and really has nothing to do with this

You seem to be primarily opinion based. Predicting change in a quantitative trait of interest to agronomist definitely has to do with evolutionary biology. The food industry is an important private sector that hire plenty of evolutionary biologists.

No they dont. It's an almost entirely ivory tower field

You know nothing about this field you are describing (as it is made obvious from your other activity on this site). You are opinion based without having ever opened a book of evolutionary biology (as it is made obvious from your other activity on this site). I will stop answering to your comments from now on as I have better to do with my time. If you are genuinely trying to understand evolutionary processes on a successive post, I'll be happy to help you with that.

If you say so..

Reading your question again, I realize that I mainly answered to the question is the title but I haven't been very specific to the content of the post. I therefore added a section in my answer hoping that will help you. Good luck!


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relative-rate of evolution
I am supposed to calculate the relative rate of evolution of two sequences (human and sheep) with a chicken serving as the outgroup. The sequences are pretty long, so I will just create a short example since I just want to learn the process (we are expected to use online resources to figure out our homework problems since it is an online class, but I can't find any examples).
Human:   GGATGCGCCT
Sheep:   GGACGCGCCT
Chicken: GGACACGCCT
Can someone show me how to do this? Here is my guess from the limited info I found, but I have little to no confidence that it is correct:
p-distance of human/chicken = 2
p-distance of sheep/chicken = 1
relative rate of evolution = 2/1 = 2
Is this correct? If not, can someone show me how to do it correctly?

This kind of thing is normally calculated using the $K_{a}/K_{s}$ ratio, the ratio of synonymous to non-synonymous substitutions. It is not enough to count mutations for coding sequences, you should also take into account whether or not that mutation will actually change the resulting product.
There are various online tools that can help you do this, for example Phylemon:
http://phylemon.bioinfo.cipf.es/evolutionary.html


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Rabies virus mortality
Why rabies virus has nearly 100% fatality rate in human (see this virology blog; thanks to @iayork for the link) if not vaccinated early, even some people have survived Ebola, then why does rabies doe not get extinct as its most virulent form will kill host and virus also?

Would be good to have a reference for the claim rabies virus has 100% kill rate in human if not vaccinated early

@Remi.b http://www.who.int/mediacentre/factsheets/fs099/en/

@murmansk Maybe I looked poorly but I failed to find the claim you are making. Sorry to be a pain but could you highlight where the claim is being made?

Speaking as a virologist and veterinarian it's absolutely true that the mortality for human rabies approaches 100%. How lethal is rabies virus?, List of human disease case fatality rates, Rabies - Prognosis

@Charles http://www.who.int/rabies/resources/SEA_CD_278_FAQs_Rabies.pdf question no 11

@Charles there are a half-dozen known survivors, but considering that the virus kills over 50,000 people every year, bloviating about the difference between 100% and 99.9999999% seems pretty silly.

@Remi.b if you want to mark this as a duplicate for the question you answered, I'd suggest significantly improving your answer there; it completely ignores a very large literature on pathogen selection.

@Charles I've now edited OP's post.

@iayork If the current answer at the other is not fully satisfactory, then a new post should address the reason why it is not fully satisfactory, not just ask the same question over again. I would not mind if the OP wants to argue that his post is specific to rabies and it is interesting because... but it should be clarified then IMHO

@Remi.b There are already better answers in Why have parasites not evolved to be harmless?

It's a common misconception that pathogens "don't want to kill their hosts". In reality, pathogens don't "care" at all about killing their hosts. All pathogens "want" to do is transmit from one host to the next. (Taking out the teleogenic language: There's no natural selection on a pathogen to reduce virulence as such. The selection on a pathogen is for transmission.)
In some cases, transmission is optimized when the virus is less virulent. In other cases, transmission works just fine when the virus is highly virulent. Rabies is one of the latter cases.
If a pathogen is spread by, say, respiratory contact, then having a host that is ambulatory and seemingly healthy may allow the first host to contact many others, so reducing virulence may enhance transmission in that specific case.
If the pathogen is spread by sand fleas (as in myxoma in Australian rabbits), then rapidly killing the host is counterproductive, because fleas leave a dead body. But keeping the host healthy is also counterproductive because a healthy rabbit scratches away its fleas. Optimal transmission turned out to work with a virus that kills 50-75% of its victims, because that makes the host very sick for a long time, allowing the fleas to bite it unimpeded.
Rabies spreads by damaging the brain, making the host aggressive, and spreading through bites in saliva (among other ways, but that's an important one). Serious brain damage to the point of wildly abnormal behavior is really not compatible with a host living a long time, so optimal rabies transmission means very high host mortality.
Finally, humans are not natural hosts for rabies and rarely transmit the virus, so in any case there's minimal natural selection for any virulence changes in humans. But it likely wouldn't matter, for the reasons above.


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What does ensemble-based model of enzyme mean?
I am reading Pan et al. (2000), a paper about dihydrofolate reductase (DHFR).  They claim using a ensemble-based model of DHFR.
What is a ensemble-based model?

Can you please link to the paper? Does DHFR means "Dihydrofolate reductase"?

@Remi.b,yes it is dihydrofolate reductase, I edited the question to add the link

An 'ensemble' is a set of related models of a structure.
For example, conformational ensembles describe the structure of flexible proteins. There is a database of such structures here : http://pedb.vib.be/.
When NMR is used to determine a structure, the result is an ensemble of structures (see this paper for a comparison with crystallography). However, it is possible to see multiple structures for crystallography as well. This paper on "Accessing protein conformational ensembles using room-temperature X-ray crystallography" describes limitations to the idea of crystal structures having one unique structure.

Does that mean: using a ensemble-based model of DHFR is using one conformation of DHFR (e.g. there might be multiple DHFR forms in E. coli, and the study used one of them)?


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First life forms to evolve controlled flight
What was the first living organism able to fly in the skies and control their direction , not just Aeroplankton like bacteria and viruses carried by the winds but something  like an winged  insect or fish  or  something  similar,  and when did it evolve?

It was probably an early Pterygota (winged insect).
To my knowledge, the phylogeny of Pterygota is not completely resolved.

Hennig (1981) describes the following phylogeny

Boudreaux (1987) describes the following phylogeny

Wheeler et al. (2001) offers good evidence for this phylogeny

Odonata encompasses dragonflies and damselflies. Ephemeroptera are commonly called mayflies. The origin of pterygotes was about 300 million years ago.
The very first flying(ish) insect had three pairs of wings (Kukalova-Peck, 2005). The pair present on the first segment of the thorax (counting from the head) was then lost in all extant species. Note however than membracidae are using the developmental pathway for this third pair to make elaborate display (mainly for defence; see below).

Some clades further lost both pairs of wings and one clade, the Diptera (flies) lost only the last pair of wings. This last pair is replaced by halteres that are particularly visible in crane flies (see below)

Re "Some clades further lost both pairs of wings...", does this mean that the ancestors of all present-day insects once had wings, but some lost them?  Or were there other lines that never developed wings at all?

There are lines who never had wings such as collembola, archeagnates and silverfish who never had wings. Most lines people generally think of when talking about insects either have wings or had wings in their ancestry.


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What are constrained genetic elements?
I am somewhat of a newbie in evolutionary biology currently taking my first steps in bioinformatics. I was reading a paper when I came across the term  "constrained genetic elements", referring to sequences in the genome.
From what little I found googling the term, a constrained genetic element is a sequence/region in the genome that can be found preserved in many generations of a species. Is my understanding correct? What are the criteria by which those regions are identified?
The paper is Analysis and Classification of Constrained DNA Elements with N-gram Graphs and Genomic Signatures.

In what paper did you find the term? And in what context in the paper?

@kmm I added the paper title. The term is mentioned when explaining that classification is applied to "conserved sequences" in the genome, but no further explanation is given.


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Explain allelic complementation at molecular level
I know that Allelic complementation is a phenomenon where two recessive loss-of-function allele generate a functional gene product by compensating each others' defect. But I don't get how do they compensate each others' defect.

I don't know much about molecular genetics but you should probably specify that an example of the mechanism by which such "allelic compensation" occurs would be welcome to answer your question.

Allelic complementation meaning that the offspring could have functional gene product

As Matej said, mutations in two different genes (or even a gene and a non-coding regulatory element) can lead to complementation and as they pointed out, the complementation test is designed to check if mutations are on separate genes or not.
Molecular mechanisms that may lead to complementation (apart from Matej's example):

The double mutation in two enzymes in a pathway basically that does not alter the metabolic flux. Lets assume the pathway is linear i.e. no branches. The net flux would be limited by the slowest enzyme in the pathway. If a mutation increases activity of the rate limiting enzyme-1 while another mutation reduces the activity of enzyme-2 then the net flux may not change.
If a regulatory gene acts on another gene by some kind of molecular recognition (protein-DNA, protein-RNA, RNA-DNA, RNA-RNA, protein-protein), then the effect of a mutation in the recognition domain in the regulator can be complemented by another mutation in the target such that the binding affinity is preserved. For e.g. a miRNA regulating a mRNA. If a mutation in miRNA, A→G, is compensated by a mutation, U→C, in the target, then there may be no change in the molecular phenotype. This logic also applies for two gene products that function as a heterodimer.

However, different mutations in the same gene may also lead to complementation like effect. I cannot cite an example but there is a theoretical possibility. Therefore this answer is speculative. There can be two cases here:

Two different mutations in the same allele
Two different mutations in two different alleles

For case-1 you can imagine a situation in which the activity of the gene product depends on intramolecular interactions (secondary and tertiary structures). Two mutations can preserve the intramolecular interaction in a manner similar to the case of intermolecular interactions discussed above.
For case-2 you can imagine a gene-product that functions as a homodimer. If the two mutations preserve the intermolecular interactions in the dimer then you would see complementation. Case-2 can also be observed in a situation when the mutations occur in two different functional domains of two different alleles such that finally the dimer is still capable of carrying out its activity.

The main principle is that the loss-of-function mutations have to be on different genes and recessive. Source
I wouldn't say they compensate each other. If either of them was in homozygous conformation, their effect would be full-shown.
The thing on the molecular level is that often less than 50 % of the gene product is necessary for the gene to "work", to fulfill its function. (in other words, the loss-of-function mutation is recessive and one functional allele is sufficient to show its effect). If the individual is recessive homozygot for the mutation in the gene, there isn't enough functional product to fulfill the function.
However, sometimes, mutations in two different genes can result in the same phenotypic outcome (e.g. one gene making colorless precursor of stain, the other one making protein which turns it into the actual coloring molecule). If there is a homozygous conformation for mutation in either of these two genes, the molecule of stain won't be produced and the flower will be colorless.
However, if two individuals aaBB and AAbb (both colorless) pair, the offsprings will all have colorful phenotype (AaBb) because there will be some of the stain precursor and some of the enzyme that makes stain molecule from the precursor, hence there will be some stain. This event is called complementation.
This was actually used in the past to determine, whether some recessive-trait-carrying individuals had mutation on one gene or on two.


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Insect Identification. Moth or dragonfly or?
Found on the exterior wall of my house taking cover from the rain it seems. Wingspan is approximately 5cm. I live in the South SF Bay and it has been rather cold and rainy this week.

t has two long cerci, so I guess it can't be a crane fly, an odonate (dragonflies and damselflies) or a moth/butterfly. It has winged hair but it really does not look like a caddisfly. The butt seems to come back up but it does not look like a mecoptera (scorpion fly). This thing look like the wings can't move, like a plane! Was it alive? Did you notice any behaviour? Can you say anything about the mouth part?  I think I would think those arenot cerci and it is some kind of moth.

Found it. Amblyptilia acanthadactyla from Europe. He must be tired.
Update: It's a Geranium Plume Moth! Beautiful pics! I have geranium plants in my garden. Why have I never seen these? Thanks for the right find, Arthur!

Oohh a plume moth. That would make sense. Probably a sister species given that you found it in the USA. It could be a Geina sp. maybe or some other plume moth.

Could be! And it's alive, btw. I carefully captured it safely in a jar before having identified it. Since it doesn't eat people or pets, I have set it free to enjoy the low growing plants in my garden. Thanks for playing, Remi.b

Agreed as to the family; the genus as given originally is possible (according to this site the genus has two species north of Mexico); it doesn't look like all Nearctic species have images online (the site I just linked to does have a few photos accompanying a fairly recent species checklist [the most recently described species therein dates from 2017] and does link to other sites with photos).

Could you add an image and some backgrounds why you think this is the correct ID? Such as global distribution and whether it fits OP's location and so forth.

The species as given in the answer is not correct; the genus might be (bugguide's coverage of a Nearctic congener here does look similar -- and the species is Californian); I would upvote the answer if it were changed to that species.

@ArthurJFrost I think you owe Johnny an upvote :p


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Visual and clear example of the idea that "animal doesn't need to understand the evolutionary function of its actions"
This is a question about education. I am trying to come up with a very visual and clear example, to explain a particular concept in evolution.
The concept I am trying to explain is,

the fact that an animal does not need to understand why it's doing something in order for that behaviour to be selected

(by "why" I mean, the evolutionary/functional role of that behaviour, the reason why it increases the animal's fitness).
Students who don't yet intuitively understand evolution, sometimes mistakenly think that in the theory of evolution, animals need to understand why their behaviour is leading to offspring in order to do that behaviour. (they might say: "the bee looks for flowers because it wants to feed his children", although bees (probably) don't actually make this computation, but simply act on stimuli).
(Note by the way that this is not simply about anthropomorphization: e.g. humans also don't need to understand what sex is for, in order to produce offspring).

What I'm looking for is an example of an animal, and a behaviour that is characteristic for that animal, that very clearly shows this principle:

It should be clear and intuitive, that the animal doesn't understand "why" it's doing what it's doing, because to reason about this would clearly be too complicated for the animal (I don't think the bee example really satisfies this).
It should be visual, and memorable.

I may give an answer at some point. But what you're referring to is the distinction between ultimate and proximate explanations for a phenomenon. You can see the Wikipedia article for one example. This is also widely discussed with many examples in many books on animal behavior, for example in chapter 3 ("Hormones and Neurobiology") in the book "Principles of Animal Behavior" by Lee Alan Dugatkin. This part is actually in the free preview of the book on Amazon, so you could look there.

@Eff, I would say that the category I'm referring to is an example of a ultimate and proximate explanations, but that concept is far more general. In any case, thanks for the comment :).

just use things that don't have a brain like trees.

@John, that would actually not bring the point accross, since people would retain the intuition that it holds with things that have brains

if you can show how it works in plants you can only explain it works the same in animals. Trying to use an animal as an example has a big problem, if the person does not know basic evolution they will have no idea of what an animals brain is or is not capable of. You are expecting two vastly different levels of biological knowledge from the student.

Use human behavior, they're human, do they understand why they like salty foods or why thiols smell bad to them. These behaviors still work even when you have no idea why you are doing them.
Using humans circumvents the problem of them not understanding animal behavior, which they already have to do to grasp your explanation for animal behavior. Using any other animal requires them to understand that animals mind which an entry level student will not, however as humans they can assess their own knowledge directly.

It's very hard for people not to see volution in actions of external entities. Thus, use the students themselves: choose a completely autonomous motor function like the contraction of the pupil in different lighting to give them the opportunity to observe themselves during an involuntary act.

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Hardy-Weinberg sex linked formula
The "big five" assumptions are the ones listed in the main text. However, the basic formulation of Hardy-Weinberg equilibrium also relies on a few other assumptions;
Allele and genotype frequencies don't differ between males and females. That is, the basic form of Hardy-Weinberg does not cover sex-linked genes.
so, is there a modified formula?

What "main text" are you referring to?

Also, exactly what is your question (modified formula of what?)? Is it on how to calculate genotypic frequencies in the presence of sex-linkage, or on how sex-linkage affects the HW-equilibrium?

Solving Hardy-Weinberg problems
First of all, you might want to have a look at the post

Solving Hardy-Weinberg problems

and eventually at

Assumptions of Hardy-Weinberg rule

After reading the first post, you should be able to answer your question yourself. I encourage you to try it before reading what follows.
Hardy-Weinberg for sex-linked loci
I will make an example. Let's consider a case where males are XY and females XX (like in mammals for example). Let A and B be two alleles of a bi-allelic present on the X chromosome. The frequency of these two alleles in the entire population are $p$ and $q$. Let's assume the locus is present on the X chromosome. We will assume that the allele frequency do not differ between males and females.
In males, there are two possible genotypes. A and B. Their frequency among males are noted $f_{m,A}$ and $f_{m,B}$ are
$$f_{m,A} = p$$
$$f_{m,B} = q$$
In females, there are three possible genotypes. AA, AB (or BA) and BB. Their frequency among females are noted $f_{f,AA}$, $f_{f,AB}$ and $f_{f,BB}$ and are
$$f_{f,AA} = p^2$$
$$f_{f,AB} = 2pq$$
$$f_{f,BB} = q^2$$
If the sex ratio (the ratio of the number of males over the number of females) is $r$, then the genotypes frequencies in the overall population are the ones from above multiplied by $r$ and $1-r$ for males and females, respectively.


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Why is the mechanism of inheritance for this disease autosomal dominant?

An unrelated couple has a daughter and a son with the same rare condition. Neither parent has any obvious signs of the condition, but the father's mother (paternal grandmother) and her brother have the same condition. Select the most likely mode of inheritance:

A. X-Linked
B. Autosomal recessive
C. Autosomal dominant
D. Multifactorial
E. Mitochondria

The correct answer is C. But I'm confused why it would be autosomal dominant when neither parent has the phenotype. I thought it might be autosomal recessive, even though this mode usually does not have a family history, just because of the fact that the paternal grandmother and her brother both had the disease, and this is consistent with the horizontal pattern associated with autosomal recessive inheritance. For it to be autosomal dominant, the disease would have to be incompletely penetrant, which seems like a less likely scenario than it being autosomal recessive.
Can someone explain why it is dominant, not recessive?
Thanks!

Why does incomplete penetrance seem less likely than autosomal recessive?

I think this question is not possible to answer without knowing the frequency of the deleterious alleles in the population.  There's no way to assess whether incomplete penetrance is more or less likely than an undetected mutation in the mother's side.  Since the question doesn't mention the mother's family at all, and only the father's, that suggests to me that the question writers don't want you to think that anything is wrong in the mother's side.  That would make it dominant with incomplete penetrance.

Yes. I'd add in addition to using the magical key word "rare", they've specified the couple is unrelated. You have to read between the lines a bit, but whenever you see "rare condition" in a test question, be suspicious of any answer that would require two unrelated individuals to be carriers.

Thank you! And thank you for the tips on how to read between the lines for these types of problems. Many of these problems are very poorly/unclearly worded, so half the battle is just trying to decipher the wording.

Possible answers

A. X-Linked

It is possible. However, it is unlikely. The condition is claimed to be rare and as the daughter carries it, it means that the mother must have been a carrier. As the paternal grandmother also express the condition, it means both of her parents must have been carrying it. It is therefore a little unlikely. We would mainly see the condition in men but much fewer cases in women.

B. Autosomal recessive

It is indeed possible. As A, it is unlikely though. As the condition is rare, it is unlikely that both the parents of the paternal grandmother were both carrying the mutant allele and also the mother of the two kids is carrying the mutant allele. I would tend to think it is therefore unlikely. If we had more information (such as the frequency of the disease and/or how many siblings bother the paternal grandmother has), then we could have a better opinion about the likelihood of "B." being the good answer.

C. Autosomal dominant

No, it can't be as none of the parents don't express the condition

D. Multifactorial

The term "multifactorial" is a little unclear to me. It might mean that there is environmental variance and/or it might mean that there are several loci that affect the inheritance of this condition (with eventually some epistasis). All of these are definitely possible and likely (see below).

E. Mitochondria

It is unlikely as 1) the disease is rare and 2) the father's mother expressed the disease. The father did not transmit the mtDNA (as mtDNA is inherited from the mother only).
What I would answer
For the vast majority of phenotypic conditions we consider, the inheritance is controlled by several SNPs and there is some non-zero environmental variance (that is, heritability is different from 1; see this post).
In my opinion, the question is hard to answer, not because it is a hard question but because it lacks information (and clarity). If I really had to answer, I would probably answer "multifactorial".

Sons are more likely to exhibit X-linked conditions, not less.

Autosomal Dominant with incomplete penetrance can be fairly common, for example
SPASTIC PARAPLEGIA 3, AUTOSOMAL DOMINANT; SPG3A
HYPOPHOSPHATEMIC RICKETS, AUTOSOMAL DOMINANT; ADHR
There's also the chance of mosaicism in the father. Check OMIM for incomplete penetrance and autosomal dominant to get an idea.


text:
What are some possible causes that might explain why the global temperature has remained relatively constant in the last decade?
First - I do not know if this is the best site to pose this question.  However, stack exchange does not appear to have an ecology sub-site. That said, this appears to be the most appropriate place post this question.
Consider this chart:

The chart was retrieved from here here.
I am curious as to whether anyone has any thoughts regarding this trend - note, however, that this is one chart among several that I came across on reputable site. All seem to depict this observed "capping" effect between roughly 2000 and 2010+. Unfortunately, I don't have much to offer right now since I am still looking into it.
Any input is appreciated.

This question appears to be off-topic because it is about meteorology.

Like I mentioned, it does not appear that stackexchange has any sites that may be more appropriate.

There is a Geoscience proposal in Area51 that you might want to follow. Also, your question could maybe find a home at http://skeptics.stackexchange.com/, where there are a couple of climate change topics.

Not my field but I have a couple of thoughts:

According to your link, the blue line represents the change in the trend and the red bars are the temperatures. These have not remained that stable, it is the bar that gives that illusion:

A much more important point are the grey bars extending above and below each year's value. This is the range of uncertainty, the actual values could be anywhere within the range of those bars. Notice how the uncertainty decreases the closer you get to the current date.

I think a lot of the stability you observe is probably due to the line hiding the detail and the far lower precision of the older measurements.

I was thinking the same - and I agree. However, a quick google search reveals many articles published in the last few months about this trend.

@Mlagma in that case I refer you to my first sentence, not my field :). That was my 2 cents. You might have better luck over at Physics.SE.

I do not mean to criticize - I simply wanted to bring out what I recently found.

@Mlagma This question is on hold so I won't put this in a true answer, but basically it's because El Nino peaked right before 2000, the Sun was at a lower point in its cycle and, because China is using lots of coal.  http://www.newscientist.com/blogs/shortsharpscience/2011/07/why-global-temperatures-held-s.html


text:
How does the enzyme Dicer function in the RISC complex?
I know that the RISC (RNA-induced silencing complex) is one of the primary complexes involved in gene regulation through RNAi.  What I want to know is, what role exactly does Dicer play in this complex?

Dicer is an endo-ribonuclease belonging to the RNAse-III class. Dicer is not a part of the RISC. It however helps in the formation of RISC by cleaving dsRNA or the stem of hairpin RNA on two ends which liberates a small dsRNA product. Then one of the strands is loaded into the RISC.
There are several reviews on this topic and there is a video as well which you can find on youtube.


text:
Beetle Identification - Oregon
My dad found it so I don't have a lot of good information, but it was probably about 2.5 inches, somewhat west of Portland, and was found on a sidewalk. I don't know the area so I can't say what habitats are there that it might have come from.

I agree that overall appearance is very longhornish. However, I cannot get the shape of the pronotum to fit with the rest of the animal (when thinking about possible tribes/subfamilies) @Charles

Too bad that the tarsal formula cannot be seen in the picture, which could rule out several families.

I think this may be a male of Trichocnemis spiculatus (Cerambycidae, subfamily Prioninae). This species is known from Western USA/Oregon, based on this key: Screening Aid for the Cerambycidae of the Western U.S.A. (from Oregon Department of Agriculture). By overall appearance, this species fits well. However, females have more pronounced spines at the sides of the pronotum, which points to a male for the individual in your picture.

(picture from http://cerambycidae.org/taxa/spiculatus-(LeConte-1851), also more pictures at bugguide.net)


text:
What factors affect the number of individuals in an animal group?
Social animals can live in groups whose numbers vary greatly according to species (for instance wolves vs deer herds vs buffalo stampedes vs lemmings).
Is this number regulated only by environmental factors (resource abundance, position in the food web etc) or is there a genetic upper bound to this number which prevents overcrowding? Put in other words, would a species with endless food resources (but finite space) grow endlessly?
If the genetic regulation is common, then why humans don't seem to be subject to it?

What is the relationship between your title and the content of your post? Can you please try to make this clear?

Also, generally speaking, avoid saying "I heard" or "I've read" but always try to cite a source for your claims ("according to www.canislupus.com/groupSize, ...")

I am terrible sorry i am still know on this site and my english is not good as it was. But this idea come to my mind in a late night. I have just want to know if a specific number of members in groupe was evolved. I am not quite sure that wolf ancestor hunt always in 6 ( that was number from my memory, i didnt know that i have to always source for my opinion, the number is not important to me). But the question should be is the number of members important to species fylogenesis?

Don't worry, you don't have to be sorry for your english or for not asking perfect questions. It takes time to learn a language and to learn the details of the working of the SE websites.

"We are only species on this planet which have tendency to increase our population". Wrong. Every species tends to do so. Thats pretty much what reproduction is for.

Again i hit a language barier. The last comment was quite insolting. I am just want to know if some kind of animals which commit group suicide od their population Is overgrove!! I am not from preschoole. If you dont want to help me. Vote And dont let comment like this!!

@Remi.b since I think I understood what the OP wanted to ask, I decided to give it a shot and I've rewritten completely the question. L.Dodo, feel free to roll back the edit if this is not your intended question.

@LinuxBlanket Wow, there is quite a stretch between the original question and your rephrasing. Apparently the OP is happy with your rephrasing so good job!

You know the main idea was actually this, but not much people understands me even in my language. I just tried to say example, but obviously it was not the right way.  But this is exactly how my question would sound in my mother language. Anyway guys i am glad u gave me this lesson and hope i ll get answer.

Thanks @Remi.b! I think that it is actually a very good question and I'm eager to see what the others have to say about it (I remember reading something about this topic some time ago). Now I hope that the downvoted can be reversed to get some attention!

this depends on what you mean by group.
If you mean population then it is mostly environmental factors, although part of the environment can be other member of your species, some groups have a minimum functional size, such as passenger pigeons and breeding in groups behavior, or have density controls(if you are too spread out you might never run into another member of your species to breed with) , these internal factors are fairly rare however compared to basic resources availability, things like food, water, territory, shelter, nutrients, ect.
If you mean size of individual packs, herds, ect, then it is a mix of both, behavior which is almost always genetic is the main cause. However this behavior can be alter or triggered by environmental factors and its ultimate evolution is strongly affected by those factors as well. for instance large herd behavior will never evolve if the environment cannot support it, and if the environment changes the behavior may stop being beneficial.


text:
What is the name of this plant with small, 5-leaved divided pink blooms?
I found this in a forest in Karlsruhe (Germany).
The blooms are pink and have 5 leaves. Each leave is divided into two parts. It is pink and has a diameter of about 1-2cm.

It looks like a Red Campion, which is native to northern and central Europe.

It would be nice to see a close-up of the calyx (which is usually striped) and the leaves to be sure; it may be a cross between a White and Red Campion.
There are many members of the genus, and many look alike. Your close-up is of a male flower (anthers only). The plants are male or female.

Looks kind of like a species in the genus Silene. Interesting group, I believe some species in this group are dioecious and have sex chromosomes.


text:
What kind of beetle is this (2cm long, brown, "V-shaped" body)?
I've seen this brown beetle, which was about 2cm-3cm long (I guess) near Loch Lomond (Scottland) a few days ago.

What kind of beetle is it?

Now it's free to use: https://commons.wikimedia.org/wiki/File:Stink-bug.jpg

I agree, it is a forest bug. But be careful, when someone kills it, it produces a extremelly bad smell.

Honestly, that looks like a stink bug, family Pentatomidae.
You can see some slightly different coloured ones here on Insects of Scotland
Here is a photo of the one that I used to see in the States (From Master Gardening):

More commonly referred to as shield bugs in the UK.

It's not a beetle but a shield bug, probably a forest bug (Pentatoma rufipes): Wikipedia. The Collins Complete Guide to British Wildlife describes these as widespread in the UK, with adults seen from August to October.
Beetles are from the order Coleoptera, bugs ("true bugs", rather than the informal use of the term to mean, basically, any creepy-crawly) are Hemiptera. Beetles have two pairs of wings, but the front pair is hardened and acts like a shell and only the rear pair is used for flying. Bugs have either one or two pairs of wings. The front half of the forewings is usually hardened for protection, but the rear half is unhardened; if there's a second pair of wings, they're usually unhardened and all wings are used for flying.

In some insects one of the pairs of wings is modified into halteres.

Pentatoma rufipes would be my suggestion as well, without knowing the Pentatomidae fauna of the british islands in particular.

@fileunderwater Good point. I added a reference attesting to them being common in the UK.


text:
What is the name of the plant with the down-falling light purple leaves?
I've seen this flower in Scotland in August 2015:

What is the name of that flower?
To help people google it:
The plant has light purple leaves with some white spots. On those white spots are dark purple points. It is sometimes quite high (about 1.70m I guess). The bloom points downwards.

I'm asking this question because I would like to upload the photo on Wikipedia Commons. And for personal curiosity.

The common name in English is "foxglove". Note that they are poisonous.

It is a Digitalis purpurea
From the wikipedia page:


text:
Is this a spiders net or a wasp net?
I have found something scary on my attic (Bavaria, Germany - found in June):

Size: The small one is a bit bigger than a ping-pong ball. The big one is smaller than a soccer-ball... maybe the size of a small handball ball?
Is that a spiders nest, a wasp nest or something different?
I could not see any alive wasps or spiders ... and I didn't want to get too close to that thing.
I'd be very happy if anybody could give me more information about that thing. I'll probably get a bit closer tomorrow (when it's hopefully very bright ... )
My research
I looked up wasps nets and spiders nets. To be honest, this makes me feel pretty bad (especially the thousands of spiders ... less the wasps).
We do have wasps once in a while in the house and I haven't noticed spiders in the house at all so far. I do see some dead wasps on the picture. My hope is that this is a "dead" wasp nest.

It looks like a wasp nest to me, but it is hard to see the texture of it in this photo (is it paper-like?) Needs better focus to be sure. Whatever it is, it looks old and abandoned and dusty.

You make me happy :-) I hope I find the courage to approach it tomorrow. Then I'll make a better photo :-)

It is probably a European Hornet nest but I'm not an expert nor an entomologist.

This looks pretty much like a paper nest of a Vespinae, the subfamiliy where wasps or hornets belong to: typical is the ball-like, gray construction with the entrance on the bottom (latter is not visible on the OP's photo) which is built from chewed wood fibers.
Here is a Vespula vulgaris queen during the construction of her paper nest (image source: Murmelade     CC-BY-SA-4.0):

Wasps and hornets are both protected in Germany - in consequence, removing a nest is only allowed under certain circumstances (although I doubt that this law is ever executed). Still, wasps and hornets are beneficial insects that are usually relaxed, but always foraging for their colony (what makes them kind of stubborn once they have found a food source). The Süddeutsche Zeitung has just published some recommendations on living together with these insects recently.

I've been a second time up there. It's definitely a wasp net, as there were several dead wasps around. I'll now wait until winter to be sure they are give e

Your answer would be improved by explicitly indicating why you believe the OP's nest belongs to a wasp. Right now you just speak authoritatively without providing any explicit evidence for your opinion. Answers should preferably be able to answer the question convincingly without the need to go to external sources. You should cite sources, but you should also summarize relevant portions of citations directly in your post so as to provide clear evidence for support.

Thank you for your comment, I added some more details...

Very good. Thanks!


text:
What is the name of this fly?
I've seen the following insect in Austria at the border to Bavaria (high resolution). It was quite small. I would guess not longer than 1cm:

Could somebody identify it?

Type of robber fly perhaps?

Not a robber fly; I think Empididae; doing a search on https://diptera.info/infusions/aw_forum_panel/search.php for that family name might suggest a deeper identification

@GerardoFurtado Thank you :-) I like taking close-ups and this one was a lucky one. I almost touched the insect with my camera lens but it didn't move. A really professional photo model; I wish more insects were like this ;-) And usually I put those photographs under CC0 on Wikipedia Commons to make it easy to use them.

yes, definitely Empididae with that long "snout". (but i can't be more precise than that.) i've also notices that a lot of them seem to be nice and slow!


text:
What is the name of this green plant with thin leaves?
I've seen this in Scotland between Balmaha and Inversnaid:

A higher resolution is here: https://commons.wikimedia.org/wiki/File:Balmaha-Inversnaid-9.jpg
What is the name of this green plant with very thin leaves?
(I guess it was most of the time about 60cm high, but I don't quite remember)

Some kind of Equisetum? https://en.wikipedia.org/wiki/Equisetum With this picture it is pretty hard to figure it out more detailed.

@AlwaysConfused Thank you for the link. For future questions, I will try to follow these guidelines. However, I have no idea how reproductive structures look like for plants.

This is a moss of the genus polytrichum, most likely it is P. commune or P. formosum


text:
What light intensity starts melatonin release in humans?
I'm interested in whether any studies have determined the intensity of light at eye level that starts melatonin release in humans.
I know that:

melatonin release is suppressed by blue light with peak suppression
occurring at 420-480nanometer range.
This light is registered by Melanopsin, a photopigment in the
eye.
Melanopsin signals the Suprachiasmatic Nucleus, the master clock of the human body.
The suprachiasmatic nucleus makes a decision to suppress melatonin
release in response to blue light observed.

What I need to know is how much light is "enough" to trigger the suppression by the mechanism described above. I've seen a mention of as little as 200 lumens of white light, but do not have any reference to verify that. Additionally, the figure of 200 lumens was given for a typical smartphone screen, not necessarily translating to 200 lumens at eye level.
I'm aware of this experiment involving rats, where the light intensity at eye level was quantified. I'm looking for a similar measurement in humans.
Here's my original question on the subject, but I've learned quite a lot since then to refine the question
I appreciate your input!

Ps. Different numbers for melatonin sensitivity (ex: starting at 420) are because the eye somehow changes the light, thus pure melanopsin responds to less wavelength than through the eye

Not looking for a new answer, just want to award bounty for the great answer already posted

There is a bounty message for that. something like , 'Reward existing answer
One or more of the answers is exemplary and worthy of an additional bounty.'

The question piqued my interest, but after hunting through the literature for a bit, I hadn't found any direct answers.  Then I went back and read the mouse study you cited a bit more carefully. The mouse study only made a reference to mice being affected at 4 lux, ~100x more sensitive than humans.  However, for that number it cited a paper in Science that has a direct answer.

http://www.sciencemag.org/content/210/4475/1267

Melatonin concentrations decreased 10 to 20 minutes after the subjects were exposed to 2500-lux incandescent light and reached near-daytime levels within 1 hour (Fig. 1). After the subjects resumed sleeping in the dark, the melatonin concentrations increased immediately and within 40 minutes were at the levels measured before exposure. The fluorescent light (500 lux) did not reduce melatonin, and there was no change after the return to darkness. In the two subjects who were exposed to 1500-lux incandescent light, melatonin concentrations decreased to levels intermediate between those measured during exposure to 500 and 2500 lux (Fig. 2). The return to normal nighttime concentrations after subjects were exposed to 1500 lux was similar to that occurring after their exposure to 2500 lux. The concentration of melatonin in subjects awakened and exposed to 500-lux fluorescent light did not differ significantly from that measured while they were asleep in the dark.

Since that was the granddaddy study of the subject, I just checked the recent citation list on that page for modern articles.
Using pure blue LED lights at 446-477 nm wavelengths, West et al. measured light intensities necessary to induce melatonin suppression. Table 1 of that study converts LED irradiance/lux into retinal irradiance (uW/cm2) based on mean pupil size.  Figure 2 shows plasma melatonin falling (p<0.05) at 20 uW/cm2 of corneal irradiance (then curve fit to 14.19 uW/cm2). It's at least twice as powerful as white light, which didn't show significant suppression at 40 uW/cm2, but was "numerically similar" to 10 uW/cm2 exposure.  If I've got the conversions right, 20 uW/cm2 is about 136 lux, which is about the brightness of an overcast day or half the brightness of typical office lighting.
http://jap.physiology.org/content/110/3/619.full
As for the discrepancy between the two studies (1500 lux vs. 136 lux), I would blame it mostly on technological advances since 1980.  The original study used gas chromatography. You can see the huge error bars and noisy data in the Figure.  The modern study uses a radioimmuno assay using antiserum, and is presumably far more sensitive.

I was also going to mention a nice review paper that summarizes more findings, but apparently I can only post 2 links as a new user.  So I'll just paste the abstract and citation.

Light is a potent stimulus for regulating the pineal gland's production of melatonin and the broader circadian system in humans. It initially was thought that only very bright photic stimuli (≥ 2500 lux) could suppress nocturnal melatonin secretion and induce other circadian responses. It is now known that markedly lower illuminances (≤ 200 lux) can acutely suppress melatonin or entrain and phase shift melatonin rhythms when exposure conditions are optimized. The elements for physical/biological stimulus processing that regulate photic influences on melatonin secretion include the physics of the light source, gaze behavior relative to the light source, and the transduction of light energy through the pupil and ocular media. Elements for sensory/neural signal processing become involved as photons are absorbed by retinal photopigments and neural signals are generated in the retinohypothalamic tract. Aspects of this physiology include the ability of the circadian system to integrate photic stimuli spatially and temporally as well as the wavelength sensitivity of the operative photoreceptors. Acute, light-induced suppression of melatonin is proving to be a powerful tool for clarifying how these elements of ocular and neural physiology influence the interaction between light and the secretion of melatonin from the human pineal gland.

Photic Regulation of Melatonin in Humans: Ocular and Neural Signal Transduction
Brainard, Rollag, and Hanifin
J Biol Rhythms December 1997 vol. 12 no. 6 537-546

If you need more information, I'd start by checking the papers cited by the second paper. Alternately, there's probably more historical information available by looking at papers which have cited the first one.

This is probably the best answer I've ever received here:) starting a bounty so you can claim it!

@AlexStone if you plan to split and distribute your bounty for each quality answer, that's a great idea indeed.

Thanks! It's satisfying to harness that abstracted science knowledge, dig deep through the literature, and come up with a simple and practical answer. :)


text:
Do male animals visually perceive females as more/less attractive?
If we somehow remove pheromones, do animals experience a phenomenon similar to human "visual beauty" when looking at members of the opposite sex? For example, given a set of 20 female ducks observed through a glass panel, would male ducks attempt to court/mate with a small subset of female ducks first(more attractive ones), or is it based on some other criteria (most receptive, random, closest, fittest, pheromones, etc?)
If there is some "visual attractiveness selection criteria", is there a requirement of certain complexity of the brain and/or visual system for an animal before this phenomenon starts to occur?
I'm aware of the existence of this question: Why does sexual selection evolve beautiful features?, and my question deals with the members of the same generation, not long-term evolution.

One related idea is that they have found in some species of fish that, no kidding, a male being seen with other females is attractive to a female who see this situation. This makes some sense evolution-wise, I think. I am sorry but have no link.

I have read that among human cultures, standards of beauty vary but all cultures want symmetry and asymmetry probably indicates some developmental/genetic disorder. I would bet that this symmetry thing also holds among non-humans. I also believe that visible signs of sickness will cause an member of non-human species to be ostracized, not just avoided as a potential mate.

There are numerous examples of visual attraction in animals. An absolute classic of an experiment, taught to most/all evolutionary biology students, is the widowbird tail length experiment by Andersson. He experimentally manipulated the tail lengths of male widowbirds at random. Some tails were made longer and some shorter. From this experiment Andersson showed that females choose males with longer tails more preferentially. Another classic example is the lek mating system where there is a bias in reproductive success towards attractive males, in some cases 10-20% of the males get 70-80% of the matings.

A lek is an aggregation of males that gather to engage in competitive
  displays that may entice visiting females who are surveying
  prospective partners for copulation. Leks are commonly formed
  before or during the breeding season. A lekking species is defined by
  the following characteristics: male displays, strong female mate
  choice, and the conferring of male indirect benefits. Although
  lekking is most prevalent among avian species, lekking behavior is
  found in a variety of animals such as insects, amphibians, and
  mammals

Beauty could be a an example of a an indicator trait:

Indicator traits are those that signal good overall quality of the
  individual. Traits that are perceived as attractive must reliably
  indicate broad genetic quality in order for selection to favor them
  and for preference to evolve.

I'm sure there are some studies in fish, likely guppies or zebra fish, which gave individual fish the opportunity to visually assess potential mates (placing tanks next to each other and observing courtship) which would be very similar to your hypothetical duck example. Despite often being a paradox, female mate choice is well documented. Further, male mate choice is now coming to light, even in species where female mate choice and male-male competition exists.
I don't think selection on "beauty" would require some kind of particularly special neural system, obviously some visual capacity is necessary for visual attraction and some basic neural pathways linked to that. I have done experiments myself in Drosophila simulans which looked at good gene benefits of mating with attractive males (indirect genetic benefits of female mate choice) and another which assessed precopulatory selection (female mate choice) for a secondary sexual character in the same species. Even in such a small-brained species there appears to be some degree of (partially visual) mate choice going on.

Those articles mention 2 examples of bird visual preference: a) better diet translates into more plumage pigment in some birds b) parasites dull the color of certain parts of plumage

@AlexStone Thanks, could you please include a citation on that quote you've edited in

I added the link

Absolutely.  Quality by appearance is sometimes a big part of mate selection and sometimes it is not.
The size and cognitive capacity brain is probably important but not always. Primates are closest to us and have most similar tastes to us, have varying levels of interest in mate appearance.  Most primates have a troupe dominance where a dominant male mates with all the females and sires as many offspring as he can before he loses his place on top.  Many smaller primates rely more on sperm competition and the females mate with all the males they can when they are in estrus - the offspring just emerge from the most competitive sperm.  Note I studied Sarah Hrdy a while ago.  I hear Robert Sapolsky is another great source of insight on primate/human behavior.
Neither of these modes are quite so focused on visual beauty as our culture is.  Other cultures are also not selective based on appearance, e.g. cultures where marriages are arranged would often consider the social and economic relationships between the families more than we do.  This is a broad generalization, but just to point out that just looking at someone to decide mate choice isn't as dominant as sometimes it feels.
But to look at some tiny brains I know that snakes often mate in gigantic balls of snake and mate choice is pretty indiscriminate, on the other hand, spiders where female choice is dominant, males will experience rejection.  This is a bummer for the males because they only often live long enough to offer to one mate.  Its probable that the females are not hungry or have recently mated with another male, but just an example to demonstrate that even small brained animals can be discriminating.

It would be interesting to know if an alpha primate male, while mating with all his females still shows stronger preference to some of them, and if so, what controls that attraction

Good observation.  There are definitely favorites amongst primates (i mean besides humans, who obviously play favorites).  Hrdy and Sapolsky's books have examples where females in the troupe are definitely favored recipients of mating behavior - younger females have an easier time producing offspring and so are favored just as they are with humans for instance.  There are also observations that female apes will break away from the alpha male for males who treat them better.

You seem to be dissociating physical beauty from fitness. In fact, beauty can be taken as a measure of biological fitness. For a classic, if simplistic example, many male humans find large breasts attractive and beautiful, however, large mammary glands are also an indication of fertility and robustness that would imply the prospective mate would be a good mother.
Anything that we consider beautiful in a prospective mate can be interpreted in terms of fitness. Another classic example is symmetry. Humans are attracted to symmetrical faces and bodies. Since we are a symmetrical species, symmetry is an indication of fitness. In other words, lack of symmetry may indicate a developmental problem and by extension decreased fitness.
There isn't really a qualitative difference between the way we define attraction and the way other animals do. In both cases we have instinctive attractions to healthy and fit (in the evolutionary sense) mates. It is simply that our complex society has marked these choices as "aesthetics" while we call them "instincts" in other animals.

In addition to the answers stated here, it is also important to remember that we, humans, are more guided by vision than many other animals. Therefore, the idea of separating an animal from a potential mate with glass would also inhibit other important mate selection criteria that other organisms use (calls, pheromones, nest tending, etc.).

Since asking this question, I've learned that 97% of male mammals do not have concept of "beauty" and will mate with every female indiscriminately. These species do not have any paternal investment, so the males are not picky.
In other 3% of mammals (~100 species) and a lot of birds, there is a significant degree of paternal investment in offspring. Species that have developed a "pair bond" mating strategy, have males capable of perceiving "beauty" in females and become much more picky. Humans are a pair bond species.
On the other hand, because mammal females have high investment in their offspring, without the pair bond females go straight for the top alpha male to secure his DNA.
The 97% -3% number is quoted multiple times in this podcast on Evolutionary Psychology: https://hosts.blogtalkradio.com/beatyourgenes/2016/03/24/gender-dynamics-biological-differences-of-men-and-women
There's also this article on social monogamy in mammals that quotes 3-5% figure

Can you provide a reference to the numbers you refer to?

@fileunderwater I have added a couple links


text:
How diverse are dogs in their traits other than appearance?
I've asked this question about dogs not so long ago, and the short answer was - dogs are the most diverse looking species of mammals because they got a small number of genes that have a big impact on appearance.
I would like to ask a follow up question- differences in appearance are easy to notice, and I would like to learn about other traits that might be genetically based.
Are there other major differences between dog breeds, like longevity, cognitive performance, friendliness, etc? Or are all dogs more or less the same in traits other than appearance?
Are there plots of traits like these among different dog breeds that identify outliers?

Since diversity isn't absolute, or doesn't have a maximum, it might be good to compare it to a wild species, like wolves, or something similar with a broader range and larger population.


text:
Any forms of pneumonia that can be caught?
I am aware of the fact that there are several different types of pneumonia.

However, I am wondering if any of these types of pneumonia are contagious from person to person.
Is this possible?

Pneumonia caused by bacteria or viruses is contagious.

@canadianer Thanks, I would appreciate a longer answer, but that does answer my question:)

Please refer to the "How contagious are different types of pneumonia" part in this article. Hope that clears your question.

Pneumonia means inflammation of lungs- especially alveoli.
There can be many causes of it including infectious agents, autoimmune condition and  chemical irritants. Pneumonitis is a more accurate word for lung inflammation, the causes of which includes the abovementioned agents; Pneumonia in common usage refers to the condition due to infectious agents such as bacteria, viruses and fungi.
In almost all the cases the infectious agents are airborne in the form of aerosols (spread by cough) and infect the respiratory tract directly. Some cases of fungal pneumonia (Pneumocystis, Penicillium) are observed more commonly in immunocompromised individuals, such as AIDS patients, and dissemination happens via spores.
As you can intuitively figure out the infectivity is different for different pathogens.


text:
Difference between ‘tagging’ and ‘conjugating’ a fluorochrome to an antibody?
The Wikipedia entry on fluorescence repeatedly states that “a fluorochrome must be tagged or conjugated to the antibody”.
How is tagged or conjugated different? Is this a mistake or are these indeed different concepts?

Your link is a null link.  I'm pretty sure thought that tagging is merely an alternate way of saying the fluorophore is bound to something. Either directly to the macromolecule of interest or "conjugated" first to an antibody that has preference for said molecule of interest.

Conjugated and tagged mean the same thing here, although I would advise against using tagged here.
In the context of antibodies, tagging means the addition of a (short) peptide sequence to a protein. Either to do something useful (degradation tag, HHHHHH-tag) or just as an epitope for an antibody.


text:
What is the cause of the packaging capacity limit of recombinant adeno-associated viral (AAV) vectors?
I am working with recombinant AAV and I am puzzled by the limit of their  packaging capacity (around 5Kb ssDNA), that is really a huge drawback for gene delivery.
I have tried to look more in deep into this problem but I couldn't find any paper that could clarify what is the reason of this limitation. Is it the size of the capsid or something else? I suppose that it is the size of the capsid but there are smaller capsids able to accommodate more DNA so it could be due to other factors. Either way, I could not find the proper literature to solve my doubts.
Do you know the answer? Or, can you point me to good papers on this topic?

Cf. http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2835018/ and http://www.ncbi.nlm.nih.gov/pubmed/17328683

It's not the size that counts, it's how you pack it (sorry couldn't help myself).
Wild-type bidensoviruses do a lot of interesting things to pack genome like splitting its genome into two virions(1), inverted terminal repeats (ITRs) that form panhandles that can stack instead of hairpins (2), and overlapping positive and negative ssDNA strand ends (2 and 3) that clip closely together.  So on the whole, I don't know that it's a fair comparison.
Also remember that you can go too small with AAV genome size, not just too large (if you go too small you will even get 2 genomes per virion).
If you want to orderly pack ssDNA (or DNA in general), you have to use some nucleoproteins to help.  Free ssDNA has the added problem of being unstable.  Going back to basic biology, you can think of nucleosomes allowing the packing of eukaryotic DNA at a much higher density than would otherwise be energetically favorable.
Viruses use a wide variety of methods to pack genetic material, one of which is through binding directly with the capsid as with AAVs.  One should remember that the capsid proteins also are tasked with entry into the cell, trafficking, and entry into the nucleus.  All while protecting and packaging the genetic payload.
AAVs, being small (wt is ~4.7kb w/7 proteins), only have the capsid proteins VP1-3 to work with.  The ITRs are known to be the cis active sequences of the genome (4, 5), and these ITRs form normal hairpins.
A portion of the AAV ITR binds (hooks onto) an interior facing portion of the VP3 gene (6, 7).  But the virus has to push in this ssDNA, and it uses the Rep proteins to do it (8).  The Rep proteins (Rep52 and Rep78 specifically), are larger than the capsid proteins, and bind the ITRs at multiple sites.
While the exact insertion pore hasn't been identified at the structural level, the way I like to picture it is a series of hairpins have to bind on spokes of the Rep proteins to be pushed into the virion, where in turn the hairpins have to hook onto the inside of the capsid.  If you put too much ssDNA between your ITRs, then you lose the ability to be passed along (or bind) to both proteins in packaging.  You start to lose the tight packing onto VP3 found in wt virus, and instead get more sporadic VP3 binding (every 3rd as opposed to every other).
It would be incredibly hard to just "increase" the size of the capsid without messing up the assembly and the other functions of the capsid.  The VPs only oligomerize in the cytoplasm (9) suggesting that host proteins are required for proper assembly.  I think the process of successfully increasing the optimal genome size would be quite a task and achievement if done.  One would likely have to optimize additional ITRs, the internal binding bind sites on VP3, and the structure of Rep52 before such a thing would be possible.  Alternatively bringing in a novel or chimeric packing mechanism, but again this would be exceedingly difficult (probably prize worthy).


text:
What is the name of this bush with red fruits?
I have seen this on Corsica (Island of France):

@AlwaysConfused I'm sorry, but I'm not several 100km away from it. However, in the future I will think about cutting the fruit and photographing it. Thank you for the hint.

It is Arbutus unedo, called "strawberry tree" in English, "arbousier" in French and "medronheiro" in Portuguese. The fruits are ripe around October or November. They are full of little seeds, but if you bear the annoyance, they can be quite tasty. They are used to distill an alcohol in Portugal.

The fruit looks like lychee (Litchi chinensis). But this was a hasty guess and now I see that there is a much better answer here!

(image from Wikipedia)

The leaves look different. Lytchee have a kind of crust that can be peeled. This is not the case with Arbutus. Besides, I'm not sure they can grow in Corsica.

You're probably right! I was misled by the fruits.
In the Wikipedia it says "They require a warm subtropical to tropical climate that is cool but also frost-free or with only slight winter frosts not below −4 °C"

@AlwaysConfused It looked so similar that I didn't check if it is possible to grow there. Corsica isn't frost-free, so I guess it is rather the Arbutus unedo.

@AlwaysConfused Do you have a justification for why this answer would be useful to people and not misleading?

@WYSIWYG The discussion below an erroneous answer might be useful. And it is useful to know that one might make this kind of confusion between lychee and Arbutus. But maybe it would be better to edit the answer to warn the reader.

i added a note about being wrong. the downvotes should also be a good indication to not listen to me!

also, of course it would be nice to have it removed since it's embarrassing, but hey, if it's possibly useful it can stay!


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What is the name of this about 5cm high, grey, Beanie shaped fungus?
I found those below some stone stairs in Germany. The grass gives you an impression of the size (I guess the grass is about 5-7cm tall)

I think this is Coprinellus disseminatus, also known as "Fairy Inkcap". Size (they are pretty small) and also the color fits pretty well. See the image from the Wikipedia:

Some more information can be found here.


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What is the name of this flower with purple leaves and orange inner part in NYC?
I've photographed this flower a few days ago in New York City:

Does anybody know the name of it? (and how is the orange part called?)

It's Echinacea. I've linked to one site but if you run an images search with Echinacea as the search term you'll see lots of examples.
And here is the WP page.
Supplementary
Echinacea are members of the Compositae. The flower (the head) in your picture is actually made up of lots of individual smaller flowers (i.e. it is a composite flower). The petals are formed by ray flowers, and the central part, the disc is made up of disc flowers. More details at the WP page I have linked to for Compositae.

And how is the orange part called?

@moose it is the head inflorescence which consists of ray florets and disk florets

@moose it is not a flower actually but an inflorescence which resembles like a flower. ray florets in general are situated at the peripheral parts of inflorescence and disk florets are situated in the centre which is a unique feature of asteraceae (other name for compositae)

@moose ray florets are the female flowers and disk florets are the bisexual flowers

The first link is dead.


text:
What is the name of this big plant with a purple trunk and green to purple berries?
I have photographed the following plant in our garden in Pittsburgh, PA.
Do you know the name of the plant?

cf http://gardening.stackexchange.com/questions/2609/what-is-this-fast-growing-plant-with-blue-black-berries/2610#2610

also cf http://biology.stackexchange.com/questions/19612/what-is-the-name-of-this-plant

So clearly we need to start pokeweedID.stackexchange.com, where the only correct answer to any question will be "Phytolacca"...

The plant looks like Pokeweed (Phytolacca americana) to me, a common "weed" in the U.S.

3cat looks like you're right. I have to dig this up all the time, and it's not fun. Of course, being a professional horticulturist/arborist/landscaper means you want to never see this plant again, al least in beds. This is the fouth SE question asking for the id of this weed.


text:
What is the name of this plant with many purple blooms with orange inner parts?
I have photographed the following plant in Pittsburgh, PA. It has many blooms and every bloom is very small (about 5mm diameter), purple on the outer and orange in the inner. You can see it here:

What is the name of that plant?

This looks pretty much like Buddleja davidii to me. They are available in a range of different colors, see this image from the Wikipedia:


text:
What is the name of this about 10cm high, grey, "flat hat" fungus?
I found this fungus on Corsica (France). Can you please help me to identify it?

In fungi, you should always look at the underside of the hat, which gives big clues to group/species determination.

Try looking up Chlorophyllum  brunneum or commonly called a shaggy parasol.
http://www.mykoweb.com/CAF/species/Chlorophyllum_brunneum.html
Hope this helps.

Thank you. I think this goes in the right direction. However, it could also be https://commons.wikimedia.org/wiki/Category:Chlorophyllum_molybdites or any other Chlorophyllum, I guess?

Most Lepiota don't have such dark lamellae.

Besides the lamellae colour, the foot seems too wide in proportion to the hat for a Lepiota, in my opinion.

Based on the dark lamellae and the ring around the foot, I would bet on something in the Agaricus genus. The French Wikipedia gives quite some details about common species in this genus: https://fr.wikipedia.org/wiki/Agaric


text:
What is the name of this yellow / orange fungus?
I've seen this in October 2016 on Corsica (Island of France):

I would guess each one is about 5cm - 15cm in diameter. Obviously, they come in small groups.

It would be nice to see how they look under the hat, and also the stem.

Do you have a picture of the stem or underside??

@theforestecologist No.

Most fungi need to be studied under a microscope to determine a species. I think this belongs to the genus of Pholiota. I couldn't find an English name, if I translate the Dutch name, it would be 'Bundle mushroom'. This name refers to the fact that they always grow in groups, usually on (dead) trees or trunks.
At first look thought this was a Honey fungus, but these are parasitic so usually don't grow on dead wood.

From the article you've linked: 'Because Armillaria is a facultative saprophyte, it also feeds from dead plant material, allowing it to kill its host, unlike parasites that must moderate their growth to avoid host death.'

Pholiota aurivella http://fieldguide.wardial.me/Mushroom%20pages/falllog.htm


text:
Are there animals / mammals which only have one eye?
Do all animals (of a certain size and not thinking about worms) have the possibility to perceive depth?
Do all mammals have at least two eyes? Are there mammals with more than two eyes?

Not all two-eyed mammals have depth perception. Many herbivores have eyes on the opposite sides of their head to increase their range of vision for predators, and are so widely separated that they barely overlap at the front, if at all.

Also, please clarify "all animals (of a certain size and not thinking about worms)".

@MattDMo Thank you for your first comment; I didn't think of that. For the second: I am aware of the fact that some worms (all?) don't have eyes. Also, I'm not interested of animals which consist of a very small number of cells (by a quick search I found Myxozoa as an example). So for the sake of clarity, lets say the animal has to have at least 5cm of height when standing on the ground.


text:
RNA-seq analysis - q-values in cuffdiff
I'm using cuffdiff 2.1.1 to look for differential gene expression between two conditions. Each condition has 2 biological replicates. The results I get look promising from a log fold change perspective - lots of genes that I would expect to be affected have the highest fold change values. However, from a q-value perspective very few of the results look promising, having q values > 0.05.
My question is, given 2 replicates, how is the q value calculated? Surely if there was high variance between replicates but the difference between experimental conditions was also large then the q-values would be correspondingly high?
In this case, can I, or should I, really trust the q-values?

http://cufflinks.cbcb.umd.edu/manual.html#gene_exp_diff

If after a few days you don't get good answers here, consider reasking the question here:
http://www.biostars.org/
It's basically stackexchange specifically for bioinformatics.  About a third of the questions over there are about next generation sequencing.

q-value is the corrected p-value to account for multiple testing (i.e. you are testing thousands of genes). Those with q-value <0.05 are significant experiment-wise. Cuffdiff uses Benjamini-Hochberg correction to compute FDR (i.e. q-value). The calculation does not depend on the number of replicates it's based on the distribution of p-values those, yes, are influenced by the number of replicates. The more replicates you have the better).


text:
Bee (?) identification
I live in Michigan.  I just saw a bee that I think I've seen before, but only this time was I so struck by its uniqueness and - for lack of a better word - scariness.
I'll describe it.  It was maybe an inch and a half long.  Maybe bigger, maybe smaller (I'll admit that I was hurrying to get away from it).  It looked like a queen bee, but longer and slightly thinner.  However it had wings that were very profoundly orangish-red.  Like burnt orange maybe.
I haven't been able to find any matching pictures online.  It is theoretically possible that it was covered in pollen, and I am incorrect about what I think I saw, but assuming it wasn't (as I do believe this isn't the first time I've seen this guy or one of his friends), does anyone have any clues as to what this could be?
EDIT:  PHOTOS
After considerable patience. I was able to capture some photos of this guy.  One of these photos is post-processed a little to emphasize the color.
A couple things about these photos.

They were extremely difficult to take because the bee never stops moving.  I don't know if this behavior is useful for identification, but he is always in the same place (in front of one house), and he flys back and forth between a small crack in the sidewalk (a nest?), and between 5 and 10 feet away.  He moves like a dragonfly (that's the best way I can think to describe it), and he doesn't stop - he'll seem like he is going to land, and then flies off.  This morning was an exception.
These photos do not fully capture the depth and vividness of the redness of his wings, nor do they adequately convey just how large he is.

"Thin" and the red color of the wings makes it sound like a bit like a hornet, as Damien says. Here in Asia, I'd guess the Japanese Giant Hornet, but it doesn't range to the US, so maybe a similar species? Although if you do think it's a bee, often the scarily large bees you see in the US are carpenter bees. They're on the rounder side though, so perhaps not.

Well - I've seen pictures of the scary Asian hornets, and the body type isn't all that far off.  I only say thinner because it was longer, but the overall body shape came closer to a large furry bumblebee than to a yellow jacket.   It resembles a big Queen bee in shape and overall appearance more than anything else.  Definitely did not look like what I commonly associate with a hornet or wasp.  Do carpenter bees match that description (with the red wings as well)?

Nice pictures! From the back pattern, size, and antennae shape, I'd say this is very likely a Cicada Killer wasp (Sphecius speciosus), cf., for instance, this picture taken at a similar angle to yours.
There are many good resources online about Cicada Killers, including this page from the MSU Extension Office, and the Wikipedia entry Sphecius speciosus.
It would be interesting to see if you could find the distinctive burrow (photo / video) of your resident wasp!

Interesting observation about the flight patterns seeming similar to a dragonfly. It's possible you're seeing flight strategies that are good for aerial predators, like dragonflies and Sphecius. I imagine a pollen-gathering insect's flight might look very different.

Wow!  That is almost certainly what it is.  The links were great.  I especially like how the first one mentions people having reactions just like my own.  Thanks!

And reactions like my own, in guessing that it was a Japanese Hornet!

Regarding the flight patterns - that's an interesting correlation.  It sounds logical.

@Oreotrephes, is there any particular reason you didn't embed the image you linked? From a UX viewpoint, it's surely better to embed? Are SE services really so hammered by doing so? If the answers to those are "embed", I'll take that as "go ahead" and do it myself as an edit... the only explanation for "no way", is perhaps users would be "too scared" to see such a "graphic image"?

@hello_there_andy for SE I tried to avoid embedding pictures that were not creative commons shareable, see for example my answer to http://biology.stackexchange.com/questions/9576/goats-are-so-fearless-but-sheep-are-not-is-there-any-genetic-difference-respons/9577#9577. However, I don't know whether there's now a meta consensus for this. I'd say best way forward if you want to embed is to ask for permission from GCMGA.

Handy info @Oreotrephes, thanks. Also nice goat pictures in that answer :)


text:
What happens during metamorphosis?
We were studying butterflies in class and I asked my 7th grade teacher, but she deemed the concept "too complicated." I'm really curious now, not only about butterflies but insects in general...
Thank you!

Could you add some detail to your question? To start, what species(s) are you interested in?

It depends of what order and even what family of insects we are talking about. Insects may have complete or incomplete metamorphosis, being the complete more complicated. Even inside the first group (wich in fact contains most of the insects since coleoptera, diptera, lepidoptera and himenoptera have complete metamorphosis) there are important differences. However, I'll try to explain some basics.
First of all, metamorphosis is a molting-related process. It's regulated by the same hormones and they share many characteristics. In insects with uncomplete metamorphosis, this is very visible, since the "metamorphosis" is the last molt, wich usually involves growth, sexual maturity and the development of functional wings.
The choice between a regular larval molt is determined primarily by the levels of juvenil hormone, wich decays during the last larval instar (pupae and adult are instars, too). The molting is triggered by a peak of ecdysone, an steroid.
Once the insect has entered into the state of pupae, the organs start to suffer diverse changes. The formation of adult organs de novo arise from some special structures called imaginal discs, wich are clusters of stem cells that are more or less isolated in the larvae.

Position of the imaginal discs in Drosophila. Source.
Note that diptera larvae lack legs, mandibles and even head, while coleptera larvae usually have true legs, a set of mandibles and many other adult features.

A typical larva of a coleoptera of the genus Lucanus. Note the mandibles and the legs. Source.
Some other organs remain more or less the same, such as the hearts or many parts of the nervous system. On the other side, some larval organs needs to dissapear and suffer programmed cell death. The gut, many parts of the nervous system, between others, suffer modifications that may be more or less drastic. In many cases this happen by simple growth and differenciation of the tissue or degeneration by apoptosis, but in some others the whole organs suffers apoptosis and regenerates itself with adult characteristics.  For example, the innervation of the abdominal parapods (false legs) in caterpillars suffer a progressive degeneration, while the opposite happens in toracic nerves, wich will have to control legs and wings. This whole process is pretty similar to embrionic development and it shares many traits with it.
Finally, metamorphosis in other animals, such as crustaceans, vertabrates (fishes and amphibians), echinodermae, annelidae, cnidaria and many others will probably vary widely. I know for sure that amphibians metamorphosis is regulated by tiroid hormones, but I'm not even sure that many of the other examples have even been studied at a phisiological level.


text:
Insects or Birds covering least distance but most wing moves
I was in search in of list or detail about Insects and Birds which move their wings most but cover least distance.
I know that in insects house fly moves its wings about 200/sec and covers 5mph (about 7.3 feet) distance and in birds Hummingbird moves its wings about 80/sec and covers 60mph (about 88 feet) distance, but I am in search of about 10 in each insects and birds. And also about their heart beats.
If you have combine list, it will be much appreciated. If you know any book or website about same topic it will much helpful.

When hummingbirds are hovering, they go 0 distance at ~80 Hz flapping frequency and ~1200 bpm heartrate. http://www.hummingbirds.net/about.html#wingbeat


text:
Leaves not liked by herbivores
I at times have many goats grazing in our locality. Recently a few cows were seen too. I just offered one of the cows a few leaves from Jasminum sambac plant growing in our garden. The cow smelled and left those leaves untouched. However on being given mango leaves, not a bit of it remained. The same situation did I observe with goats.I have the following questions:
What is the difference between leaves of others and leaves of Jasminum sambac?
Why do herbivores avoid consumption of these leaves?
Does it happen with other leaves too?

No idea why the cow hate it. Its a rabbit safe plant: http://wabbitwiki.com/wiki/Vegetables

I havent ever experimented with rabbits. However this is a practical situation in case of cows and goats. I have observed this a number of times, since I was small

Some animals don't like any unusual smelling or textured foliage. I've noticed that deer will avoid many non-toxic plants that rabbits enjoy. I've noted that deer avoid aromatic, slimy, prickly, hairy, spicy, etc, and prefer plants like hostas, which taste similar to lettuce.

what about regular herbivores...cows and goats??

Goats will eat almost anything, including the canvass on your convertible mustang :(.

Goats will eat bark off a full grown oak tree.

We havent got oaks growing here...yes, I have seen goats eating leaves of different types...but I wanted to know, why they do not like the above mentioned!!!

I have noticed goats eating film posters and banners stuck on walls but yes I do remember them avoiding certain leaves. Could be just like some of us hate some food items while other might hate it.. They have their preferences. Might be that the leaf you offered   could have been eaten by another cow.

I have seen cattle eat the flowers off thistles if they get hungry enough, they wrap their tongue around the back of the flower and pull it off. The rest of the plant is too thorny. But about herbivores avoiding some plants, many plants have defensive mechanisms such as raphides, tiny needles of calcium oxalate which are extremely irritating to the tissues in the mouth and esophagus and can create holes in cells that allow toxic plant proteins inside. Maybe some of these plants have raphides.

Cattles actually hate shrubs which are very tough to break and tasteless(for a cow). Some plants they won't touch are:

Lantana urticoides (West Indian shrub verbena),
Malvaviscus arboreus var.drummondii (wax mallow)
Rhus copallinum (winged sumac)
Viburnum acerifolium (mapleleaf viburnum).
Morella cerifera (wax myrtle)
Ilex vomitoria (yaupon).

Source:
https://www.wildflower.org/expert/show.php?id=2108

Lantana urticoides
http://www.wellgrowhorti.com/Pictures/Landscape%20Plants/Shrubs/Web%20Pictures1/M/Malvaviscus%20Arboreus.jpg
Malvaviscus Arboreus
http://www.floridata.com/wallpaper/jpg/Rhus_copallinum_frt800.jpg
Rhus copallinum

(source: naturallandscapesnursery.com)
Viburnum acerifolium

Morella cerifera

Ilex vomitoria

Also see 'Is there a grassy plant that's unattractive to livestock without being poisonous?' and 'What kind of landscaping plants do livestock avoid eating and need minimal attention?'