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Why don't vegetables taste good despite being healthful?
This is more a question about the evolution of taste than about the chemical composition of vegetables. Why don't vegetables taste good despite being healthful?

Probably because vegetables are usually the parts of plants that plants don't want to be eaten by others.

This question might in fact be a question about the inferior quality of vegetables that are grown in greenhouses or other industrial facilities.

Who says vegetables don't taste good?  Depends on the vegetable, of course, but IMHO peas picked fresh from the vine are in the top 10 or so of yummy things.  Carrots, cucumbers, peppers (or are they a fruit?) and more are all quite good.

@jamesqf Everyone agrees they don't taste as good as fruits.

@Thomas: Everyone does NOT agree.  Of course it depends on the particular vegetable and fruit, and on the individual.  But there are a great many vegetable that IMHO taste better than say an uncooked quince, cornelian cherry, or even some of the modern store varities of apples.

@Cell What is the basis for saying that?

We are evolved to survive starvation, and live to be perhaps 35. So fatty foods with lots of calories taste good to us. Our genes (and preferences) lag thousands of years behind our present environment.

I'm not sure about your statement that humans evolved to live 35 years. Prior to modern medicine, that was the mean, but it was skewed left by very high infant mortality. If they survived infancy, neandertals would live 60-70 years.

I have not heard that @kmm. What is your source. Mine is admittedly a TV show, and I am an entomologist. But as far as I understood, Neanderthals lived to be 30 or 35. Even if they lived longer, it does not matter, because evolution only acts on child bearers.

Because your primary school cafeteria used to serve canned vegetables, you've hated vegetables ever since, and you haven't tasted them cooked properly yet.
To make vegetables taste good, one thing you can do is going to your local farmers market, buying whatever looks appealing to you and asking the farmer for suggestions on how to cook it.


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How to edit manually pdb structures?
I would like to manually movement some b-sheets from a 3D structure of my PDF protein to represent a change in its structure.There some tool i can do that?

Using PyMOL, (see Nicolai's answer and my comment), you can also generate movie of a transition between two structures (conformations). Question: why do you want to edit the structure manually?

If I remember correctly pymol can edit pdb structures (as well as visualize them).
I've used a student version though (which is a free full version) and I'm not quite sure if its possible to use pymol without buying a license nowadays (though the source code is still open source, so can in principle always install it from that)

PyMOL 0.99rc6 is available for free: https://sourceforge.net/projects/pymol/files/Legacy (i have been using this version since 2006 and it still fulfills all my macromolecular visualization needs)

source: Stack Exchange

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

sort: votes


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Why is amylose insoluble in water?
In a handout the following is stated:

Amylose is insoluble in water, therefore a good storage compound e.g. in stroma of chloroplasts

This is with regard to the chemical structure of the molecule.
However it has left me wondering, what is it intrinsically about the structure of a molecule that makes it soluble/insoluble in water?
My thoughts at this stage are perhaps to do with whether the molecule is hydrophobic, and if that is the case - how is amylose hydrophobic?

The availibity of -OH groups for hydrogen bonding with polar water molecules is reduced in amylose due to its coiled nature (resulting in part by H-bonds between the glucose monomers).  Amylopectin is even less soluble due to the additional 1-6 glycosidic bonds on the branch chains, further reducing its H bonding potential and therefore reducing solubility in water.

Welcome to Biology.SE! Your answer sounds reasonable, however, it is likely to receive a more favorable response if you include supporting references (primary literature is best, but a textbook available online would seem sufficient for this question). ——— You may also benefit from taking the [tour] and then consulting the help pages for additional advice on [Answer] effectively on this site. Thanks!

There are a couple of other questions that address this point indirectly:
here and here.
In my answers to the first of these questions I mention that amylose is semi-crystalline because of its regular extended structure. I imagine that the semi-crystalline state is more thermodynamically favourable than the solution state, but suspect that a rigorous chemical answer might be quite complex.

Depending on molecular weight of amylose and because of its helical structure formed by two macromolecules makes it partly soluble in water.
Heating amylose solution leads to formation of colloidal suspension of soluble fraction and remining insoluble higher molecular weight fraction of amylose does not dissolve. On cooling this suspension, certain portion of polysaccharide precipitates. This is because of the glycosidic linkages between these glucose molecules.
Reference
Cuevas et al. Structural differences between hot-water-soluble and hot-water-insoluble fractions of starch in waxy rice. Carbohydrate Polymers 81(3):524-532

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


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A Hadeeth on the fly
I think most biologists here on this site will not  consider my question below to be unfit for posting on Biology SE.
I came across this article about the hadeeth (a hadeeth is a saying of the Prophet Muhammad (peace be upon him)) on a fly:

"If a housefly falls in the drink of anyone of you, he should dip it (in the
  drink), for the one of its wings has a disease and the other has the cure of
  the disease." [Bukhari, vol. 4: 537].

where an attempt is made to show the truthfulness of the hadeeth with an experiment: they dip a fly into water in a petri dish wholly and partially in another petri dish and different kinds of bacteria appear in each petri dish. This experiment is carried out 3 times and results are different in each round. (Please, read that article thoroughly before answering) I want to know biologists' point of view on that experiment, i.e.
Do you believe this hadeeth based on the experiment? (i. e. do you consider it to be pseudoscience or not? If yes, please provide your proofs.)
Can pathogenic bacteria arise in such an impressive quantity in water just by dipping fly into water? If yes, could you explain how?
Do you agree with the notion in the hadeeth 'he should dip it (in the drink)?
Thanks very much for your answers in advance!

Can you explain what hadeeth is, for those who do not know?

@kmm I have added the explanation.

It would be a good idea to summarize the experiment here in the text of your question, rather than just linking to a report of the experiment.

@DeNovo I edited it a bit.

Please read the guidlines about asking questions on this site. When your question involves asking whether people "believe" in assertions in religious texts (whether or not based on published peer-reviewed work) or agree with notions in religious texts, you are clearly asking a subjective question. Such questions are, I am afraid, most definitely off-topic here.

I think most English speakers would be more likely to understand the spelling "Hadith".  That said, it would improve the question if you just explained what the claim in the Hadith is, rather than expecting people to follow links or do research.  Even then, I'd expect it to be unsuitable for this site.  Perhaps the Skeptics site would accept it?

The problem begins with literal interpretation of a metaphor: "If a housefly falls in the drink of anyone of you, he should dip it (in the drink), for the one of its wings has a disease and the other has the cure of the disease."

@Martin Klvana: Who says it's a metaphor, and not a statement meant to be taken literally?  Other than people trying to defend the claims of their particular religion, of course :-)

@jamesqf There are two extremes: (1) considering ancient philosophical/theological texts literally, and (2) considering ancient philosophical/theological texts as 'fairy tales.' Both of these extremes are wrong, but the understanding of this fact comes with studying the original texts and with studying commentaries on those texts written by people 'infinitely' smarter than me, such as Ananda Kentish Coomaraswamy (his writings on metaphysics and theory of art are excellent). [Note: i am neither an atheist, nor do i adhere to any particular religion.]

'The text no doubt has many interpretations. For a start, petri dishes were a different technology 1300 years ago, so it depends on what kind of petri dish. Agar for example is a kind of sugary jel which has been raised above 100'C, I dunno who in the arabic world knew that kind of biotechnology. perhaps add to the wiki page on petri dish history.

@Martin Klvana: The Hadith aren't really philosophical texts.  They are simply people's recollections of the words and actions of Muhammed, collected after his death.  See the Wikipedia article as a start: https://en.wikipedia.org/wiki/Hadith

@jamesqf "People's recollections" of this kind are myths. And, to paraphrase Ananda Kentish Coomaraswamy, every myth is true or else it is not a myth at all. A myth is not a recollection of historical events (if it were it wouldn't be a myth) but a device for storing and transmitting man's understanding of the cosmos, both from its material (physical) and immaterial (metaphysical) perspective.

@Martin Klvana: That is simply not true.  There are many, perhaps most, myths which simply aren't true, from the myths about various gods (what we normally think of as myths) to the stories about George Washington and the cherry tree.  The Hadith are not myths: the closest modern-day equivalent would be oral history projects.

What about Articles #1 to #4 on http://www.answering-christianity.com/hadiths_of_the_fly.htm concerning the hadeeth.  Maybe those can serve as evidences?

@jamesqf Good luck.

Rephrasing your question
Allow me to start by saying that I barely know the term Hadeeth / Hadith mean. Of course I have checked on wikipedia but its definition is vastly unrelated to any concept in science. I think it won't be necessary for me to use this term, I will use a more classical, scientific terminology. As I barely understand the term, I do not really understand your question phrased as

Do you believe this hadeeth based on the experiment?

I can however answer to the questions

Is this document a fair description of a natural phenomenon?
Is this document contribute to our understanding of a scientific phenomenon?

The answer to both of these questions are "absolutely not"!
Lack of methodology and definition of the expectation
The document is extremely unclear, provides a very poor description of the methods and does not provide any suggested interpretation of the results. After reading it several times, I have little idea what the treatments are.
Note that this document is not peer reviewed and does not follow an appropriate format (no introduction, no method section, just a religious quotes, a citation from the Quran and images with a vague legend). It is just a document that someone wrote and uploaded online.
As @BryanKrause perfeclty said in the comment below

[I]n science the burden is on the person making a claim to defend it and provide appropriate support - there is no point in proving a claim true or false if it lacks documentation of the methodology. Being poorly written in terms of lacking adequate description is hardly better than lacking any experiment at all

In short, this document does not make any contribution to our understanding of a natural phenomenon.
The claim is very unlikely to be true
The expectation implicitly suggested to be tested is something like (my own phrasing)

If a fly barely touch (with one wing only) the media, then the media will be full bacteria but if the whole fly (with both wings) touch the media then the media will remain clean.

This expectation is highly unlikely to be true. If it were to be true, it would probably lead to a major revision of our understanding of microbiology or of the biology of flies (whichever species is considered)! Also, there is no reason to expect that in some petri dish only one bacterial species would have invaded, while in another only another bacterial species. Also, the pictures don't really match what the species described IMO. Hence, if the authors claim that this document report the results of a scientific experiment (I am not saying they make this claim), then I very much think this is a case of scientific dishonesty or at least a case of very poor understanding of how to perform a scientific experiment.

I used the term 'Hadeeth' meaning a 'saying'. I agree that the document is poorly written (lacks description).

@Tug'Tegin It is not only an issue of the phrasing however. Please consider reading my edited answer.

@Tug'Tegin An important part of this answer that isn't made completely explicit is that in science the burden is on the person making a claim to defend it and provide appropriate support - there is no point in proving a claim true or false if it lacks documentation of the methodology. Being poorly written in terms of lacking adequate description is hardly better than lacking any experiment at all.

While I sometimes wish I could down vote some comments, I would wish I can double upvote @BryanKrause comment!

I wish there were more people like Abdus Salam among Muslims.

The problem begins with literal interpretation of a metaphor: "If a housefly falls in the drink of anyone of you, he should dip it (in the drink), for the one of its wings has a disease and the other has the cure of the disease."

Some may (rightfully) disagree with my phrasing of the expectation (but I had to write out an expectation as the document does not offer any). That being said whether or not the expectation is met in an experimental set up and what it means for the islamic faith is of course not to be discussed on a science website.

You can read Articles #1 to #4 on http://www.answering-christianity.com/hadiths_of_the_fly.htm concerning the hadeeth. Maybe those can serve as evidences?

Diseases and infections carried by house flies include, but are not limited to:

typhoid
cholera
dysentery
salmonella
anthrax
transmission of the eggs of parasitic worms

Of these, exactly zero have been shown to be cured or in any way influenced by flies in a positive sense.
And, of these, exactly zero have proposed mechanisms (however outlandish the claim) of treating or curing any one of the above-mentioned diseases.
To paraphrase, there does not exist a hypothesis, nor an experiment, nor evidence for the claim. It is entirely and scientifically unsubstantiated.

On a less scientific note: it's clearly and demonstrably unwise to assume that there is any prescient scientific validity in this claim. It reads and sounds like a metaphor, perhaps somewhat along the lines of what doesn't kill you only makes you stronger. Taking metaphors literally is a very erroneous mistake to make, and unfortunately this error is a dead giveaway of exactly how shallow and uninspired one's interpretation of a religious text is. I don't think it's unreasonable to say that such an interpretation today would be a bastardization of the text. My two cents!

"If a housefly falls in the drink of anyone of you, he should dip it (in the drink), for the one of its wings has a disease and the other has the cure of the disease."
The quoted text above is not meant literally(!), it is a metaphor, the figure of speech in which a name or descriptive term is transferred to some object different from, but analogous to, that to which it is properly applicable.
Kid-friendly metaphor: "The classroom was a zoo." Does it make sense to perform an experiment aimed at determining number of monkeys, zebras, elephants, dolphins, . . . in the classroom? (No, it doesn't).
Further reading: writings on metaphysics and theory of art by Ananda Kentish Coomaraswamy. There one can learn about what "figure of speech" is and why it is used in philosophical/theological texts.

We do not know, at least without more information which I haven't been able to find (I don't read Classical Arabic, and so must depend on translations posted on the web) whether this was meant as a metaphor, or as a simple statement of fact.  I've found two hadith that contain the statement about the fly, Al-Bukhari and Ibn Maj’ah.  Both seem to be simple statements, but the translations I've found lack context.  It could be something philosophically profound, or as fundamentally ignorant as today's anti-vaxers or the dietary restrictions of Leviticus.  Who can tell?

@jamesqf (1) When the information is limited, apply Occam's razor---if applied skillfully, it works instantly and most of the time; (2) yes, the text can be interpreted in both profound (wise) and profane (ignorant) way---which of the two is the primary one if myth is a device for storing and transmitting wisdom?

But a myth isn't that.  If we apply Occam's razor, the result is rather rude.  Muhammed was an Arab tribesman, blessed with charisma and imagination, but woefully ignorant of microbiology and the mechanisms of disease transmission and treatment.  So his pronouncement, by Occam's Razor, is on the same level as the many folk remedies for baldness, such as Hippocrates' "cure" rubbing the scalp with a mixture of opium, horseradish, pigeon droppings &c.

@jamesqf Good luck.


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Are these two same insects?
 These guys are infesting my place. I searched through this site and came to know that they are cloth moths. All these days I used to see the left one type in the image. Recently I started to get the ones looking like the right ones.
As you can see the the right ones have a black border like thing at the end of the casing which the other kind does not have. Also , it looks like it has a different kind of structure from the left one, no ? I don't know..
So, are they the same ones or different kinds ?


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Can Anyone Identify this Tissue?
I am hoping someone can identify the image below

My wife felt a bug bite her and found this in her hair now she's worried that it was a tick.
the photo is at 40X under microscope. I'm guessing it's an arthropod maybe some kind of beetle but I haven't seen anything like this before.

One usually doesn't feel tick bites. To me it looks like some kind of beetle too.


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Help identifying spider found in central Indiana US
I noticed this spider outside my garage tonight, and I'm curious if anyone can help identify what type it is.
A few details to help:
I live in central Indiana, United States.
I saw it for the first time at night.
It's body was roughly 3/4 inches (might be slightly bigger).
Each brick in the picture is about 2 1/8 inches.
It seems to have a black velvet like texture.
It was sitting on a gas pipe that leads into my house.
It was under a bush.
Sorry the pictures aren't great. Being under a bush and trying to use a flashlight made it a bit harder.

More photographs

This looks like a black lace-weaver, or Amaurobius ferox. Based on the size you described it seems as though this one is an adult female. These spiders avoid bright spaces and if they feel cornered they might bite you.
For pictures of it you can look here https://www.arkive.org/black-lace-weaver/amaurobius-ferox/ and for more information you can look here https://en.wikipedia.org/wiki/Amaurobius_ferox


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Book on the history of Darwin's discoveries and development of his theory
This question is a book request. I am wondering if there are any books with these elements:

Tells the history of Darwin's discoveries.
Captures Darwin's changing views of the origins of species, because of his discoveries and his thinking on the subject.
Is a modern text but incorporates some of Darwin's writings (e.g. from the Voyage of the Beagle, etc).

Note: I am not asking for a book that is just explaining the process of natural selection, rather I am looking for a historical book about Darwin's discoveries and the inception and development  and eventually his publication of his theory of natural selection.

On your second point, for the most part, Darwin's views were fully formed within a few years of his return from the Beagle. They didn't really slowly change. But he was slow to publish for a variety of reasons.

@KarlKjer While that is somewhat true, I think there is a lot of nuance missing from that description, and Darwin certainly wavered on things and shifted his views prior to that time; the slow publication is only one aspect of the story.

I'm not certain it fills every element of your question, but I really enjoyed Michael Ruse's "The Darwinian Revolution: Science Red in Tooth and Claw."
It's especially good for setting up the collection of worldviews that predated Darwin, and the influence on him by both biologists/anatomists as well as very crucially geologists like Charles Lyell (Darwin really thought of himself more as a geologist; the long time prior to publishing Origin was largely because he was trying to build up some scientific chops as a biologist).
The aspect it is most likely to lack is references to original source material from Darwin. While it certainly draws on such writings, I don't recall it actually containing reproductions of those writings, at least not on a substantial basis.
Importantly, however, this book is not a biography - it is a history of the scientific community at the time, centered around Darwin and Origin and placing them in relevant context.

Thanks a lot (+1). To not discourage others from answering, I will wait some time before accepting.


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Insect identification request. Long anteni. Grasshopper legs

Found in solo cup used to catch drips from toilet valve. East coast of U.S.

Possible duplicate of Do you know what type of insect this is?

That is a camel cricket, Rhaphidophoridae. https://www.pestworld.org/pest-guide/occasional-invaders/camel-crickets/
Likely some species of Ceuthophilus


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Why doesn't oligodendrocyte produce neurilemma
I was searching literature related to neurilemma and oligodendrocyte and came across these lines from WP (Neurilemma)

Oligodendrocytes do not have neurilemma because excess cytoplasm is directed centrally toward the oligodendrocyte cell body.

I tried tracing more scholarly articles in this  context but I wasn't satisfied.
So my question is: Why doesn't oligodendrocyte produce neurilemma. Any  reference articles would also help.

This statement is made in contrasting oligodendrocytes with Schwann cells. Both of these cell types are glial cells involved in myelination of neurons, but their morphology (shape) is different.
Oligodendrocytes in the CNS "reach out" with extended processes that then envelope axons as a myelin sheath. You could imagine an octopus reaching out arms that then loop around a stick. Like an octopus, they have multiple arms, and each arm can cover a different axon. The nucleus and other cellular machinery is located in the 'head' of the octopus.
Schwann cells in the PNS instead wrap around a single axon. You can think of them more like a fried egg, wrapped around a stick. The egg white is the myelination, the yolk is the nucleus. The outermost wrap is where all the other machinery of the cell is, and this area is called the neurilemma.
The actual presence/absence of the neurilemma isn't that important for the function of myelination, it's just a different shape of the cells.


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Basic question about phylogenetic trees
The following is an illustration rom my book of the phylogenetic tree of 6 animal phyla (the red stuff is mine):

I think what's causing some confusion is that there are no names/years at the circled nodes.
My first question is, was there an actual population between nodes (ex.) 2 and 3?
I would like to check if my understanding of the tree is correct:
Before node 1, there was a population which split into two populations: Porifera and the population between nodes 1 and 2 which we will call population 1-2. This population is unnamed on the diagram, either because we don't have a name for it, or because members of that population no longer exist, or to keep the diagram simplified.
Next, after some millions of years, population 1-2 split into the Cnidarians and population 2-3. Etc.
Is my understanding correct?
Thank you very much.

Yes, your understanding is correct.
That being said, it is standard to refer to population / species at specific points in time. Also, it is standard to refer to these ancestral populations relative to what they are the ancestors of. For example, we generally don't refer to the population 2-3 (as you named it) but we rather refer to the node/population/species 3 as the Most Recent Common Ancestor (MRCA) of Athropoda, Mollusca, Chordata and Echinodermata. The tree presented here is not complete but all Athropoda, Mollusca, Chordata and Echinodermata are Bilateria while Cnideria and Porifera aren't. Hence, you could say that the ancestor at node 3 is the MRCA of all Bilateria.
Related posts

This intro to phylogeny
If dinosaurs could have feathers, would they still be reptiles?


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The protostome/deuterostome distinction and why it is important
As I unerstand it, at some point an embryo develops a hole; this hole continues to punch through, and eventually makes an opening at the other side of the embryo. If the original hole becomes the mouth, then the organism is called a protostome. If the second opening becomes a mouth, then the animal is called a deuterotome.
My first question is, is this distinction made only for organisms who have two openings? In other words, would an organism with only one orifice be called a protostome, or would it be neither?
Why is the protostome/deuterostome distinction important? Why does it matter whether embryo develops a mouth from the first or second orifice?

The terminology is really just describing the process in embryonic development that you describe: deuterostome means "second mouth"; protostome means "first mouth."
The significance of these groups is in evolutionary history and cladistics. All of the deuterostomes have a shared common ancestor that is not shared with any protostomes, and vice versa. Regardless of developmental pattern or number of openings during development, no other organism should be given these names (and if it is, and the correct ancestry is determined later, they would be moved out of those categories accordingly).
This is actually really important in biological classification of organisms, and before modern genetic techniques these types of shared characteristics were the best way to determine shared ancestry. Think a bit about what it means for an organism with two openings to differentiate one as mouth and the other as anus: once they are strongly differentiated, there is a huge barrier towards going "backward" and "switching" openings because mouth and anus have very different functions. However, if you go from having one or no openings to having two, before there is specialization, the distinction of which one develops first isn't likely to be that advantageous one way or the other.
Nephrozoa contains the deuterostomes and protostomes, consisting of almost all extant animals. However there are also other animals that are neither. For example, Xenacoelomorpha might be the closest thing to a bilateral animal with only one orifice, though they don't really have a true gut at all.

Thanks for the answer; if I could as a follow up question: In my class we are just focusing on 6 phyla of animals: Porifera, Chordata, Mollusca, Cnidaria, Arthropoda, Echinodermata. Is it possible to say that some of these phyla are completely composed entirely of protostomes, and some of deuterostomes?

@Ovi I can't really help you with your homework more than I already have, but if you see the Wikipedia pages for deuterostomes and protostomes (and most likely your textbook as well...) the answer to your comment question should be quite apparent.

Thanks for all your help; I will check the wikipedia article. Anyways it's not a homework question, I am studying for a test. My book is very short (written by professor specifically for this class) and doesn't seem to answer this question.


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Can humans eat green leaves to get necessary daily energy intake?
Green leaves make carbohydrates by photosynthesis. This means that green leaves are abundant source of energy. Can humans eat enough green leaves off the trees and get necessary daily energy intake?

Welcome to the site! You may know this already, but early-season leaves of many common trees are edible, including hawthorn and beech (apparently also linden, birch and spruce, but I haven't tried those). Later in the season they accumulate tannins and other secondary metabolites that can be toxic. Unfortunately, I can't find much about their calorie content (although I'm sure it's low), so I can't post a full answer, but I'll leave this here for anyone else who's planning to. My gut feeling is it would be very difficult; assuming similar calories to lettuce, you'd need to eat 13-14kg per day.

Do you mean exclusively the leaves of trees?  If not, there are a number of common foods that are leaves: lettuce, spinach, cabbage, green onions...  Offhand I can't think of any tree leaves commonly used as food, but bay leaves are a common seasoning for soups and stews.  And I like to nibble the new green leaves of spruce when out hiking...

Something can be called a food when it is edible, and most tree leaves are not.
Carbohydrates or other nutrients can be a source of energy when they are digestible, but cellulose and (most) other carbs in leaves are not (Elmhurst.edu).
Finally, to get "necessary daily energy," you need to consume, for example, 2,000 Kcal. So, even if you find edible tree leaves with digestible carbs, they will still not likely provide enough calories. Think of lettuce: 360 grams of lettuce = 54 Kcal.


text:
Should the infraspecific epithet agree in gender with the genus name?
Let's take the following plant name

Gymnocalycium mihanovichii

So we were to designate the yellow form of the plant, would it be

Gymnocalycium mihanovichii f. aurea

because forma is feminine or

Gymnocalycium mihanovichii f. aureum

because Gymnocalycium is neuter?
Hope the question is on-topic

This is governed by the International Code of Nomenclature for algae, fungi, and plants or by the International Code of Zoological Nomenclature.
For plants, infraspecific names are covered in Article 24. Article 24.2 states:

Infraspecific epithets are formed like specific epithets and, when adjectival in form and not used as nouns, they agree grammatically with the generic name (see Art. 23.5 and 32.2).

Article 23.5 reads:

The specific epithet, when adjectival in form and not used as a noun, agrees with the gender of the generic name; when the epithet is a noun in apposition or a genitive noun, it retains its own gender and termination irrespective of the gender of the generic name. Epithets not conforming to this rule are to be corrected (see Art. 32.2) to the proper form of the termination (Latin or transcribed Greek) of the original author(s). In particular, the usage of the word element ‑cola as an adjective is a correctable error.

Article 32.2 states that names are still validly published, even if their terminations are incorrect.
In this case, since "aureum" is an adjective, it should agree with the genus name.


text:
How different can the Tm be between 2 primers?
I have a forward primer with Tm 85 degree Celcius. I cannot change this primer. But I have two options for the reverse primer. One with Tm 65 degree Celcius (Annealing at 65 degree Celcius) and another with 72 degree Celcius (Annealing at 72 degree Celcius).
First of all, will either of the primers work for me?
If so, which pair would be better?

You should check with the manufacturer of your PCR kit. I use NEB and their online tm calculator warns you when tm difference is greater than 5C suggesting that 5C or less difference is best.

Simple: try both.

The default parameter provided by "primer-blast" is 3 degree (max difference between the melting temperatures of the pairs) .
that said I think it really depends on the application. in case of cloning (in my experience) you can allow wider ranges of delta Tm between primers (in this case I used to use the average Tm of the two primers as annealing temperature). you accept to have a bad efficiency but eventually you can pull out your insert from the gel and clone it in a vector for a prep.

Thanks, Pedrini. This is the case of cloning. With all your suggestions, I am just gonna try with the same primers.

@RKK what do you mean "with the same primers"? if none of the two reverse is working you can even redesign one by elongate at the 3' to match the Tm of the forward.

This really depends on your application, but from my experience 2-3 degrees with a max of 5°C difference usually works. The more the melting temperature differ, the more you need to optimize all the other parameters like salt and magnesium concentration, amount of enzyme, annealing and elongation times and so on.
85°C melting temperature seems very much for me, as you are 13°C over the optimal working temperature of the Taq polymerase. This willmost likely  lead to a lot side products with incompletely bound primers. You can change the annealing temperature by shortening the 3' end of your primer (I assume that you need a specific starting point) so you get down at least a bit. Then I would probably order both other primers and test which ones works better, but I wouldn't expect that this works immediately and will need at least some optimization.
Can you give some more information why you can't use other primers and on your application?

Thanks, Chris. I cannot change my forward primer as it incorporates a restriction site in 5' end and a point mutation near 3' end. I think i just have to try it out and play with the parameters. I will comment once I do my experiment. I welcome any other suggestions.


text:
There are small parts between Genes in an Operon that does not encode for any amino acids. What is the purpose of these parts?
What is the purpose of these parts in the translation process ?
Picture to demonstrate below :

The regions between the genes on a prokaryote operon are transcribed into the messenger RNA  but are not translated into proteins.  Because they are not translated, they are characterized by the general term UnTranslated Regions (UTRs).  A typical operon having two genes is shown in this diagram from Wikipedia:

The UTR which occurs between the protein-coding genes contains the sequence for a ribosomal binding site (RBS) in the transcribed mRNA.  An RBS is a site where a ribosome can attach to the mRNA so that the Start codon of the following gene is in the correct position to begin translation of the protein.  (Of course, the 5' UTR preceding the first gene also has an RBS sequence.)  An RBS contains a particular nucleotide sequence to match up with a complementary sequence of the ribosomal RNA of the ribosome; this sequence is known as the Shine-Dalgarno sequence.
(Note that these inter-gene UTRs are not called introns; introns occur only in eukaryotes and occur within a gene, between the Start and Stop codons.)

You might add, in answer to the specific question of "purpose", that having separate RBSs allows the independent translation of the cistrons in a polycistronic mRNA, i.e. each cistron can be translated at a different rate producing different amounts of protein product.

Not sure about the role in this particular case of lac operon but normally such noncoding sequences in eukaryotic system (intron regions) have some regulatory roles, may be on the same gene or other genes located elsewhere on the chromosome. For example intron 3 of gene A may act as an enhancer sequence of gene B located 500 bp downstream of gene A
In this case the operon is producing three different proteins, if there were no gaps then a fusion protein may have been produced which is not desired

Introns, enhancers, what are you going on about?  This is a question about prokaryotes.

I think I clearly mentioned about I am not talking about lac operon, I just explained what the roles of non coding DNAs may be. My bad if my answer sounded otherwise


text:
Why do the host cells containing iC3b fragment not undergo phagocytosis?
As far as I understand, in complement system C3b gets deposited on pathogen surface but it can also be deposited on host cells. Host cells have some negative regulatory system such as membrane cofactor of proteolysis MCP, decay associating factor DAF etc which either removes C3b or cleave it using factor I to iC3b which can not form a C3 convertase or C5 convertase so no production of membrane attack complex on host cells.
However, phagocytes contain complement receptors CR2, CR3 etc that specifically recognise iC3b and engulfs the cells bearing it. While it is very useful for pathogens bearing iC3b (In those cases where pathogens contain sialic acid residue which attracts factor I and prevents forming MAC on those pathogens) wouldn't it be very dangerous for host cells?
So if there is receptors against iC3b on phagocytes then what is the point of host cells converting C3b into iC3b, they get killed one way or another anyway

There's a relatively new concept of self-associated molecular patterns (SAMPs), which much like DAMPs and PAMPs, help immune cells make a decision in a slurry of signals. There's at least a fair article on SAMPs here, and to go even further, the suggestion that tumor-associated SAMPs can dampen immune clearance of cancer cells.
In my head a few things are going on:
(1) The opsonins are potentially binding to everything. Of course, there are surfaces like ECM that don't have any receptors or patterns that you don't want getting damaged, and there's at least some evidence that complement clearance by factors I and H (paywall) may contribute to ablating that effect.
(2) The actual targets for the immune system are expressing patterns that specialized pattern recognition receptors on your phagocytes and so forth can recognize.
(3) Self cells are expressing receptors and patterns that tell the very same cells there's no threat, either through direct inhibition or degradation of kill signals.
Remember that when self cells are damaged, the expression of DAMPs help macrophages and the like come clear them away, so there's obviously a way for self cells to control that effect.


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Is there muscle hyperplasia or hypertrophy after surgery?
After exercise there is hypertrophy only. I am curious, if a surgery removes muscle, will there be hyperplasia or hypertrophy to restore it?

It does not required much research to find the answer. After injury and surgery the muscle undergoes inflammation to clear up the debris. After that myogenic cells start to proliferate and differentiate, so as expected, there is hyperplasia by restoring injured muscle. Which means that the body can fully restore muscle function if the injury is not too severe.

Effective fiber hypertrophy in satellite cell-depleted skeletal muscle.
Cellular and Molecular Regulation of Muscle Regeneration
Regeneration of mammalian skeletal muscle. Basic mechanisms and clinical implications.

I investigated this a little bit further. Muscle regrowth is mediated by the BM (basement membrane) which is the extracellular matrix that sorrounds the muscle fiber. If that is badly damaged or the nerve is cut, then the muscle fiber won't grow back and we will get scar tissue instead. The muscle will compensate this at a certain level by hypertrophy. There is an interesting new treatment for severe muscle injury, which removes the scar tissue and adds pig extracellular matrix to regrow the muscle.

Implant Lets Patients Regrow Lost Leg Muscle

"Which means that the body can fully restore muscle function if the injury is not too severe" – as far as I remember, connective tissue proliferates a lot faster and most of the damage is "hot-fixed" that way, that is musles do not fully regenerate their physical capacity, unless the damage is very localised and limited. I might be wrong though: I only had two basic courses on morphology and histology many years ago.

@EliKorvigo Well we can find it out.

@EliKorvigo I read yesterday that muscle can grow back if the basement membrane is not removed. I just need to read a little bit more in the topic.

@EliKorvigo As far as I remember healing has nothing to do with how fast a tissue type proliferates. It depends on what type of stem cells you have and what signal they get. But maybe I am wrong. I have only superficial knowlegde in the topic.


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Are wasps attracted to UV light emissions?
I remember seeing a documentary where it was shown that bees and wasps are attracted to UV components of a flower colour (please correct me if I am wrong).
Does this mean that they could be attracted by neon lights (that I suspect are emitting also in the UV part of the spectrum)?
I am asking because I have neon lights in my office and if I have the lights on I can't open the window, or a wasp will almost immediately enter the office. I've experimented a bit, and turning off the light makes the wasp go out rather quickly, hence my hypothesis.
I am located in Europe, if that makes a difference for the species involved. Outside the window we have some tall trees, so we keep some lights on even when the sun is out.


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What is this strange-shaped fruit?

The fruit has form of a cube or icosaheder. It is green but quickly becomes black. The meat of ripe fruit is easily separated from the seed, is sweet and tastes as dried plum. The seed has strange icosahedrical form, like two pyramids connected.
The fruit is seen on Mediterranean coast of Israel.

I don't have the answer, but a warning: the flowers, to the degree I can see them, look like the family Apocynaceae -- 5 petals, tubular, twisted/overlapping petals.  Break off a leaf and see if there is white sap, another characteristic of the family.  These plants are typically very toxic, at least the sap containing parts.  However, the fruit looks pretty atypical for the Apocynaceae, and I don't know if the fruit in the family is typically toxic.  But I guess you've already done the experiment!

@Bryan Hanson: And if the OP never posts again, we can reasonably assume that it was indeed toxic :-)

You funny! Let’s hope we get a positive report!

Now I have the answer, and if you are reading this soon after eating the fruit you should probably seek medical attention.
Looks like Cascabela theviata which is in the Apocynaceae and the Wikipedia article makes clear that the fruit is also poisonous.

I did not eat it, only tried yesterday morning, I experienced no problems so far.

@Anixx that's good to hear!  I think it could have been unpleasant...

I did not swallow it, that's why possibly there are no effects. But I testify it tastes like a dried plum.


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Is the "Manhattan Ant" a new species; still only found in Manhattan's Upper West Side?
I've stumbled upon the viewing.nyc article Upper West Side Has Its Own Ant Species Dubbed the "ManhattAnt" which says:

Columbia University biologist Rob Dunn has discovered a unique species of ant living between 63rd and 76th streets along Broadway on the Upper West Side of Manhattan. Dubbed the "ManhattAnt", the ants have a higher concentration of carbon in their bodies, indicative of a high corn-syrup diet, likely from eating trash and discarded street food.

Biologists stumbled upon a new species of ant in the Broadway medians at 63rd and 76th streets […] The ant looks like it hails from Europe, but so far the scientists have not been able to match it with any of the approximately 13,000 species of known ant. “It’s new to North America, and we believe it’s new to the entire world,” biologist Rob Dunn, whose team discovered the insect, told the Post. The ant doesn’t have a scientific name yet, but it’s fondly nicknamed the “ManhattAnt.”

and references the Simthsonian Magazine article NYC Has Its Own Ant, the “ManhattAnt” with the subtitle:

A new ant species joins a menagerie of other creatures cut off from their kind in isolated patches of urban green in NYC

A "new species" is not the same thing as a "creatures cut off from their kind in isolated patches of urban green in NYC"
Question: Has the "Manhattan Ant" or "ManhattAnt" turned out to be a new species, and is it still only found in Manhattan's Upper West Side?

I'm not sure that the species-identification tag fits here. Those who are monitoring the tag and have species-ID skills may still be interested in answering this question, but I don't have independent images or measurements of the ant. Since "Columbia University biologist Rob Dunn" is cited, there should be some reliable information out there somewhere in the literature, but I don't know how/where to find it.

I'm not sure what we can add to this. The article states that for the moment, this does indeed look like a new species. But it was only identified a few months ago, so there's not much more to say. It's not as though this was several years ago so you can expect a consensus to have been reached.

@terdon the site has a substantial number of active users; I wouldn't write each and every one of them off so quickly. Sometimes people actually happen to know specific information on a topic, and this species, having been reported in several news sources, and relating to an interesting new topic in biology (species differentiation affected by urban development), might just have an extra amount of notability in the field. Let's wait and see!

I say this because your question suggests you were under the impression that the species was discovered years ago:  Has the "Manhattan Ant" or "ManhattAnt" turned out to be a new species, and is it still only found in Manhattan's Upper West Side?

@terdon based on the answer below I found essentially the same article published in 2012! https://nypost.com/2012/09/02/new-breed-of-ruffi-ant-found-in-manhattan/

yes indeed! I'm glad you found out more :)

Rob Dunn is a professor at North Carolina State University (though apparently taught at Columbia University at some point). I recall him mentioning this specific NY ant discovery to me 4-5 years ago. A better pop-sci article can be found here that suggests this discovery was circa 2012. Another related article can be found here.
You can find a few other papers regarding urban ant populations by Dunn and collaborator Amy Savage and others via Rob Dunn's website, (Ex: Savage et al. 2014 and Penick et al. 2015).
However, I could not find evidence in the few relevant papers I skimmed for the the so-called "Manhattant" or evidence of any publications formally introducing this as a new species.
Pećarević et al. 2010 ("Biodiversity on Broadway - Enigmatic Diversity of the Societies of Ants (Formicidae) on the Streets of New York City") lists a number of species found by Dunn and others in Manhattan, but again makes no mention of this specific discovery.
My conclusion is that since Dunn has not listed this as one of his many publications on his website it's either burried in another paper as an ancillary artifact, or, more likely, has not been formally described...
You could reach out to Rob directly [email | twitter], I suppose, and update us all on this question!

This is great, thank you! The Biodiversity on Broadway paper (Pećarević et al. 2010, yay, open access!) is quite interesting, and google for example gives 55 citations and many related papers So this will keep me busy for a while. I'm too shy to reach out directly to any of them being outside my field, but that's a good idea and someone may follow up on it.

apparently there is an Ant Wiki for this too! http://www.antwiki.org/wiki/Ants_of_New_York_City


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What are the differences in the two possible methods to calculate the Hardy-Weinberg Equation?
I am more than flabbergasted by calculations of Hardy-Weinberg equilibria. The formula's theory assumes a binomal distribution of allele frequencies in a population, and hence allows the comparison of observed phenotype frequencies to an ideal model distribution.
$$
p^2 + 2pq + q^2 = 1
$$
with
$p^2$ = Frequency of homozygous phenotype PP
$2pq$ = Frequency of heterozygous phenotype PQ
$q^2$ = Frequency of homozygous phenotype QQ
There are two different methods of working with the HW equation that I have come across, and they do not seem to be compatible; used on the same data sets they yield wildly different results. I feel like I'm not seeing the forest for the trees, to be honest.
Is either of these methods (technically) wrong? How do I decide which one to use for each data set (i.e. is it valid to use method #1 on 3-allele-data sets)? Or do I just use whatever method is easiest? Doesn't this lead to discrepancies in the results? This seems like a big thing, especially when comparing real-world observation data to assumed HW distributions.
Example data set (EST/California) and results of HW calculations. I'm using observed phenotype in the place of the original data's observed genotype.
Phenotype     n  |   HW1   HW2p   HW2q
PP           37  |  33.9   37.1   28.8
PQ           20  |  25.0   23.0   28.2
QQ            7  |   4.5    3.8    7.0

Calculation method #1
As suggested by above-linked data set source and Beebee/Rowe's Introduction to Molecular Ecology, alleles are simply added up to get values for p and q respectively:
Phenotype    n  |   P    Q
PP          37  |  74    0   (37 * PP = 74 P)
PQ          20  |  20   20   (20 * PQ = 20 P + 20 Q)
QQ          7   |   0   14   ( 7 * QQ = 14 Q)
Sums        64  |  94   34

From this we can directly infer p/q: $p = 94/(94+34) =0.73$ and $q = 34/(94+34) = 0.27$; with the condition $p + q = 1$ remaining true.
Using these values for p and q in the HW equation yields:
$$
p^2 + 2pq + q^2 = 1
\\
(0.73)^2 + 2(0.73)(0.27) + (0.27)^2 = 1
$$
And a population-wide phenotype distribution of
Phenotype      n
PP         33.92    p^2 * 64
PQ         24.96    2pq * 64
QQ          4.48    q^2 * 64

Calculation method #2
The second method of utilising the HW equation is a lot more direct, and just about every text book I could find uses this method to solve 3+ allele problems (as, for example, blood types); Wikipedia commends its usefulness in calculating heterozygote frequencies of genetic diseases in large populations.
In this calculation frequencies are directly inferred as per the definition of the HW equation. This means $p^2$ is equal to the frequency of the phenotype PP (see above).
$$
p^2 = \frac{37}{64} \\
p = {\sqrt 0.578} \\
p \approx 0.76
$$
$$
q = 1 - p = 0.24
$$
Leading to a HW distribution of
$$
(0.76)^2 + 2(0.76)(0.24) + (0.24)^2 = 1
$$
With a new ideal phenotype distribution:
Phenotype      n
PP          37.1    p^2 * 64
PQ          23.0    2pq * 64
QQ           3.8    q^2 * 64

Inverting the calculation by starting with $q^2 = 7/64$ leads to even more diverging results:
Phenotype      n
PP          28.8    p^2 * 64
PQ          28.2    2pq * 64
QQ           7.0    q^2 * 64

Using both $p^2$ and $q^2$ inevitably violates the condition $(p+q)^2 = 1$.

Welcome to SE Biology, which is a question and answer site about biology. You have obviously put a lot of effort into this, but at present I don't see any question. This is, admittedly not my field, but if there is no question posed in the title, begining or end of your post, it is difficult to know what you wish to know. Are you asking which of two types of calculation is correct? If so, please edit your post to make that clear at the outset, otherwise it risks being ruled "off-topic" on the basis of "unclear what you are asking".

Hi David, I thought his post was clear. Perhaps the title needs to "rogatized," but the questions are in the end of the main post before the computational addenda: "Is either of these methods wrong? Do I have to decide which one to use for each data set? Can I even use method #1 on 3-allele-data sets?"

Hej David, hej vipatron!
You're right that my questions are not as clearly defined as I thought they would be. I would like to know where the differences between those two (three) equation stem, and if either is more valid/accurate than the other model

G'Ra. Please use the @ so I know you have responded to my comment. Only the poster gets automatic notification. You need to edit your question. A comment response is insufficient. @vipatron — A question needs a sentence with a question mark.

And then there's Gene driving which destroys all of your calculations :-/

Okay, so the Hardy-Weinberg Equilibrium is just that: an equilbrium.

In physics, a system (some object) is at equilibrium when no net energy crosses its boundary with the surroundings.

no energy change means no change in motion (the state of the object) due to outside influence on the system.

In chemistry, a system (the beaker/reaction container/cytosol) is at equilibrium when no change in the concentration of the chemical species inside of it occurs over time

no chemical makeup change means the (molecular) state of the atoms in the system is free of energetic influence from the outside world.

In the H-W Equilibrium, a system (the gene pool) is at rest when no change in the frequency(concentration) of its alleles occurs over time.

no change in the frequency of alleles means that there is no outside influence on the state of the gene pool.

Just like in basic physics, we have to define our system. If our system is the gene pool, then even the behaviors of the organisms in whose cells those alleles are found are outside of the system. The system is only the alleles aka gene pool.
The most important part about understanding the H-W Equilibrium is that it only applies when those conditions of the gene pool being free from outside influence hold. In fact, in the link you gave, the introduction has it in the second sentence (don't feel bad, I missed it the first few times, too—too focused on applying the algebra to understand what it was really saying):

The model has five basic assumptions:
1) the population is large (i.e., there is no genetic drift)
2) there is no gene flow between populations, from migration or transfer of gametes
3) mutations are negligible
4) individuals are mating randomly
5) natural selection is not operating on the population.

Let's break them down/group them:

2: Obvious in terms of equilibrium == system is in isolation from surroundings
4 & 5: Selection pressure (4: sexual selection, or 5: natural selection) is not pushing on the system.
1 & 3: Random effects are not pushing on the system (1 = statistical sampling error that can push small populations, and 3 = mutation that pushes the system like adding a new chemical species to a system at rest.)

With that solid grounding in the theory, let's move on to your questions about the algebra. Remember, the equilibrium only applies when the gene pool is not being pushed around by external factors. Which means that the physical copies of alleles (gametes) should pair randomly with the possible gametes at every mating. If those assumptions didn't hold true, then the math of the equilibrium wouldn't hold up. If you run the numbers on a system at equilbrium, barring small amounts of sampling error (reducible with a bigger n), the H-W Model's predictions will be accurate. All the methods will yield similar results.
However, if the predicted values don't match the actual with one method, you can assume that other methods will also yield inaccurate predictions, and that the two different calculation methods' predictions will vary widely from each other, largely because of the assumptions you are making (Method 2: 1 = p+q), or aren't making (Method 2).

Hello vipatron!
Thank you for your clarifications. I am aware of the limitations of the HW model, but have to be honest with myself in admitting I've never given them this much thought.
But if I'm understanding this right, both modes should -- in an ideal HW population -- yield the same results, but will inevitably lead to skewed distributions as long as "real" (i.e. "non-ideal") populations are observed? Considering that measuring real deviations from the HW model ideal is most I've seen HW used for, doesn't having two options lead to two significantly different results?

I’m not a pure biologist. So, I don’t think I can answer your question except with a supposition backed by experience. Let’s say you were testing a hypothesis: you need to make some estimate of the values for p & q, and then be able to quantify the degree of deviation. Using the “exact method” of allelic frequency count, you can get a single estimate of allelic frequency and then create a null hypothesis about what the gene pool would look like if it were in equilibrium. But, I would prefer to see someone’s real work and explain why they did that rather than talk into the wind.

Oh, and you are understanding my answer.

@vipatron Under the listed assumptions, HW equilibrium is reached in a single generation. The term "equilibrium" is hence a little funny and there is not much over time dynamic that would lead to equilibrium. The expression HW rule is also common and it avoids the term "equilibrium".

You are throwing numbers into an equation without understanding it.
If you know the numbers for pp, pq and qq, you don't use HWE to recalculate them.  So your last statement in Calculation 1 is nonsense.  What you've done there is calculated the proportions for a population in HWE where the p=0.73, but you were already given the actual distribution in the population, so pretending like your theoretical calculation trumps the given data is nonsense.
Calculation 2 only works perfectly if your population is exactly in HWE.  Yours is a little off, that's why it won't give you quite the same p and q's as calculating it properly, by actually counting up the p alleles in the homozygotes and heterozygotes.


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Birds brewing beer?
There is a slight bend in the rain gutter next to my window.
Over the last 4 years, I observed birds (ravens, magpies and newly doves) to dip their beaks in. I observed ravens to dip what I think was bread in.
There are many other opportunities around to take up water and just quench their thirst.
Doves drinking where ravens are around looks dangerous to me.
Maybe I'm completely mislead, but all I see makes me think these birds are kind of brewing beer.
Has anything like this be seen before? What should I think of this?

Most likely there is no fermentation going on. For fermentation to occur you usually must deplete oxygen from the system. Here is more information about it.

You don't need an oxygen depleted environment to ferment (produce ethanol). Baker's yeast (S. cerevisae) is Crabtree positive and will metabolize glucose to ethanol as the main source of energy under atmospheric oxygen conditions.

I think you're observing drinking and food moistening.  Since birds have no teeth, food like bread, especially if dry, is easier to consume if it is moistened first.
Drinking from a gutter is attractive because most other water sources are at ground level, which means there are potentially attacks by ground-based predators as well as aerial ones.  Cats are a major predator of birds.  Also, it may be easier to take flight from an elevated place like a gutter than from the ground.  I expect that is attractive for a large bird like a raven. Landing is easier too, as the bird's tail can be below the level of the perch and braking can also be eased by the final part of the approach being a dip with the last part being upwards which will reduce speed.

It was hard to decide which answer to accept. The reason I choose @BPinto is that it gave the reason to rule out fermentation.


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T-Cell Motility: does motility require direction specific actin polymerization?
T-cells have been shown to migrate inside concentration gradients - both in the direction of the source or away. Even under shallow gradients, t-cells move. I argue that, to be able to move in a directed manner, a cell must be able to have a differential response of actin polymerization and philipodia. But I find it hard to believe that it is a differential response unless the sensor resolution not only communicates centrally, but is also extremely sensitive. How does this work?

I don't have a direct answer to your question, mainly because I'm not an expert on T cell motility. There are, however, some fine resources that help me make sense of it. Video of T cells moving within a lymph node. A paper from the same group talking about T cell motility.

Yes! I have read this fantastic paper, but it simply does not answer the mechanism of action of motility. The video shows clear evidence of philipodia→move, but i wonder how the philipodia is requested to be built in the first place. Perhaps a more direct question would be: is it possible that cytoplasm concentration gradients of phosphatidylserine are creating differential actin polymerization zones based on cell membrane signaling from extrinsic stimuli? I am just not sure if that is even the right question, better to keep it broad... I am just an engineer though, not a biologist.

Okay so you've had some readings, I tried very hard to come up with something sensible. It's a tough one because I work with T cells quite a bit, but mostly in commercialization and manufacturing of T cell-based therapies. So we don't really have to care how they move about.

It's understood at least that leukocyte motility is dependent on cytoskeleton remodeling and actin dynamics. In the blood, as the T cells tumble past the activated endothelium of an affected site, they're grabbed by selectins and integrins expressed on the endothelial surface. These are often illustrated as the adhesion and rolling phases of T cell migration.
Chemokines, which normally form a gradient for T cell chemotaxis, induce changes in the cellular morphology that promote migration into the surround tissues. The cells polarize into a force-generating lamellopodium with a leading edge in the front, and a uropod in the back. It appears as though actin polymerizes in the lamellopodium and juts the cell out toward the direction of the signal, and the uropod contracts in a myosin-dependent manner, releasing molecules bound there, thereby allowing the cell to tug in the direction of the lamellopodia (1, 2).
The mechanism has in fact been characterized by leading-edge redistribution of chemokine receptors such as CCR5 and CXCR4, which may have to do with actin/myosin dynamics and lipid rafts. This makes the receptor distribution asymmetric as well, and so a weaker response to the chemoattractant in the back end of the cell. The best way I could describe it is using the formation of the cSMAC in T cell receptor biology (Figure 1) (3). The SMAC is basically a synapse formed during T cell activation where receptors are concentrated to a particular area where the T cell is meeting the APC.

Figure 1. TCR-mediated cytoskeletal remodeling
The way the authors describe it is the downstream signals from the TCR localize actin pathway molecules to the site of signaling, and causes cytoskeletal remodeling at that particular site.
Studies in neutrophils have shown that polarization leads to a frontness and backness to the cell, regulated by different proteins and inhibit the formation of one another. This is a good paper to read through on that matter, though it's a tougher read in my opinion: https://www.researchgate.net/publication/8957894_Cytoskeletal_remodeling_in_leukocyte_function


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How cnidocytes work?
I have googled  for the structure of cnidocyte but images of google is unclear or complex .so please draw a simple understandable structure of cnidocyte .I know that cnidocyte works by osmosis but I don't know how exactly osmosis make cnidocyte to function .so please explain the mechanism of cnidocyte.

A cnidocyte is a poison-loaded harpoon connected to a pressure plate, implemented at the microscale level in a cell. Something triggers the plate, the harpoon jets out. Simple enough.


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Is there a reliable source for storage and stability of reducing agents like DTT?
Reading the literature on DTT, one is confronted with a confusing mass of papers; some claim that a 1M solution in water is stable, other papers say it is not. I use the reaction with DTNB to show that the DTT is still good, but that is cumbersome.
Is there some source of reliable (as in data driven) information on how to store compounds like DTT and other reducing agents?

Thiol-Based Reducing Agents
The instability of thiol-based reducing agents in solution is due to their propensity to form disulfide bonds by the following half reaction:
$$\ce{2RSH -> RSSR + 2H+ + 2e-}$$
It is clear that disulfide formation requires:

Deprotonation of the thiols to form thiolates (RS-).
An electron acceptor.

Therefore, solutions of thiol-based reducing agents would be most stable when:

The pH is buffered to where the thiol form predominates. The pKa of the thiol in β-mercaptoethanol is 9.5 and in dithiothreitol are 9.2 and 10.1  (Whitesides et al., 1977). Buffering the pH lower than this should increase stability.
Electron acceptors are removed. In aqueous solution, the electron acceptor is molecular oxygen. Degassing the buffer and storing the solutions under an inert gas such as argon should increase stability.
Reaction catalysts are removed. Divalent metal cations, especially copper (II) (Cu2+), catalyze oxygen dependent disulfide formation, even in trace amounts (Smith et al., 1994). Therefore a chelator such as EDTA should increase stability.
Temperature is low. As with most chemical reactions, rate increases with temperature.

The stabilities of the thiol-based reducing agents β-mercaptoethanol (β-ME), dithiothreitol (DTT) and glutathione (GSH) have been determined in solution as a function of pH at 20°C (Stevens et al., 1983):

...and temperature at pH 8.5:

...as well as in the presence of copper (II) and EDTA at pH 8.5 and 20°C:

Below is the tabulated raw data (this is the actual data from the paper which I used to create the above graphs, but take note that I found it difficult to plot “>100”):
                               Half-life (h)
pH    Temp (°C)    Additive    β-ME    DTT    GSH
6.5   20           -           >100    40     16
7.5   20           -           10      10     9
8.5   20           -           4.0     1.4    1.3
8.5   0            -           21      11     8
8.5   40           -           1.0     0.2    0.2
8.5   20           Cu(II)      0.6     0.6    1.2
8.5   20           EDTA        >100    4      70

As expected, stability decreased with increasing pH and temperature, and also with the addition of copper. Stability increased with the addition of EDTA.

Non-Thiol-Based Reducing Agents
Han and Han (1994) studied the effect of pH and buffer composition on the solution stability of tris(2-carboxyethyl)phosphine (TCEP). Though this is not a thiol-based reducing agent, it is still subject to oxidation. However, it is quite stable in solution:

pH    Solute/Buffer     % TCEP Oxidized After 3 Weeks
7.5   Tris-HCl          18.7 ± 0.6
8.5   Tris-HCl          16.8 ± 0.5
9.5   Tris-HCl          14.5 ± 0.5
8.2   borate             6.6 ± 0.2
10.2  borate             5.3 ± 0.1
6.8   HEPES             14.8 ± 0.4
8.2   HEPES             13.6 ± 0.3
9.7   CAPS               9.8 ± 0.3
11.1  CAPS               4.3 ± 0.1

Stability increased with increasing pH, though the effect was not large. Interestingly, the buffer composition had a larger effect on stability which was especially pronounced with phosphate:

        % TCEP Oxidized After 72 Hours
 pH     0.15 M phosphate    0.35 M phosphate
 6.0    not determined      11.2 ± 0.3
 6.8     8.1 ± 0.4          56.8 ± 2.3
 7.0    23.5 ± 0.9           100
 7.2    33.4 ± 1.0           100
 7.4    56.5 ± 1.4           100
 7.6    56.8 ± 2.1           100
 7.8    48.9 ± 2.5           100
 8.0    36.6 ± 1.7           100
10.6    not determined      11.7 ± 0.5
11.6    not determined       9.1 ± 0.4

References
Han JC, Han GY. 1994. A Procedure for Quantitative Determination of Tris(2-Carboxyethyl)phosphine, an Odorless Reducing Agent More Stable and Effective Than Dithiothreitol. Anal Biochem 220(1):5-10.
Smith RC, Reed VD, Hill WE. 1994. Oxidation Of Thiols By Copper(II). Phosphorus Sulfur Silicon Relat Elem 90(1-4):147-154.
Stevens R, Stevens L, Price NC. 1983. The stabilities of various thiol compounds used in protein purifications. Biochemical Education 11(2):70.
Whitesides GM, Lilburn JE, Szajewski RP. 1977. Rates of thiol-disulfide interchange reactions between mono- and dithiols and Ellman's reagent. J Org Chem 42(2):332-338.

Very useful references, thank you. Do you know if there is a similar, probably more recent article that also addresses the stability of TCEP?

@Guillaume I might have some; I’ll check when I’m at work tomorrow. I work with TCEP frequently and, in my experience, it is very stable in aqueous solution, though I don’t have any quantitative data.

@Guillaume I've updated the answer to include the data about BME and glutathione as well as TCEP.


text:
Why Is Gray Matter Gray?
When I researched I found  different reason for this, the  popular
ones are
1) white matter is mylinated .this reason was given in reference books and   this website
while others say
2)cell body concentration causes grayish appearance ,as in brain the cell body is concentrated outside. As mentioned in this .i.e cell body orientation.
also my teacher agrees with 2nd one, that the nissls granules contribute to the grayish appearance.orientation causes the effect of gray matter and white matter
I feel 1st reason to be more appropriate as there are billions of it couldn't be arranged as depicted in the second reason.
kindly help  me out to choose the accurate one, with appropriate reason of-course!

so whats is your question ? :) Just teasing you but kindly i higly doubt you will get anything more than just comment on it.

why is that true  ?

man i just say that this type of question is rather fit to the chat room rather posted like that. In my opinion SE its about sharing information not discuss like that. Still i hope that somebody try give you proper answer not jus opinion.

@L.Diago the question is clear and definitely answerable, you just might not be familiar with it if you haven't worked with gross specimens.

You are right that was the reason of my special interest to this question so thank you man. :)

The terms gray and white matter relate to their color in gross specimens (i.e., not microscopic specimens) that have been formalin fixed. Nissl granules describe a microscopic structure, the rough endoplasmic reticulum, and aren't directly related to the color of gross specimens. Here's an example of a frontal cross section from a University of Utah slide set:

You'll see it's generally a tannish-yellow (at least on my monitor, this image is a pretty good representation of what it looks like in person), but there are lighter "white" parts in the white matter areas, and darker "gray" parts in the cortex.
A live, or a recently deceased and not formalin fixed brain has different qualities, including color and consistency.
The color of the formalin fixed tissue is an artifact of the process of fixing, so it's not necessarily accurate to describe the gray color as something inherent to the cells in the gray matter, but generally yes, the whiter color in the white matter of formalin fixed brain is because of the high lipid concentration. The grayer color of the gray matter is because of the lower lipid concentration. This lovely old JBC article from 1929 discusses some of these issues, mostly regarding white matter in response to staining after fixation, but also gray and white matter before staining.

Nice answer but i still dont see that answer to question what exacly makes gray matter gray ? :)

@L.Diago "the grayer color of the gray matter is because of the lower lipid concentration."

I know, actually i am trying to give you constructiv criticism. But the other part was about the fact what makes gray matter gray (i am not telling that your answer is bad but he put on tabel something about nissle substance )

@L.Diago can you please clarify your suggestion? I'm not sure what you're getting at.

I think the criticism is a bit nitpicky. It's not like there is a "gray chemical compound" in gray matter. This answer provides the correct one: gray is the color of formalin-fixed brain tissue that contains less lipids than white matter. Unfixed brain tissue is not gray.

@BryanKrause I just tried to get him inculed something about the nissle substance. You know only to makes the answer perfect, but i know doesnt need to be included. But still i think he wanted oppinion about the nissle substance. Still wrote that i just teased him.

@L.Diago Nissl granules don't have much to do with it, but I've added it to the answer to clarify that.

@DeNovo I am sorry for that, but you know  this type of question can be usefull for anybody new in neurosciences so i wanted that to be perfect answer.

The grayer color of the gray matter is because of the lower lipid concentration. Is it known, why the lipid concentration differs between the inner outer parts of the brain?

@Marzipanherz myelin

so you are saying first answer is correct right? i.e white matter is mylinated , inturn mylin is made up of lipids. but the problem with that is mylin sheath is formed in between shwaan cell and axon how could you see the color of middle layer

@sudhanvab plasma membranes are not opaque. The intracellular contents of a tissue are typically what give that tissue a characteristic color.


text:
How does body fat leave your body?
So I know that it’s not from tears or sweat because they are composed of mainly water and sodium, it’s not from going poo or pee as poo and pee are made of the parts of food that supply your body with no nutrients and your body also doesn’t “burn body fat” because there is a theory that no matter is ever destroyed so it’s none of those but another thing is it’s not your hair, ear wax, finger nails or anything of that sort because people can lose over 17 pounds in 3 months but you can’t build up that amount of hair , ear wax or whatever else in three months so how does body fat leave your body

there is a theory that no matter is ever destroyed - what theory is that? Do you have a reference?

@Nathan welcome to Biology SE.  I see that you are new contributor, so i highly recomend you to take a tour in help center. There you can find what we expect from an question. For now your question is full of oppinion based claims, with unclear poin of what you exacly want to know. Please feel free to edit your answer or according to rules of Biology SE it can be close.

Where does wood (or gasoline &c) go when you burn it?

Many of the statements in your question are false, including your ideas about waste products.
Ultimately, fats, just like carbohydrates, end up as water and carbon dioxide if they are used in cellular respiration for energy. The reaction path is different, but the ultimate reaction products are the same as you would get from burning fat in a fire: reaction with atmospheric oxygen oxidizes the reactants to carbon dioxide and water.
This is the reverse process of photosynthesis, where carbon dioxide and water react to form sugars, with oxygen as a byproduct.
The mass leaves the body as exhaled carbon dioxide and as metabolic water through the urine, vapor in exhaled air, etc.


text:
Mating patterns and genetic superiority
In peacocks and peahens, the peahens prefer mating with peacocks having a large and bright tail. But how is having a large tail an indicator of genetic "fitness" (in survival terms) ? If having a large and bright tail is not related with genetic superiority, then what is the point of having the mating ritual?

Darwin thought quite a bit about this. He even said "The sight of a peacock makes me sick". https://www.ncbi.nlm.nih.gov/pubmed/10824193
He added to his ideas about natural selection to include sexual selection. Traits selected by females, even when they are non-adaptive for males, will increase the males fitness (as defined by his number of offspring). There is also the idea that perhaps possessing such an outrageous and non-adaptive tail proves that you a good mate, the same way we would think that a guy who could win a sprint while carrying barbells must be superior.

Evolution of traits under sexual selection is relatively complex subject that isn't easily summarized in a post. In short, these are the most important concepts you will want to read about; Fisherian runaway (aka. runaway selection), the sexy son hypothesis), the good genes hypothesis and Zahavi handicap principle.
All these concepts are somewhat related and the semantics can quickly become a little complicated and has been subject to a number of papers (e.g. Kokko et al. 2003). My understanding of the semantics details is limited. To my understanding, the Fisherian runaway selection and the sexy son hypothesis are very similar and the good genes hypothesis and Zahavi hanicap principle are related. What you will be most interested in is the Fisherian runaway selection.
I will below just cite some popular sources and I will leave to you the pleasure of understanding and misunderstanding the differences between these concepts :)
evo101 > Fisherian runaway

Imagine a bird population in which females choose mates at random. Males with slightly longer tails fly a little more adeptly, avoid predation, and so, survive better than males with slightly shorter tails. In this situation, a gene for female choosiness (longer tail = sexier) will be favored, since by choosing a long-tailed male she will have sons with longer tails. This trait will spread through the population until most males have long tails and most females prefer long-tailed mates. So far so good.
However, once this has happened, the process may run out of control, until the male trait becomes so exaggerated that it is disadvantageous. In other words, female preference, instead of survival advantage, may begin to drive the evolution of ever-longer tails, until males are encumbered by showy plumage that no longer helps them avoid predation.

evo101 > good genes hypothesis

Imagine another bird population in which females choose mates at random. Some males in the population have better genes for survival than others, but it is difficult to tell whether a male has good genes or not. In this scenario, long tails make it more difficult to survive�they are costly to produce and maintain. Because they are so costly, only males with good genes have the extra resources to produce them. In this situation, a long tail is an indicator of good genes. A gene for female choosiness (longer tail = sexier) will be favored, since�by choosing a long-tailed/good gene male�she will have sons with good genes. This trait will spread through the population until most females choose long-tailed mates and males that are able to produce long tails are favored.
If females choose males with “long and costly” tails, they are guaranteed to get good genes! If they choose males with “short and cheap” tails, they may get good or bad genes.

Wikipedia > Sexy sons hypothesis

The sexy son hypothesis in evolutionary biology and sexual selection—proposed by Ronald Fisher in 1930—states that a female's ideal mate choice among potential mates is one whose genes will produce male offspring with the best chance of reproductive success. This also implies that a potential mate's capacity as a parental caregiver or any other direct benefits the father can offer the mother, such as nuptial gifts or good territory, are irrelevant to his value as the potential father of the female's offspring. Fisher's principle means that the sex ratio (except in certain eusocial insects) is always 1:1 between males and females, yet what matters most are her "sexy sons"' future breeding successes, more likely if they have a promiscuous father, in creating large numbers of offspring carrying copies of her genes

Wikipedia > good genes hypothesis

"Good genes" theory proposes that females select males seen to have genetic advantages that increase offspring quality. Increased viability of offspring provides compensation for any lower reproductive success that results from their being "picky". The good-gene hypothesis for polyandry proposes that when females encounter better males than their previous mates, they re-mate in order to fertilize their eggs with the better male's sperm.

Clearly, the good genes theory is not the one you are interested in with the peacock tail example.
Wikipedia > Zahavi handicap prinicple

The handicap principle suggests that reliable signals must be costly to the signaler, costing the signaler something that could not be afforded by an individual with less of a particular trait.

Note that the term "genetic superiority" is never used in evolutionary biology. In fact the term sounds very social science related and make me think of the ugly side of eugenics. We usually talk about "fitness difference", "low fitness" and, "high fitness".


text:
Why does resting potential not become continually more negative?
(Firstly, I know this is similar to other questions, but I have read those answers and they do not really cover this topic).
My understanding of resting potential: action potential is not being transmitted; by way of action potentials via Na+ and K+ pumps, for every 2K+ pumped in, 3Na+ is pumped out of the cell. This process is termed "resting potential" and the transmembrane pd roughly = -65mV.
If more Na+ are pumped out than K+ in, why does the resting potential difference remain at -65, why does it not continue to decrease (until an action potential is triggered)?

The resting membrane potential is due to internal/external differences in ion concentrations and very importantly differences in permeability to those ions.
The fact that the sodium/potassium pump does not move an equal number of ions in each direction hardly matters at all for resting membrane potential; the resting membrane potential would be almost the same if that wasn't true. What is important is just the overall concentration of the two ion species, and the permeability of the membrane to different ions (almost all of this permeability is through specialized ion channels, because ions don't otherwise flow easily through a lipid bilayer).
You can calculate the resting potential/equilibrium potential using the Goldman equation - note that nothing in this equation involves the sodium/potassium pump moving different numbers of sodium and potassium ions.
The reason the membrane potential is negative is because the membrane at rest is most permeable to potassium, and because there is more potassium inside the cell than outside. Therefore, there will be a net flow of positive ions out of the cell, until enough ions have left that there is some negative charge inside the cell to counteract that net flow.

As you mentioned, the pump will keep generating an ionic gradient (and the membrane voltage should decrease)
Nonetheless there is still open ion channels at these negative potentials. Then the resting potential will be the voltage at which the net ion Flux (ion channels + leak + pump) is zero.
Since the pump is electrogenic (generates a current) the standard Goldman equation is not applicable and has to be modified.

Here $I_{pump}$ is the current generated by the pump. This equation can also be applied when other electrogenic pumps or transporter are present
You can see the derivation in this paper.

This answer is a bit misleading, the resting potential is almost entirely due to the differences in permeability, only a couple mV has anything to do with net flux through pumps.

@BryanKrause I expanded the answer a little bit  to show how the pump affects the membrane voltage


text:
How similar do proteins have to be to trigger the same immune response?
The title really says it all. How precise or vague is the immunity we get from vaccination or from having encountered a germ before?
Is it about protein parts that are recognised if they are identical? Full proteins? Which kinds of mutations break the recognition and which don't?

What is your level of understanding of immunology? Your question — which is really quite  broad — suggests that you may be better reading some introductory account of the topic. For example some of your terms are vague or strange. "trigger the same immune response doesn't really mean anything". If you are concerned with the utility of flu viruses, for example, against annual strains, then the phrasing would be something about antibodies recognizing the same protein. And what do you mean by "which kind of mutation?" @KarlKyer is correct, but does his answer clarify things for you.

I work in genome assembly, but I'm not a biologist. So my question is posed from a sequence point of view. A virus has a certain gene sequence, this sequence is expressed as a protein (i.e. a sequence of amino acids). Which part of this sequence is recognised by the antibodies and how precisely does it have to match, is basically my question. A mutation is just a change in the sequence. Karls answer takes me most of the way, I would say.

Fine. Just wanted to check what type of answer would be appropriate.

Immunoglobulins don't recognize entire proteins, but rather,specific shapes (called epitopes). These epitopes must also be present on the surface of the invading bacteria or virus for the immunoglobulin to have access. The epitope must be exactly the same. Any change in the amino acid sequence would change the shape. But an epitope is a relatively small part of the larger protein. If the shape is the same between different proteins, it would trigger an immune response.

Thank you for your answer. I just posted a follow up question about conformational epitopes: https://biology.stackexchange.com/questions/77952/what-is-the-length-and-number-of-the-subunits-of-a-conformational-epitope


text:
Why do hot water baths affect only males' fertility? Why not females'?
Here is the link where urologists are warning men not to take hot water baths.
Why does it affect only males' fertility? Why not females also?

@PeterMortensen By two tags, ignoring the question?

@PeterMortensen Posting xkcd links is fun but they should be actually relevant. A comic about memes popular in 2009 doesn't become relevant to a question about male fertility just because both involve pregnancy somehow.

For what it's worth, the article is making unsubstantiated scare claims that, as far as I know, have no basis in research. Temperature affects sperm production and viability but is not believed to have any adverse long-term effects on the body. There is (unfortunately limited in number of studies and sample size) research on contraceptive use, credited to Dr. Marthe Voegeli.

I dont know if baths last long enough to really reduce sperm count, but wearing synthetic underwear can elevate scrotum temperature enough to be used as a contraceptive. The effect is also reversible. Ahmed Shafik won the 2016 igNobel prize for reproduction for this research. Unfortunately, the study had a small sample size. Anyone care to reproduce (the study, not yourselves, obviously)?

@Ivana: Unless you like really, unpleasantly hot baths, I seriously doubt it's going to have any effect. It seems you need sustained temperatures above 37°C, which requires either really good insulation, ongoing heating or replacement of the water, or initial temperatures that would likely be scalding.

A mature human sperm has some mitochondria, a nucleus, an acrosome, and a flagellar apparatus. That's it. Because of the lack of other organelles in the sperm, they have to be kept in a kind of 'cold storage' so that they are viable for at least some time (usually a couple of days). The ideal temperature would be 1.8 °C to 2.5 °C below normal body temperature, i.e. 37.6 °C or 98 °F. If a man takes frequent hot water baths, his sperm count becomes low as the mature sperms get dessicated quickly.
The reason that women don't require this strict temperature regulation is that the mature ovum has the complete cellular machinery at its disposal- mitochondria, nucleus, golgi bodies, ER, the works. So it can remain viable for a much longer time (about seven days after ovulation) and has higher temperature tolerance than sperms.

can you add please some refferencis? Specially this "Because of the lack of other organelles in the sperm" made me quite suspicious.

@K Sai Harsha how do you know that this answer is scientifically correct let alone accept it?

I don't know about all other organelles but mature sperm certainly lack some of them, like endoplasmic reticulum. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2736672/ however it appears that has little do do with temprature sensativity, temprature appears ot be the regulator for sperm activity levels so they they can't remain dormant at highr tempratures. https://www.ncbi.nlm.nih.gov/pubmed/29963982

Well, the answer by @An J has already explained the prima facie of your question which is: sperms need lower temperature for development. But I will be explaining in my answer: Why do the sperms actually need a lower temperature for their development?
This is a debatable subject, but there have been several models or hypothesis about this. I found this literature on it, and it summarises the thing excellently. Hope it helps:

Throughout the Cenozoic, the fitness benefits of the scrotum in placental mammals presumably outweighed the fitness costs through damage, yet a definitive hypothesis for its evolution remains elusive. Here, I present an hypothesis (Endothermic Pulses Hypothesis) which argues that the evolution of the scrotum was driven by Cenozoic pulses in endothermy, that is, increases in normothermic body temperature...
The model argues that stabilizing selection maintained an optimum temperature for spermatogenesis and sperm storage throughout the Cenozoic at the lower plesiomorphic levels of body temperature that prevailed in ancestral mammals for at least 163 million years. Evolutionary stasis may have been driven by reduced rates of germ‐cell mutations at lower body temperatures...
The fitness advantages of an optimum temperature of spermatogenesis outweighed the potential costs of testes externalization and paved the way for the evolution of the scrotum. The scrotum evolved within several hundred thousand years of the K‐Pg extinction, probably associated initially with the evolution of cursoriality, and arguably facilitated mid‐ and late Cenozoic metabolic adaptations to factors such as climate, flight in bats and sociality in primates.

About the function of the scrotum from the article

The scrotum is a sac‐like thermoregulatory structure that houses the testes at a temperature lower than the core body temperature (Tb; Moore, 1926; Wislocki, 1933; Ruibal, 1957; Setchell, 1998). The cremasteric muscles in the scrotum contract and relax to draw the testes closer to or allow them to dangle further away from the body in order to maintain the testes at an ‘optimal’ temperature for spermatogenesis (sensu Moore, 1926; Tsperm) and sperm storage of 34–35 °C (Setchell, 1998; Gallup et al., 2009; Mawyer et al., 2012). In humans, the scrotal temperature is maintained about 2.7 °C lower than the Tb (Momen et al., 2010). Notwithstanding the relative fitness benefits of a cooled epididymis vs. the cooled testis, four nonmutually exclusive hypotheses currently dominate explanations for the evolution of the scrotum: the Cool Spermatogenesis Hypothesis (Moore, 1926), the Galloping Hypothesis (Frey, 1991), the Mutation Hypothesis (Short, 1997) and the Activation Hypothesis (Gallup et al., 2009).

Cool Spermatogenesis Hypothesis

...argued that Tsperm and the maintenance of sperm viability during storage in the epididymis is about 34–35 °C (Moore, 1926; Appell et al., 1977). Scrotal temperatures that approach those of the core Tbcompromise fertility (Moore, 1926; Bedford, 1978b, 2004; Setchell, 1998), particularly if evaporative cooling of the scrotum is impaired (Momen et al., 2010).

The Galloping Hypothesis

... (Frey, 1991)proposes a trade‐off between testes vulnerability (fitness cost) and the avoidance of strong intra‐abdominal pressure fluctuations during galloping which impair spermatogenesis in abdominal testes (fitness benefit).

The Mutation Hypothesis

... maintains that the testis is a ‘hot spot’ for germ‐cell mutations and that the lower temperatures of the scrotum reduce the rates of mutation on the Y chromosome through mutagenic metabolites (Short, 1997).

The Activation Hypothesis

... storage of sperm at a lowered temperature ensures that they undergo ‘thermal shock’ during ejaculation into the higher temperatures of the female, which increases their motility and hence the probability of a successful insemination (Gallup et al., 2009).

Finally somebody with refferences :D nice aswer :)

@user 33690 your answer lacks female's fertility

Hm, I thought that last hypothesis is closer to reality. That maybe after capacitation (which occurs in warmer environment) sperm have much shorter lifespan. Or that capacitation is limited in its time. So that it was lifespan-motility-scrotum tradeoff. But who knows.

@rus9384 yeah, I personally feel the same. But personal opinions are off topic in an answer so I considered adding all of them besides it's a hypothesis... nevertheless it's noteworthy that the male reproductive system has developed so much physiology to prevent early activation of the sperm, the last hypothesis is highly likely.

@KSaiHarsha I thought it was already there in An J's answer (& I have mentioned that)..what's the point in adding a second answer if I have to repeat the same content of the first answer

The thing is that activation is the case only for mammals (while birds do not have it). And scrotum as well. Also, wondering if difference between scrotum and body temperature is linked with sperm competition. This definitely would add points to the last hypothesis.

@KSaiHarsha Well... These four hypotheses are not applicable to women. Ova have quite a long lifespan; are not influenced much by the pressure; women do not have Y chromosome, so no mutations there; ova do not move really fast. I think this answer really explains the difference between male and female fertility under temperature influence.

To keep sperm viable in natural body conditions, they are kept at a relative lower temperature than the body temperature, and this can achieved by the scrotum. As sperm is produced in testis, and testis are situated in the scrotum outside the main part of the body, a pouch like structure. This arrangement is going to help to achieve a slightly lower temperature relative to the body temperature. Definitely, frequent hot water bath will lower the sperm count by hampering spermatogenesis as it disturbs the normal physiological conditions inside the testis by increasing temperature.
Another side, in females, the body temperature is not going to affect the oogenesis (ovum formation process). Instead of that you will see an increase in basal body temperature (about 0.5 °C) during ovulation (release of ovum). That means a hot water bath isn't an issue for female fertility.

Hi, its good aswer, but can you add some refferences to your claims?


text:
What does "novel, predicted deleterious, within autozygome" mean in genetics?
I am a medical student and just got involved with a genetic lab and research. I read a lot phrases like: "Although no mutations have been reported in this gene, we think this variant is interesting because the nature of the variant (novel, predicted deleterious, within autozygome).
Can anyone explain it to me?

Welcome to Biology.SE. Could you please give a direct quote and link to the original paper?

For a genetic variant:

novel - Not previously reported in the scientific literature.
predicted deleterious - There are reasons to suspect the variant could cause abnormal effects in a person.  This may be in part from where the variant is located (e.g. what gene), what problems were observed in persons having the variant, and many other considerations.  See the "Variant interpretation" section of this paper for more detail.
in autozygome - "Autozygous" refers to parts of the genome which are identical on both maternal and paternal chromosomes because of common ancestry of the two parents.  The autozygome is the collection of all such segments for a person, and is larger in cases of inbreeding, as when the parents are first cousins.  Autozygous segments are (usually) entirely homozygous, that is, all alleles are the same since they come from the common ancestor. (In normal segments, there will be a mix of matching and mismatching alleles.) The importance of homozygous alleles, of course, is that a recessive allele will be expressed in the person when both alleles are the same.  (Related papers: "Autozygosity mapping with exome sequence data", "Autozygome-guided exome sequencing in retinal dystrophy patients reveals pathogenetic mutations and novel candidate disease genes".)


text:
Larvae appearing after many rainy days
After a few days of raining, I found these larvae in a puddle. What animal are they from?

Is the puddle still there? I would like a better picture, your location, and additional information like size and behaviour if possible. There are so many insects out there!

Thank you very much @picapica. But I already know what those things are. They are the final stage of the mosquito larvae. Named "pupa". I will post it as an answer (just in case some one else has the same doubt).

They are the final stage of a mosquito larvae, called "pupa".

btw: You are allowed to mark your own answer as "accepted" by clicking the check-mark next to the up- and down buttons.