text:
What would it take to recognize a deer by its photo?
I am trying to recognize a deer by its antlers or any other means.
Elaborating:
I was hoping to use their antlers to recognize them but I have heard that most deers shed their antlers every year so it would be difficult to recognize it from the last year's photo unless these antlers retain the same pattern every year.
If not the antlers, what other characteristics should I be looking for?
Is there any software that can help me in recognizing a deer?

I'm not so sure about software... but it would help to know what particular trait you are examining, exactly. You can quantify fur color by spectrometry, for example.

i m not sure on what basis you want to identify a deer.. but you can use machine learning algorithms to find your deer (you have to train your classifier first)

I think the main question you have written does not quite fall within the scope of biology SE.  However, your final question, "What would it take to recognize a deer by its photo?" could be answered in biological terms.  Perhaps that might be the better title.

Changed the title, provided more explanation and even though I am a software engineer, my question is now completely biological. Please up vote me now. If zoology experts cannot not help me then who can?

It seems as though one of your only options is deer-adapted facial recognition software (as silly as it might sound) which is definitely not within the scope of biology.

One part of this question remains unanswered- does the shape of a deer's antlers act as some kind of identifier & are they consistent between years? I guess to answer this one would have to collect antlers from a group of individuals with knowledge of who owns each set, and examine how they vary within individual across years... But, if you had access to the antlers could a genetic identity test be a more reliable way to identify?

@rg255 - It is not a way of identify a living animal. Or you have to cut antlers directly from it. Someone would prefer to use their own eyes (see Dian Fossey) and a direct contact, though visual only. I'd prefer recognize my deer broder (or gorilla, or whatever) while he is living, than after the death. The problem is how to recognize deers, not to compare antiers among theirselves. In my opinion.

@violadaprile collecting dna as a form of ID can be done from living animals thus I am not advocating killing or physically interfering with a living animal. DNA can be collected from, amongst other things, faecal matter or antlers which have been shed. And I know the problem is how to recognize a deer, I raised the point of "do antlers vary between years within an individual?" and to answer this, and thus show whether deer can be identified reliably by antlers, would require comparing antlers produced within individuals. The choice of recognition method would depend on the observers needs.

@rg255 - yes, i'v seen you profile. You have right from your point of view. You are microbiologists and informatics, I am just a nature lover, my eyes are my point of contact with the world. Try to drawing two cats, they are never similar, But to me, I dont need to examine their blood to distinguish. And I prefer to leave them alone =)

There is a lot of variation in how and when deer shed their antlers. In most arctic and temperate-zone species, antler growth and shedding is annual, and is controlled by the length of daylight. In tropical species, antlers may be shed at any time of year, and in some species such as the sambar, antlers last several years. Some equatorial deer never shed their antlers.
The horns change every year and, especially, increase the number of branches (and consequently, change their shape). You can't recognize them by antlers, but by other features, such as color of the hair or the lineaments. Like us, animals have individual morphological differences that are recognizable and listable.
Biologists specializing in studies of particular animal species not only take photos, but also make drawings and write descriptions of behavior, to identify individuals within herds.
An optical examination, however, of the subject through drawings and photos (and if possible, direct observation), is more useful than a PC program. This involves identifying particular similarities and equalities that are not "identical". This is possible to do visually on a large (but limited) number of specimens. The human eye is the best computer.

I wouldn't say that automated computer image analysis should not be used to study animals. Its hard to believe that at some point it will be more common than direct observation.

it was just what i meant - you are biologists and microbiologists and informatics, i am only lover of nature and studied a lot about it. So we talk from 2 true different points of view

The Open Source Computer Vision library OpenCV is pretty popular. I'm a Python guy, but it also has C, C++, and Java interfaces. The O'Reilly book Programming Computer Vision with Python was pretty good, and their C-oriented Learning OpenCV from 2008 is coming out with a new C++ edition in July, supposedly. There are also the OpenCV online docs, linking to the reference manual, user guide, tutorial, and Java API for each release.

MATLAB also has a computer vision toolbox

Sure but... this implies that you can distinguish a deer by its photo, which is what we are trying to determine.

We have programs which use a tecnic knew as biometria. that presume an archive of thousands (millions?) of possible variants. I do not think that such an archive exists also for deer.


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Does antibody staining / immunolabeling block or inhibit protein function?
In dissociated live cells, does staining them with an antibody block the protein's function?
I am sorting cells based on their expression of a few marker genes, and culturing them post-sort for several days.
How can one assess if the protein is still functional?

That depends on a number of factors: The actual place where the antibody binds, the protein itself and also the number of available protein molecules. About which protein are you thinking?

Also, the assay for functionality completely depends on the protein you're testing. Assuming you have an in vitro assay for your protein's function, you could try performing the assay at a given protein concentration with varying concentration of antibody to see if there is a significant effect on activity in vitro. It might not correlate well in vivo, but it is a start.

Thanks for your input, @Chris. I do not have a specific protein in mind; rather I have a panel of proteins which I want to use to sort cells based on their expression, and I am worried that these antibodies will mess with the cell's behavior, as I will continue to observe them after selecting for them.

Thanks, @A.Kennard. That makes sense, although I don't have an in vitro assay for my proteins' functions. Do you know of any examples where people have verified the activity of proteins for which they added antibodies in vivo?

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How does oxygen help break down food?
I'm familiar with cellular respiration. Cellular respiration is the set intracellular chemical reactions that utilize oxygen. One example reaction is this:
C6H12O6 + 6O2 -> 6CO2  + 6H20 + heat

Another example reaction is this:
Food + oxygen -> carbon dioxide + water + energy

But there are many chemical reactions in cellular respiration. There are pathways that produce more energy like oxidative phosphorylation. There's glycolysis, the Krebs cycle, and oxidative phosphorylation, and each of these pathways has many chemical reactions.
Why is oxygen so helpful in breaking down food? Why is oxygen so helpful in chemical reactions?
With water, the answer is obvious. Water is a solvent. Water is polar. Water has a polar shape since the two hydrogen atoms are at one side of a tetrahedron and the oxygen's lone valence electrons are at the opposite side of a tetrahedron, which gives water polarity.
What properties of oxygen make oxygen so helpful in cellular respiration? I know that oxygen is an electron acceptor. Are there other properties that make oxygen helpful in cellular respiration?
Is oxidation one of the relevant properties that helps us make energy from food? Is it the oxidation of glucose inside the cytosol at a specific temperature?
When we look at the chemical reaction
C6H12O6 + 6O2 -> 6CO2  + 6H20 + heat

Is that an example of glucose oxidizing inside the cytosol at a warm temperature?
It makes sense that, since fruits and vegetables oxidize at room temperature, small molecules of glucose would oxidize very quickly at warm temperatures inside the cell.
Is oxidation the relevant property of oxygen that helps us get energy from food in cellular respiration?

This is a very basic chemical question and has already attracted three close votes. I suggest you read an elementary biochemical text — but not a biology text. In the past I would have recommended Berg et al. on NCBI Bookshelf, but that has been withdrawn. If you have $100 to spare, the 9th edition would be a sound investment in your education.

Good question. Why oxygen? Why not something else?
Fortunately the answer is well known and a rudimentary one in biochemistry. I offer a great paper on this by Babcock from 1999 in PNAS. I really recommend you read it all, it's relevant, within the scope of your question and well written in my view.
Excerpt with the answer:

Despite its biochemical versatility, however, >95% of the oxygen that
we consume is used in respiration. High-energy electrons derived from
food traverse the mitochondrial electron transport chain in a series
of exergonic redox reactions. These energetically downhill electron
transfers are used to develop the chemisosmotic proton gradient that
ultimately produces ATP. Oxygen is the final electron acceptor in this
respiratory cascade, and its reduction to water is used as a vehicle
by which to clear the mitochondrial chain of low-energy, spent
electrons.

The utilization of dioxygen by life is a very efficient strategy and the movement and control of pathways and mechanisms relating to oxygen is highly conserved and tightly controlled.

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Why do animals only eat some parts of their food?
For example monkeys/apes only eat part of a fruit and then throw the rest. Cats (big and small species) only eat some parts of their prey and then they abandon it.
Humans on the contrary leave as few leftover as possible.
What do we know about the parts that animals eat ? and how do we know it ?

Humans leave as few leftovers as possible? No, they definitely do not. They throw away a lot of good edible food.

Animals that abandon some food certainly have quite a lot of food at their disposal and they can be choosy and eat only the best. I'd be surprised that an animal that is starving would throw away some good food. If this is the case, it is probably a case where the animal is not adapted to its environment and do not recognize the good quality food as being good quality food.

It all depends on hunger. As in comment (@Remi.b), it has been mentioned, an animal won't throw if they are starving.

For example monkeys/apes only eat part of a fruit and then throw the rest.

Monkeys and apes can differentiate between good and bad part of the fruits. So, they eat what they can and if the color looks different (or however they differentiate them) they will throw the rest of them.

Cats (big and small species) only eat some parts of their prey and then they abandon it.

Cats in general are very picky eaters. They actually have a very short digestive tract, so, they need something easy to breakdown into energy rather than complex processes of digestion. Their main food consist of meat, they leave the inner organs as such.
Source:

http://en.wikibooks.org/wiki/Wikijunior:Big_Cats/Complete_Edition
http://bigcatrescue.org/feed-cats/

Image Source:

http://wordpress.as.edu.au/rspiers/2013/05/22/comparing-animals-digestive-systems/
http://cats56971.wordpress.com/2012/10/30/eating-habits-of-a-african-lion/

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What are the universal laws of Nature concerning animals' behaviour?
I'm looking for very old (centuries) treaty or recent (20 & 21th century) research that state what some of the laws of Nature are, particularly concerning wild animals' behaviour. Such as; every animal does this, no animal does that, etc.
Laws that could be then used to simulate or reproduce natural behaviours or check against unnatural ones.
Added: I'm looking for more simple laws, such as "no (wild) animal eats cooked food". Assuming it's true then humans broke that law of Nature. It's the relation to Nature that interests me. I used the word behaviour in the large sense, as in, what are the laws that animals seem to follow (dos  and don'ts) in the world. I suppose that by looking at what the human is the only one to do we can find lots of those laws.

the reference to the particular work you are referring to is more like a research project seems to me. Different times have different opinions on this and without even a century or millenium to tie it to, it does seem impossible. Origin of Species is not a bad example of such a work.

This question is just far too broad and rather vague in many aspects to be answerable here in this format.

It's really simple, but if nobody has gathered such knowledge before then of course it's going to be difficult to answer.

This seems to be rather impossible to answer! Very fundamental laws of nature are rather found in physics, mathematics or philosophy than in biology.
The theory of evolution is generally considered as a field that brings light to the whole science of biology. T. Dobzhanski famously said: "Nothing in Biology Makes Sense Except in the Light of Evolution" So I guess you might be interested to "laws" coming from that field.
I'm afraid you will some more knowledge in animal behavior than what you can acquire from this simple question before starting simulating. You can easily spend 5 years studying animal behavior and still having much things to learn from that field.
I would guess you might be interested in the concept of selfishness and altruism. I don't know your level of knowledge in biology. The following might seem a bit complicated (although it is a very brief and inaccurate summary of the real science that study these fields), if so, I would invite you learn about basic stuff in biology and evolutionary biology.
Selfishness and altruism
In order to have natural selection, you need:

variation
heritability (of the trait that present some variation)
different reproductive success (or success of copying itself) according to the trait which is heritable.

Following, this idea, an allele that behave altruistically (providing benefit (in terms of ability to copy itself) to someone else to its cost (always in the same terms)) will disappear  to the benefit of the selfish allele and therefore altruistic behavior should never be found in nature.
However, we find altruistic behavior (and that was one of the greatest flaw Darwin could think about his theory):

Because of relatedness (Hamilton's law)

An animal would always behave in order to increase its inclusive fitness (=direct fitness + indirect fitness)

Because of genetically correlated behavior
Because of upper level selection
Because behaving in a way will directly or indirectly influence the way others will behave with you

Now, that's a very big field. I can't develop everything in this answer! If you liked the discussion of selfishness and altruism, you might be interested to read the selfish gene or the extended phenotype.
If you want to go a bit deeper into mathematical formulation you might be interested in evolutionary game theory and hamilton's rule.
Here is a quick formulation of Hamilton's rule on this website

UPDATE (in reaction to your comment)
So, you're not looking for a scientific law/theory/evidence/etc... you're looking for a simple observation in the nature that fit all animals. Here are some examples:

There is no wheeled animals (see this).
There is no animal that migrate every year from Earth to Mars
All animals need a source of organic carbon
All animals possess some flagellates cells (I think)
All animals reproduce (not necessarily sexually)

If you want to talk only about behavior, then you might have some trouble to generalize things to all animals because, there are many non-motile animals, many animals that have no brain, many animals that does not even have organs, … As a side note: It is possible that if you accept that a sponge (which is at the base of the Animalia kingdom see this website if you want to learn about what is classified to be an animal) produce some kind of behavior, you will have to accept that an oak tree also have behavior
UPDATE.
Ah you meant animal in opposition to human?! Humans are included in my above list. If you look for differences then between human and all other animals, than you won't many other things than the brain and the behavior indeed. I hope nobody lost a whole life of work listing what human can do and what animals can't!

Human have a complete and articulate language (I don't fully remember what adjective we use to differentiate human to animal language)
Human are conscious that the are conscious that they are! It is quite hard to show that animals are not!
Humans are the only animals that drive a car!
etc…

You're using the word law in a weird way. You might to have a look to
http://en.wikipedia.org/wiki/Scientific_law and http://en.wikipedia.org/wiki/Scientific_law

That's a bit too theoretic. I'm looking for more simple laws, such as "no (wild) animal eats cooked food". Assuming it's true then humans broke that law of Nature. It's the relation to Nature that interests me. I used the word behaviour in the large sense, as in, what are the laws that animals seem to follow in the world.

@user2534 see the update in my answer.

Very funny. Well I guess that by looking at what the human is the only one to do we can find lots of laws. I hoped that someone had already listed them, though.

@user2534 see my updated answer.

You don't seem to grasp my idea and I don't know how to explain better. But thanks for attempting to answer. It's not about what animals can or can't do (couldn't be a law) especially not about absurd things like going to Mars, having wheels, driving cars. I meant Laws with capital L, as in established by God. Best examples I can think of are: animals may not eat cooked food, animals may eat their own kind (cannibalism), animals may not copulate with their close parents, animals may kill babies of their own kind.

I am afraid you can hardly explain the difference between some silly examples (the example with wheeled animals is actually very interesting and not silly at all!) and yours because there are no difference! Many humans have copulated with there close parents (look at a genealogy of european royalty). I think there are/were some tribute tat practice canibalism and there are many cases of human killing their own baby. I am even wondering if we couldn't find some animals that let their food some time under a big sun in order to cook it.

What do you call a Law with capital L? You can't use God's will to define anything in science.

@user2534 animals often copulate with their parents, they also eat cooked food if they come upon an animal killed by lighting. There are NO "laws" in animal behavior, none for animals and none for human animals either.

ha ha! Don't be impolite! You don't define the word "Law"! And your examples were very poorly found because   both human and animals can perform such behavior. Even if I don't quite understand what your "Law" means, I would tend to say that there are no "Law" that explains difference of behavior between animals and humans because there are no fundamental difference between humans and animals as humans are animals. Note: For further purposes I want to say that this website is for scientific discussion which means using scientific metho.


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Why is carotene in carrots?
Internet says that the carotene is an important pigment for photosynthesis and UV-protection. That explains its accumulation in leaves. I suppose colored fruits are more appealing to animals, so that explains the fruits. But why roots? Why is carrot full of carotene? The only reason I can think of is human cultivation. Is there any specific reason carrots synthesize so much carotene? Are there other similar examples of so vividly colored roots?

They're uncommon in mainstream grocery stores (but starting to appear more and more), but one can find carrots of all sorts of colors out there.

I have asked on Biology.se and it appears to be on topic there. I will therefore migrate it. It does, however, come with the advice that adding some references would be a good idea if there are any, and including what your attempts at answering the questions are. There would otherwise be a chance that it might gat closed as low effort.

I mean... it's called "carot-ene". Carotene... carrot... it just makes sense.

Carrot (Daucus carota) is a biannual plant that accumulates massive
  amounts of carotenoid pigments in the storage root.

The root of the carrot was not orange before domestication.

Although the root of carrot plants was white before domestication,
  intensive breeding generated the currently known carotenoid-rich
  varieties, including the widely popular orange carrots that accumulate
  very high levels of the pro-vitamin A carotenoids b-carotene and, to a
  lower extent, a-carotene.

As stated in the comments people did this to give a better taste to the roots. This is simply economical more beneficial because otherwise only the leaves of the carrot could be used for consumption (and not the roots which are a major part of the carrot), wasting this root would result in a lot of waste (and thus a lot of money waste) and because of an increase in carotene (and other compounds which contribute to the flavour) this would save money and provide more tastefull and appealing roots.

It is likely that wild carrot plants had uncolored roots of a bitter
  taste and a woody core but were initially cultivated because of their
  aromatic leaves and seeds.

So the only reason (as far as I can find) is that this is ineed because of cultivation by stimulating a flux in the direction of the carotenoid biosynthesis
I think this picture will explain it all:

 (source)

I'm not sure how familiar you are with biology so I described this not in that much detail about the genes and expression of them etc. If you would like to know this I would highly recommend to read these articles:

Biosynthesis of carotenoids in carrot: an underground story comes to light. (which I mainly used to write this)
New insights into domestication of carrot from root transcriptome analyses

I'd swear an onion sneaked into that picture...

hahahah it's a parijse carrot @xDaizu


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Dissection techniques for fruits and seeds
I'm doing some amateur botany, and I was keying some plants in the Brassicaceae (Cruciferae) family, which requires detailed information about the seeds of the plant. My question is, in a seed, how can one identify features such as:

Cotyledon(s)
Radicle
Endosperm (when present)
Accumbency/incumbency of the cotyledons with respect to the radicle (in dicots)

It also seems like the key parts of the seed will be within the seed coat; it's not always obvious how to remove this seed coat, or what methods exist. Are there resources for this sort of thing?
As a more concrete example, I've identified this Cardamine hirsuta from my backyard, but I'd like to verify some features of the seeds. Unfortunately, the seeds are very tiny, as this microscope photo of the silique shows, and the features are non-distinct.
Flora of North America provides these details for the Cardamine genus:

Seeds uniseriate, flattened, usually not winged, rarely margined or winged, oblong, ovoid, or globose; seed coat (smooth, minutely reticulate, colliculate, or rugose) mucilaginous or not when wetted; cotyledons accumbent, rarely incumbent

How can I figure out from dissection whether the cotyledons are accumbent  or not? At least, that's the sort of question I'd like to be able to answer.

I will answer my own question for anyone that's interested in doing something similar. First, a great reference for seed morphology is A. C. Martin's The Comparative Internal Morphology of Seeds (1954), available on JSTOR and from sci-hub.
To dissect a seed, you’ll probably want to have a good dissection microscope, two pairs of sharp tweezers, a razor blade, and a pin. Begin by opening the fruit to expose the seeds; for a silique, it’s very easy to peel the valves open. Be careful not to crush any seeds. Using the tweezers (and optionally the razor blade) separate a seed from the fruit by breaking or cutting the funiculus. Do this for at least a few seeds, more is better. The seed coats will protect the seeds from drying out, but be aware, once the seed coat is removed, the embryo will only last a minute or two before becoming completely dried out. You'll figure this out pretty quickly, if it's a problem, otherwise don't worry.

Seeds in the silique, all still in their seed coats.
Use the tweezers to position a seed so you can cut it with the razor blade. To get a good idea of how the embryo is arranged requires several dissections, cutting the seed in different ways (vertically, horizontally, parallel to the work surface); seeds are cheap so just experiment. Cut the seed open and you should have something that looks like the image below.

Seed of Cardamine hirsuta cut in half.
What you’re seeing is (a) the seed coat, and (b) the embryo. Use the tweezers and/or the pin to get the seed coat away from the embryo with as little movement as possible to preserve the formation.

Using a pin, separate the embryo from the seed case. Note that the distinct features of the embryo are becoming visible.

With the seed coat (pale green part) removed, the radicle and the cotyledons become visible and distinct. This seed is accumbent.

The two cotyledons are pressed together in this example, but you can still see a separating line between them when you hold the embryo at the proper angle.
When dissecting seeds, do yourself a favor and select the most mature fruit available. Your life will be much easier if you have a larger specimen. These stills were taken from a video I made, available on YouTube here.

Thanks for the excellent breakdown. IMHO seeds get ignored a lot in identification. This is fair at least where I live in California--the Jepson Manual revolves around reproductive organs. But I constantly encounter fruit & seeds and like to study them as well. What microscope did you use?
Edit: fixed typo

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What is the life of cell-free genetic circuits?
Can genetic circuits be tested in a cell-free environment? What would be their life if we keep them at room temperature?
The circuits which are composed of DNA-based components are commonly referred to as genetic circuits. By testing, I meant to say to test its behavior i.e. applying input signals (perhaps proteins) to see if it generates an output signal (another protein, may be fluorescent protein).
By life, I meant to say, for how long such a circuit (containing strings of dna) can survive at normal room temperature.

Welcome to Biology.SE! What do you mean by a "genetic circuit" and what kind of testing are you interested in doing? What do you mean by "life"? Are you sure these are biological questions? Please note that questions should be clear and demonstrate prior research. In addition, separate questions should be posted separately. ——— Please take the [tour] and then go through the [help] pages starting with [Ask] questions effectively on this site and [edit] your question accordingly. Thanks!

Quick search for "cell-free genetic circuit" gets this article as first result. They give time for which the transcription and translation reactions run. I wouldn't call the reactions life.

Thanks for your responses.
@tyersome: The circuits which are composed of DNA-based components are commonly referred to as genetic circuits. By testing, I meant to say to test its behavior i.e. applying input signals (perhaps proteins) to see if it generates an output signal (another protein, may be fluorescent protein).
By life, I meant to say, for how long such a circuit (containing strings of dna) can survive at normal room temperature.

@BagiM: Thanks for reaching out. I am not calling the reactions a "life". As I said in previous comment, I meant to say for how long such a system can be usable.

@HasanBaig Comments are meant for suggesting clarifications and such; it's better to edit your question in response rather than replying as a comment. Questions and answers are meant to be long-lived, comments are not.

Also it's up to you to write clearly, not to expect others to interpret your writing to discover your intent.

I just edited the question.

And I thought people are already aware of genetic circuits. This is the reason why I did not explain it in details. Next time I will try to explain in more details.

The word "survive" does not really clarify the previous word "life". The reaction mix is not living at any point in time. Are you asking at what time does the production of fluorescent protein stop? Are you asking how long it takes for reactants (ATP) to be consumed? Are you asking how long it takes for the individual components of reaction to degrade (eg. RNA-polymerases to loose function)? For the first two questions, If you have read the article I linked in my previous coment you could have find the answer yourself.


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Why do women have less synapses / neurons / brain mass than men despite having the same average IQ?
I don't mean to cause offence or suggest than men and women shouldn't be of the same intelligence — that's not something I'm here to dispute. What I want to understand is how this is possible given the vastly lower average synaptic / neurone count and weight in the average female vs male brain, in terms of both the overall brain and the neocortex.
Are there some systems that the female brain employs to compensate for a lower number of neurons, and if so is it dependent to the hormone estrogen or is it something inherent to the female brain? Is it just the case that the male brain has vast redundancies, if so why does brain weight correlate with IQ if it is redundant? Or perhaps it's the discrepancies in synapse count do not extend to areas that are most closely linked with higher order thinking. This is the explanation that I am leaning to, and if someone could explain which areas these are and link to a study that shows that the male vs female average in these areas are the same, then that would be greatly appreciated (I'm not looking for areas that are the same size adjusted for total body weight, I'm looking for areas with the absolute same number of synapses/neurones).
Studies:
Female brains on average lighter than male brains: https://pubmed.ncbi.nlm.nih.gov/8072950/
Female brains on average have lower neocortical neurone count than male brains:
https://pubmed.ncbi.nlm.nih.gov/9215725/#:~:text=The%20average%20numbers%20of%20neocortical,brains%2C%20a%2016%25%20difference.&text=Sex%20and%20age%20were%20the,no%20influence%20on%20neuron%20number.
Female brains have on average a lower cortical synaptic density: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2567215/
Context:
I am transgender (and taking estrogen) and have read that taking estrogen can move brain volume and weight closer to average "female proportions" to quote the study, and that this does not appear to negatively affect cognition. So, this is a question that is hugely important to me and does not come from a place of mal-intent.

Note the last study has a sample size of 8 meaning it is completely worthless. honestly trying to establish something for humanity as a whole with sample size of 8 makes the study a waste of paper.

In brief, so far as we can tell size matters far less than brain architecture.
Consider that humans have only about half as many cortical neurons as a number of whales, yet are clearly far more intelligent.
While we are still far from a complete understanding of the details of how intelligence actually works, neuron count is only part of the story.
For humans in particular, there is also a selection argument that would lead us to expect that relatively small differences in neuron count (e.g., between male and female average) are not particularly significant. General intelligence (not "IQ") appears to be a critical aspect of human selection, and thus under significant evolutionary pressure for both sexes. If a small adjustment in neuron count made a significant different in intelligence, cranial and cortical scale is a relatively simple morphogenetic adjustment, and we would expect both sexes to scale until they hit a more similar scaling boundary. Since that has not happened, it is reasonable to conclude that neuron count is at least not a major factor in intelligence.

If the correlation between general intelligence and brain size is so small that males and females have the same average general intelligence despite differing brain sizes, then why is the correlation large enough to even be observed? Surely if global brain size correlates even slightly with general intelligence that we would see a very small difference between the sexes?

So far as I have been able to find, it's not clear if there is any actual relationship. There are too many other factors that could be causing the correlation. For example, brain size also appears linked with nutrition, which is linked with wealth, which is definitely linked with decreased disease burden, increased educational opportunity, etc. If there's any effect, it's small, which combined with the scientific click-bait factor makes it a very messy subject to try to study.


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Can combining C3, C4 and CAM plants in a greenhouse/vertical farm increase the efficiency of plant production?
I am reading a little about different types of photosynthetic systems in plants because I want to learn something about plant production in greenhouses/vertical farms (I have no experience in this field).
Can combining C3, C4 and CAM plants in a certain way have positive effects on its production value? So for example C3 and CAM plants are planted in the same area close to each other and they have in some way a positive effect on each other because they use different methods for assimilating energy and thus one can bring down the energy use in the greenhouse/vertical farm.
This is an interesting article.
https://www.khanacademy.org/science/biology/photosynthesis-in-plants/photorespiration--c3-c4-cam-plants/a/c3-c4-and-cam-plants-agriculture
It explains the different aspects of the different plants very well. Maybe the best answer to my question is a simple: NO, because all 3 types of plants grow naturally in different environments, but I can imagine a system were energy that is gained from their photosynthesis at different times of the day can be shared among the plants and thus an increased energy efficiency can be reached. Maybe someone can


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What is this bird called?
I've found this bird.
Does anyone know what is it?

Since Asia is pretty big: Where in Asia is this taken?

You should ask him, I don't know him personally but he looks like a good bloke, he does remind of a Geoffrey though

It is White breasted Kingfisher also called White throated Kingfisher. Halcyon smyrnensis.

Why this is Halcyon smyrnensis?

Halcyon kingfishers are mostly large kingfishers with heavy bills.

According to wikipedia this genus has 11 species, some workers also include genera Pelargopsis, Syma and Todirhamphus.

Out of all the 11 species only two are comparable to H. smyrnensis; Halcyon badia and Halcyon coromanda.

Halcyon badia is an African resident.

Additional information:

They are “sit and wait” predators of small ground animals including large insects, rodents, snakes, and frogs, but some will also take fish.

The genus Halcyon in the current sense consists mainly of species resident in sub-Saharan Africa, with a couple of representatives in southern Asia, one of which, the white-throated kingfisher, occasionally reaches Europe. White-throated and Ruddy kingfishers (Halcyon coromanda) are at least partially migratory.

it looks much more nice but has a lot in common

Added more information to establish as why it is your bird and the similarities are not due to chance. Check google for images from different angles. @griffonvulture


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Why is the size of the human penis not in proportion to that of the rest of the body?
According to this research
https://qph.fs.quoracdn.net/main-qimg-2ffcc3b19663af67c96ac1be8f3d6351-c
it is more likely for tall men to have large penis
but there are still many tall not having large
It is clearly not matching the size of other organs such as arms, legs, hearts, etc.
If you see a tall man you can see he has long arms, long thighs, bigger heart, etc.
similarly for short men, they have short arms , legs ,etc.
why it is not the same for penis?
why tall men may have short penis or short men may have long ones?
why the length of the penis does not match with make height similar to other organs?

Welcome to Biology.SE! It is expected that you will demonstrate that you have done research on your own before asking questions here — at a minimum please supply a credible source showing that human penises deviate more from their expected proportions than other parts of the human body. ——— Please also take the time to check out the [tour] and then the help pages starting with [Ask] questions on this site. Thanks!

Asymmetric is the wrong word. That would mean that one half (along the length) does not appear to be the mirror image of the other. "Male" would appear to be redundant also. You should edit your question say something like "Why is the size of the human penis not in proportion to that of the rest of the body?" (Remember the question mark.)

Why are some people more intelligent than others? Why are some people taller than others? Perhaps all theses have the same or similar answer...

@SolarMike it is definately not the same. the intelligence is not a physical thing, it is not an organ. taller people have tall arms, tall legs etc. there is a percentage of proportion that goes with these organs ( like your heart size is matching your fest size) to a certain degree is accurate. but for penis there is no theory that works, foot size is false, and penis size vary for the same tall people ( so my question again why penis size vary (biologically what causing this difference in size, why it is not same as other organs matching a percentage of the human tall))

According to genetics all phenotypical characters are inherited from both biological parents. The Y chromosome is mainly responsible for appearance of male characters and the only source of getting Y chromosome is from biological father. However other traits i.e. of height  can be inherited from either biological father or mother. Therefore if the height of mother was taller and is dominant over father's height then the child will be having the mother's height. The Y chromosome related characters would remain same and you would not observe any change in male character.  Therefore, you can not relate all physical characters with Y-chromosomal characters.

but you don't see a tall man (coz the father was tall) with short arms (coz mother was short and has short arms) all organs for tall men are tall and big that matches that tall. except for penis it is vary for the same tall people

Welcome to Biology.SE! Your answer over simplifies the genetics of both penis size and height (for evidence start here:https://en.wikipedia.org/wiki/Human_penis_size). Inclusion of references is also highly desirable. ——— Please take the [tour] and then consult the help pages on the standards for [answer] effectively. Thanks!


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Image analysis of GFP-tagged protein localization bursts
I'm reading an article (full text here) that analyze the dynamics of localization of a GFP-tagged transcription factor (Crz1) over the time at the single-cell level, by taking movies in a fluorescent microscope.
In Methods section they say:

Fluorescence cell images were segmented using a Hough transformation algorithm in Matlab, provided by Sharad Ramanathan. Localization score was determined by the difference between the mean intensity of the 5 brightest pixels in the cell and mean intensity of the rest of the pixels in the cell.

The segmentation process here seems to be the identification of cells over the background. They then calculate a localization score, for each frame of the video, for every cell. Now there's the part that I can't understand:

Bursts were identified by thresholding traces at >1 standard deviations above background noise, estimated from the lowest 20% of values.

I searched some definitions of "background noise", but I can't figure out what does it mean in this particular context. Moreover, "lowest 20% of values" of what?
Is it plausible that they define it for the lowest 20% of values of localization scores over the time, at the cell each time considered?
Maybe can be useful a screenshot of a single cell in a photogram of the video:

Yep, the Hough Transform is a way to pick out shapes you're interested in, in this case they probably have it set to find circles, and they use that to segment the image.
I think that you have interpreted their methods correctly.  For each cell they make a trace of localization score vs. time, localization score defined in arbitrary units as the difference between the mean of the five brightest pixels and the mean of the remaining pixels in the cell.  I think the lowest 20% refers to the frames in the video that have the lowest 20% of localization scores.  They take the lowest 20% of localization scores, calculate a standard deviation, and then for any frame that has a localization score that is more than 1 standard deviation above the mean of those 20%, you say that frame exhibits a burst of localization.  If I'm understanding this correctly, this process would be repeated on every individual cell.
My interpretation is that the 20% doesn't have anything to do with the signal intensity from the background pixels, and it comes from analyzing the series over time, not a single image.

I don't know a whole lot about signal processing but I am a little familiar with artificial intelligence. Perhaps this wiki would be helpful http://en.wikipedia.org/wiki/Image_segmentation. I am familiar with k-means clustering discussed there and as a trivial segmentation method it would indeed identify the cell versus the background of the photo. The Hough transformation would be more sophisticated and probably more useful for this application but if you want to get a sense of the process the naive k-means algorithm may be helpful.
I interpret the "lowest 20% of values" to refer to the localization score values, the lowest being those who are darkest in your image. That is, the background the cell is imaged on. The background noise refers to the fact that a signal processing algorithm without any preprocessing may try to identify patterns from the background of the image rather than the cell subject matter, which is the part the researchers are after. This is why they perform the segmenting.
For instance, imagine a k-nearest neighbors algorithm http://en.wikipedia.org/wiki/K-nearest_neighbors_algorithm for computing a "localization score" for image brightness. Your paper is interested in the intensity of GFP for a cell. In the image, pixels on the border of the cell with its background will have artificially low score values because of the background: the adjacent pixels that are in the background and not part of the cell are dark, but that doesn't mean anything related to the biology of the problem. This is the noise.
The lowest 20% of values, then, should refer to a single image, not to a series over time.


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Meat and mushroom allergies, why are they so rare?
There are a lot of food allergies, but for some reason not to meat (mammalian meat or poultry) or mushrooms. I've googled a bit, and now I know that one can actually have a meat or mushroom allergy, although the odds of that are very-very small. Why is it so?
Is it because both meat and mushrooms are usually cooked and that kills potential allergens? What about undercooked or raw food like portobellos or carpaccio and steaks?
Or is it because animal tissues are so similar to ours and so are better digested? What about mushrooms then?
Is it something else?
Also, are there any data of what types of meat and mushrooms are most allergic?

Do you mean few mammal meat allergies? There are many fish and invertebrate (e.g., shellfish) allergies.

Yes, excluding seafood. I'll fix the wording.

I suspect that the reason mammalian meat allergies are so rare is that they cause extreme morbidity or mortality in kids. Essentially, most components of mammalian meat are going to be very similar or identical to self-antigens and therefore, your immune system will destroy your own body from the inside out.

Chinmay Kanchi, yes, that's plausible to me. But do you know anything to support this hypothesis?

What @ChinmayKanchi says makes sense, an allergic reaction is a response to unknown antigens, those antigens in meat are more likely to be our own - being allergic to these antigens would be like walking around with a giant self-destruct button on your forehead and hoping someone doesn't push it...

@ftt Nope. That's why it was a comment and not an answer ;)

Whilst it is true that animal cells are more like our own, I'm not sure that would be the reason for non-allergic responses. If we take xenografts (transplanting pig organs for example) we see a profound response.
The latter theory of it having a higher mortality is more closer to the truth. Typically we observe that things we are given from childhood causes induction of tolerance (T reg cells). However this occurs best at a young age and if given orally. Peanut allergies for example are incredibly infrequent in Japan for example. Meat is given typically from a young age.
However what about the vegetarian converts or exposure to new foods as you grow older. Well the theory suggested for this are some antigens act to signal the immune system. These proteins are similar to the cell signals our body uses to tell the body there's a fight on, we are being invaded by something dangerous. This causes an immune system reaction to build up, specfically IgE antibodies. Thus on subsequent exposure, the response is stronger due to a preformed response.
Although these are they hypotheses, they're being actively investigated because frankly they can't be that simple. And of course there is conflicting evidence.
Interestingly, I've met a person with mushroom allergy. It does occur. Maybe polymorphisms (slight genetic differences) means someone responds to antigens others don't?

I know two or three people with fungus allergies. In at least one of these people, mushrooms can trigger the allergic reaction.

@AndroidPenguin, you say these hypotheses are being investigated, can you point to any papers? Thank you!

See "the hygiene hypothesis"

Please add some references


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Is nuclear DNA immuno-privileged?
It is well known that if DNA occurs in the cytoplasm of eukaryotic cells, an immune response may be triggered through a myriad of DNA receptors and pathways as part of the immuno response. Yet, apparently the nuclear DNA does not induce any type of such response. Is it known why this happens? Is it just due to the fact that the nuclear DNA is immuno-privileged?

comment on the edit: exogenous DNA its not restricted to viral origin alone, it can occur by prokaryotic invasion as well, for example.

Was just trying to improve wording - please feel free to roll back. You mentioned the viral stuff in your original question.

Also - isn't it so that eukaryotic DNA released from cells is immunogenic in its original host? I.e., is your question valid?

I dont get the point. "eukaryotic DNA that comes from the nucleus is immunogenic", is it? lets assume it is, why would that make my question ilegitimable?, genomic fragmented DNA pieces will be retained in the cytopalsm after nuclear envelope breakdown in mitosis, so thus the nucleus would be cleaned and we are thereby talking again about cytoplasmc DNA response, which I already introduced in the question. I really dont see your point. Do you maybe refer that this putative immuno response happens already in the nucleus even before nuclear env. breakdown? I think thats a key point if so

do viral DNA INSIDE the nucleus induce any response? if so, why not genomic DNA?

You introduced "cytoplasmic DNA response" in your question. Would the following  somehow reformulate your question:  "How does the cell know whether DNA/RNA in the cytoplasm must be translated for binding and immunogenic presentation by MHCl or, alternatively, be bound by Pattern Recognition Receptors (PRR, see answer given) to trigger some inflammatory pathway?"?

Pattern recognition receptors (PRRs) can potentially discriminate between endogenous and exogenous DNA:

Microbial nucleic acids can be discriminated from self nucleic acids using various parameters, such as their sequence, their tertiary structure, their molecular modifications and their localization. In addition, mislocalized DNA and RNA can be an indicator of cellular damage and infection. [1]

and

Microbial nucleic acids are discriminated from self nucleic acids based on different parameters, such as their sequence, structure, molecular modifications and localization. On the other hand, mislocalized self nucleic acids — such as extranuclear DNA or extracellular RNA — can be recognized as DAMPs, probably because they are reliable indicators of cellular damage. [2]

Somewhat suspect is the similarity of those quotes; I only link to both reviews so as to include both in the references for further reading.
Distinguishing by sequence and structure are self-explanatory. Molecular modifications could include unmethylated CpG sites which are more common in bacterial and viral genomes and are recognized by TLR9. [3] Mislocalized DNA means any that is found outside the nucleus, which is a sign of damage or infection. Most of the well-studied nucleic-acid-recognizing PRRs are found outside the nucleus: TLRs are constrained to endosomes and the extracellular environment while RLRs are found in the cytoplasm. The as of yet identified DNA sensors like DAI also seem to localize to the cytoplasm. Extranuclear PRRs do not necessarily need to discriminate between endogenous and exogenous DNA: any that they sense is mislocalized. However, at least one dsDNA-recognizing PRR, IFI16, localizes to the nucleus as well as the cytoplasm, where it can recognize viral dsDNA. [4]

It has been assumed that cells distinguish viral from cellular DNA due to the former's presence in the cytosol. However, … Kerur et al. (2011) propose that the DNA genome of Kaposi's sarcoma-associated herpesvirus (KSHV) is recognized inside the nucleus by the DNA sensor IFI16, leading [to] inflammasome activation. [5]

IFI16 apparently distinguishes exogenous from endogenous DNA by its length. [6]

Endogenous DNA is present in vivo as chromatin and the amount of exposed linker DNA between histones is too short to promote the cooperative binding and oligomerization that IFI16 requires for signalling (B). An older model, where IFI16 binds independently, is also shown (A), but it suggests that IFI16 should bind self-DNA and doesn't fit with experimental results.
That is just one specific example of how a PRR can distinguish self from non-self. DNA sensors actually seem to be on the cutting edge of research into the innate immune system and, as such, the complete picture has yet to be determined.

References:

Broz P, Monack DM. 2013. Newly described pattern recognition receptors team up against intracellular pathogens. Nat Rev Immunol 13(8):551-565.
Desmet CJ, Ishii KJ. 2012. Nucleic acid sensing at the interface between innate and adaptive immunity in vaccination. Nat Rev Immunol 12(7):479-491.
Yoneyama M, Fujita T. 2010. Recognition of viral nucleic acids in innate immunity. Rev Med Virol 20(1):4-22.
Kerur N, Veettil MV, Sharma-Walia N, Bottero V, Sadagopan S, Otageri P, Chandran B. 2011. IFI16 Acts as a Nuclear Pathogen Sensor to Induce the Inflammasome in Response to Kaposi Sarcoma-Associated Herpesvirus Infection. Cell Host Microbe 9(5):363-375.
Unterholzner L, Bowie AG. 2011. Innate DNA Sensing Moves to the Nucleus (comment on Kerur et al., 2011). Cell Host Microbe 9(5):351-353.
Morrone SR, Wang T, Constantoulakis LM, Hooy RM, Delannoy MJ, Sohn J. 2014. Cooperative assembly of IFI16 filaments on dsDNA provides insights into host defense strategy. PNAS 111(1):62-67.

+1 But what about eukaryotic microbes? They have nucleosome wrapped DNA

@WYSIWYG Thanks. That's a good point, but IFI16 is just one example that I happened to find; there are apparently other ways to distinguish between self and non-self DNA. Also, while DNA viruses and retroviruses necessarily spend part of their life cycle in the nucleus, I don't know that cellular microbes do. Are they just constrained to endosomes?

@canadianer badass answer

@Katz I thought so too…


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Real time PCR parameter CT
When puting a real time PCR, parameter CT, which means threshold cycle, is used. What does it mean really? according to wikipedia "The number of cycles at which the fluorescence exceeds the threshold is called the threshold cycle (Ct)"
could anyone put it in conext?

Realtime PCR uses a fluorescent dye which binds to double-stranded DNA and thus allows to measure the growing amount of DNA by each cycle. The DNA added to the reaction also binds the fluorescent dye and makes some part of the fluorescent background. When the PCR reaction starts, it takes a while until enough DNA is synthesized to go over the background and to be able to reliable distinguish the signal from the noise. I think this becomes clearer, when you look at the image below (from the NIH):

The Ct is the point where the signal can be distinguished from the background when it enters the exponential grwoth phase. The no template control stays below this threshold.

and when you make the calibration curve does it really matter which range of dilutions you choose or does it have to be a logarithmic serie? besides, when you get your results for different CTs, which is the criteria when choosing the correct dilution?

If you know the concentration of your standard exactly, you could do only one reaction. However it is better to do at least a few dilutions to see if your dilutions are correct and to test if your standard is amplified linear (meaning 10x more standard gives an accordingly higher signal). I would always choose a dilution which is as close as possible to your gene of interest. I mostly avoided absolute quantifications if possible, since relative quantifications usually where sufficient for us.

what do you mean with " I would always choose a dilution which is as close as possible to your gene of interest."?

That I use the curve (when I make more than one) which is nearest to my sample of interest. This way you avoid to skew you calculation by non-linear amplifications.

and when i use the most diluted concentrations i often get fold changes really diverse when comparing to the more concentrated. Is there any criteria i could follow to discard those results?


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Cancer history on environment-cancer relationship
I am interested to know how environment-cancer relationship knowledge has developed.
I know that all began when Muller first proved that mutation could be induced via ionizing radiation, X rays in the case, and hypothesized for the first time the role that this could have on carcinogenesis. Do you know further data and the main or most significant events that leaded from that point until the current state of the art? (like when smoking and cancer were proved related)
(all factors enhancing risk would be included in the query, as human behavioral aspects (such as diet), work environment...)

Actually, "soot wart" was identified by Percival Pott in 1775. It is the first reported occupational cancer (it is a squamous cell carcinoma of the skin of the scrotum). It was shown in 1922 that an active ingredient of coal soot was a carcinogen. I'm not sure of an expansive, technical text on environmental cancers, but you may want to check out
"The Emperor of All Maladies: A Biography of Cancer" which covers the origins of man's understanding of cancer starting with the ancient Greeks, progressing to mention Percival Pott, and then moving on to modern day science and medicine. This book won the Pulitzer in nonfiction a few years ago and is well worth your time.


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What kind of larva is this?
It has a body which is divided into three parts:

The head, which is small, with a black, needle-like structure on the tip which I think is the mouth.
The upper body, which has a pure white color that is softer than the lower body.
The lower body, which is hard, has some blacks spots on the rear end with a yellow spot on the very tip and, compared to the upper part, has a clouded clear white color.

It moves very strongly when touched, but not that much.
My classmate found this when he opened a leaf from a small plant, thinking that it was a butterfly pupa because it was covered with a silk like cover but very thin to be compared to a butterfly cocoon.
Larva pictured here:

What about adding location?

That's going to be a moth. You can identify the wings forming, and which end will be the abdomen. You're upside down; the little black needle part is the eliminating end of the moth pupa. The head is at the end with multiple dots. When it is far enough along, you'll be able to make out everything: eyes, antennae, etc. They often encase themselves in silk (think silk moths caterpillars).

Location, and the plant it was found on may help.

+1 for the efforts in description. I agree with @anongoodnurse that you got the orientation wrong, though. What you see on the photo is the ventral face, with the head to the right. You can also guess the legs forming on the right part.


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What is happening to this tree?
I was walking down to my mailbox when I saw this tree:

And by the looks of the branches, the tree seems to be dying because it has no leaves.  What is happening to the tree?

They may be lichens or some other fungi.

The tree is dying.  From what you say, it has no leaves wduring a time it should, it has saprophitic growth along the trunk; it looks like there's a crack in the bark on the right, and there are shoots coming up from the base of the trunk, the last hurrah from the tree to try to regenerate.
Trees send up suckers as a reaction to stress (like slowly dying). If you cut the trunk in such a way as to discourage rot, it will likely be replaced by this shrubby growth if the roots are sound. Some loggers use this as a way to quick-start new lumber trees.


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What is this Californian shrub?
I spotted this shrub-like plant in California, USA.

found it in Los Angeles

@Charles A randomly chosen plant from So. Cal. could be from anywhere given the climate and horticultural practices, so I don't think I'd limit the search to natives.

It may be useful to add a clearer picture of the flowers.

unfortunately i don.t have another picture of it..

Almost definitely not a CA native.
It looks like a coleus to me -- cultivars are pretty diverse but typically have variegated leaves with some amount of purple coloration.
https://en.wikipedia.org/wiki/Plectranthus_scutellarioides

Flowers look very different though...

Not a Coleus. They have square stems and opposing leaves.

It is Bouganvillia. If you have pets you don't want one even if your neighbors have pets. When the flowers drop they get all over the place and if they get into any food or water source for pets they will slowly die from the Poisonous oils that seep out of the flower. Other than that they are a very easy vine to grow and easy to train.

Flowers don't resemble bougainvilla. And leaves don't either as matter of fact.

I know bougainvilla and that wasn.t it.


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What kind of spider is this from Nova Scotia, Canada?

What kind of spider is this? It was found in Nova Scotia, Canada and is about the size of a quarter.


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DNA Longevity in Keratin, Ivory and other Bioplastics
For how long is DNA viable for extraction and/or sequencing in bioplastics created by the human body? I checked out a few links online, and this article gives a record of about 7000 years for frozen mitochondrial DNA, and Ötzi's DNA remined viable for 5000 years. However, I suspect that the samples used to analyze both were not taken from anything that was like keratin or ivory, with their limited cellular matrix. What is the longest record of sequence-viable DNA being stored that way?


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Saltwater fish identification
Can someone please identify this fish. Someone had asked me to rehome this fish but they were unsure what type of fish it is. Right now I have it in a quarantine tank until I find out what type of fish it is. I know it is some sort of clown but I cannot find the specific type after that. The fish is the one in the foreground of the image being black and white. It is a saltwater fish.


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What is the point of storing biological samples in Trizol/TriSURE before RNA extraction?
The Wikipedia article on Trizol says that it helps break the cells and maintain RNA integrity during homogenisation of samples. Does anybody know by how much Trizol improves RNA integrity compared to homogenisation without it? If somebody is extracting RNA from tissues without first storing them in Trizol, can you please tell me about the quality of your RNA?

These reagents denature RNases to protect RNA from degradation.


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Isolated mitochondria in glucose rich solution, what happens to ATP generation?
I'm taking intro to biology course this year, and I was thinking about this question.

Isolated mitochondria were placed in a glucose rich solution. (With ADP and Pi). How would this affect the ATP creation in the solution ?

My very simplified understanding of the process is as follows:

Glycolysis takes place in the cytosol, and converts glucose into pyruvate.
Pyruvate enters the mitochondrion and is oxidized to acetyl CoA
Acetyl CoA enters the citric acid cycle which creates NADH and FADH2
In the electron transport chain, NADH and FADH2 electrons pass through the mitochondria membrane, this flow results in active proton transport out of the matrix, creating a gradient. And the result is diffusion of protons which is coupled with synthesis of ATP.

I was unsure what would happen when isolated mitochondria and placed in a glucose rich solution.
Reasonable options are:

My book states that ATP synthesis is reversible and ATP synthase can also act as an ATPase, hydrolyzing ATP to ADP and Pi if there is too much ATP.
There is no cytosol (due to the mitochondria being isolated), There is actually no glycolysis happening, meaning no citric acid cycle, and no electron transport chain, meaning no ATP.
There is not enough ATP to start the process: break glucose into fructose and pyruvates?
Or just nothing happens and ATP is generated regularly ?

As is usual with this kind of posting, we are being asked not about a problem or principal of biology but about a contrived examination question with ambiguous wording, the expected answer to which depends on the specific level of teaching in a given syllabus. While sympathizing with the poor student, I regard this as akin to mind reading. “How would this affect ATP creation?” Creation?  Phosphorylation of ADP? biosynthesis? Abiogenesis? “Affect” it? Was it happening already? Really, if the educator wants to test whether a student knows where glycolysis occurs he should ask it straight.

While I do agree that the wording is ambiguous, I did state that my teaching level was intro to biology course. I appreciate the sympathy, and would be happy with any biological explanation that is related to my question (simplified as it might be). I think the the question indeed meant Phosphorylation of ADP.

Well for an introductory biology course (unless it's at MIT) I would imagine the answer is what you have deduced yourself in 2. As glycolysis only occurs in the cytoplasm, adding glucose to isolated mitochondria is like spitting into the wind. Phosphorylation of ADP cannot occur because there is no enzyme system in the mitochondrion that can convert glucose into a substrate that can feed into the TCA cycle.


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Is the stuffy environment due to using masks all day, helping in spread corona virus in people?
I came across a research that stated, the most disease ridden place in a toilet is actually the air dryer. The hot and moist microcosm that develops around the dryer due to frequent use helps in breading germs.
If I were to consider the research accurate and implement the same logic on masks. The stuffy environment created around the mouth and nose due to a sweaty day wearing masks has the same, if not way better chances of breeding or maintaining germs, doesn't it?
Doesn't the constant moisture from our breath, trapped within the confines of a mask, make for a denser moist environment for microbes? Similar to those found around air dryers?

The question is not "dumb". I have chosen to reply to the precise question not to the more broad question in the title which is much more complex.

You are right, I should reword the question to be nore precise

This sort of question would be better on SE Medical Sciences if anywhere, as it does not involve any specific virus biology.

Are you talking about microbes or about viruses, e.g. COVID? Viruses are not microbes. (They do not have significant physiology independent from their hosts.)

Viruses "breed" (replicate) within infected cells, not within masks. Other kinds of microbes such as bacteria could breed within masks provided they find substances they can feed on in this environment.
https://en.wikipedia.org/wiki/Viral_replication
Sars-Cov-2 has been shown to survive for extended periods of time (hours) on various types of surfaces. There is no reason why masks would be different. The following study found that Sars-Cov-2 remains viable up to 72 hours on plastic. Surgical masks are typically made of polypropylene or other polymers.
https://www.nejm.org/doi/full/10.1056/nejmc2004973
However, a more recent study found that Sars-Cov-2 is unlikely to remain viable for extended periods of time on porous material such as fabric.
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7978145/
Also to this day the following study appears to be the only one documenting a case of indirect contamination.
https://pubmed.ncbi.nlm.nih.gov/32758198/
(Obviously, I cannot prove the non-existence of other such studies.)
As a result, droplets and aerosols (smaller droplets that remain suspended in the air) are thought to be the main vectors of contamination. Secondary contamination due to contact with a contaminated surface is thought to be a rare occurrence.
In the case of masks, one would probably have to touch a mask which has been recently worn and not wash their hands afterwards in order to be contaminated. It seems unlikely to me that this would be vector of transmission.

hmm..yes. You are right. Viruses cannot breed there, but do they survive longer in moist environments?

I have edited the answer. I have no time for more right now: I must work. I will try to add references later. Editions / improvements are welcome in the mean time. I do not think the mask being moist is relevant here. Sars-Cov-2 has been shown to survive for hours on dry surfaces.

Yes, I have also delved into some similar articles that point towards the conclusion you make. Although what I want to know about is the moist environment created around the mask, rather than the surface itself. We are constantly breathing out moist air, and masks trap it within itself for extended periods.Making for a denser moist environment similar to the ones found around air dryers.

I tried to figure out what you were interested in and made the wrong guess, it seems. So, if it is not Sars-Cov-2 you are interested in specifically, then you should change the title of this question if that is possible or create a new question. There is little doubt that bacteria would breed in masks. This is why you are told not to wear the same mask more than a few hours.

Okay, but the relevance of my question with Sars-Cov-2 is that I want to know whether due to creating such an infectious environment,  masks actually become counter productive or not

You may be right, but there is no way of telling because your answer consists of unsupported assertions. That does not cut it here.

@Apocaleone: We have abundant, if not overwhelming, evidence that the use of masks does significantly reduce the spread of the COVID virus (and other airborne infectious diseases), so theories that masks increase the spread have been proven false.

@David Originally I thought the OP was just asking whether Sars-Cov-2 replicates in masks. It appears that this is not what they were looking for. So I started adding more information and ran out of time and left my response in that state. I have now added some references. But I must admit I still do not know for sure what the OP is looking for!


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What kind of animals are these little creatures?
I have 3 tanks. 1 with my fishes and 2 other are technical.
The smallest one is 0.5l and I'm using it as trash bin where I put dead plants and algae from main aquarium and it has sand from the see at the bottom. For more than 5 monthes it was full of algae and no alive creatures. Now it has many live black dots that are very fast moving and now the tank is very clean.
Second technical was planned to used for daphnia (didn't get it yet). It has 5l volume now. In the bottom it has simple ground and rasied Glossotigma eletinoides from the seeds. Also it has many algae (including Spirogyra).
Two tanks are closed tightly.
I have a some questions about it:

What kind of animals are these?
Can I move black dots to the other tank to have it clean from algae?
Are these creatures safe for me?
Are these creatures safe for my fishes?

I recorded video, it has 3 parts (1 tank, 1 tank in zoom, 2 tank in zoom):
https://youtu.be/3jbqPiAcKOc

Update:

Tank 1. This animal is hard to catch

Tank 2. In water I see only one type and on the stick I got 2 different animals. The left one looks like one of the species of daphnia.

Update 2:
I think I found what I have in the tank 1. It is some sort of Ostracod (seed shrimp), because I saw whiskers and slit in the shell

Welcome. It's best practice to include (an) inline pictures of the critter at hand. External links are discouraged and I am personally quite hesitant to click on them (spam, phishing etc)

Welcome to Bio.SE! Two recommendations to ensure a better response (to follow up form the previous comment): 1. Use a site like ezgif.com to convert a few seconds of your video to a gif to include the gif as an inline photo in this post. 2) Is there any way to get more magnified images? -- the resolution on these videos make an accurate ID tenuous at best.

Looks like in the first picture it could be Pleidae or some Helotrephidae, or not?)

Also I dropped fruit twig inside 1st tank and these creatures occupied it fully.


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Does medication make the body dependent?
First of, I know of course that certain medication can cause an addiction if incorrectly used. But as far as I understand it, drugs prone to cause addiction have some agent in it, that makes them addictive.
What I am interested in is a bit different though: If a drug "helps your body" do something your body can not or only insufficiently do alone, does it get dependent on this drug, even if the drug does not have addictive substances in it?
Or in other words: Can the human body unlearn something because of the fact that medication helped it do it for some time?
Edit: To make the question a little more clear, I can give the following example: I recently received medication containing Etilefrine, which contracts my blood vessels and thus prevents me from fainting in certain situations. If I take this medication regularly for a year and the suddenly stop it, could it be possible, that my blood vessels "forgot" how to contract on their own?

Stopping drugs/alcohol "cold turkey" can be fatal - drug dependency is a common problem

@rg255 I checked the Wikipedia article on it, along with the one on Drug withdrawal and it had some useful information in it. However, the articles tend to discuss drugs containing addictive substances. I would also be interested in drugs without those substances.

You have now specified your question, but a different thing you might be interested in is steroid withdrawal and what can happen if corticosteroids are stopped abruptly.

@YviDe I gave steroid withdrawal a look, it is a very interesting subject and roughly the thing I asked about. Thank you!


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Why do living fossils like crocodiles remain so constant and not evolve?
Crocodiles have supposedly remained unchanged for millions of years, and several other species are considered as "living fossils". How do such species remain so constant over time given that they will have had so much time to accumulate new mutations?

I'd add that although they may appear morphologically the same as their ancestors they may well be substantially genetically different. "Unchanged" on the surface does not necessarily mean the same under the hood.

Molecular evolution != phenotypic evolution!

Evolution is a process of change by four mechanisms; mutation, migration, drift, and selection.
You are correct in thinking that, because crocodiles have been around for a long time, they could have accumulated many new mutations in that time, relative to other more recent species. However, mutation is only one of the important mechanisms underlying evolution.
How different are ancestral and modern crocodiles?
It seems the appearance of crocodiles has been fairly unchanged since their occurrence ~85 million years ago (mya).
How can they remain so unchanged?
Genetic variation may have been low in the ancestral population, this would reduce the potential for evolutionary change, as most change would have to occur through new mutations. It seems the populations of ancestral crocodiles were quite small, such that a genetic bottleneck may have occurred (which would reduce genetic variation). Mutation rates seem to be relatively low in crocodiles (also see here) which would reduce the rate at which novel mutation occurs, reducing the potential for evolution.
Note that many mutations will be neutral in their effect (or "synonymous") so won't have an obvious phenotypic effect, so there may be substantial evolution at the genetic level despite the phenotypic similarity.
Low rates of evolutionary change could suggests some other things may have also played a factor. Given that the populations have been through multiple genetic bottlenecks, genetic drift could have slowed down rates of evolution eroding genetic variance, removing rare mutations from the population.
If selection has been fairly constant over time then there is less chance that changes will occur. If selection were to change and favour new adaptations then these are likely to spread, but if selection remains fairly constant over time then it will continue to favour the same mutations. After a long time of consistent selection it is likely that most mutations will be deleterious (have a negative effect) and be removed from the population by selection. Darwin suggested that living fossils could occur because the environment they are in has remained fairly constant (from this link).

When the species is not affected by disease, The species has masterd the environment and the mutations should entirely cease. The salt water croc has a incredible immunity and a wide variety of food

@TheVoid - diseases have basically no effect on mutations. What are you even talking about?

@Davor-spontanious new mutaions that suddenly show up in slight steady numbers are signs of a upgrade to better the species evolve in other words, Should I provide a link to show the strength of a crocodiles immunity from disease and infection?

@TheVoid Mutations don't happen on purpose, they just do. They are not trying to make any species better.

The quality of a crocodiles immune system won't have any effect on mutation rates. If the immune system is very well adapted then most mutations will be deleterious and selected away, but mutations will still occur

I think The Void wants to say that a perfectly (as far as biologically/physically possible) adapted species won’t change because all mutations would only yield a disadvantage (so there would be no permanent mutations). Because of that there would even be a strong selective pressure against mutations once a species has reached that point.

that point is made in my answer I think "After a long time of consistent selection it is likely that most mutations will be deleterious" - it relates to fisher's geometric model of adaptation

Crocodylomorpha were actually once a lot more varied than they are today, so their group isn't immune to change or evolution.

The tongue in cheek answer is to say, there were a lot more forms of crocodile in the past so chances are the single form we see today would look like one of them!
A better answer is: Species often evolve to fit a niche, they become specialised in their form both externally and internally. As long as this niche stays the same and neighbouring niches remain filled, the species will only become more suited to its niche. Over time you'd expect new mutations which made an individual fitter to become rarer, or have a smaller impact on survival so be selected for less strongly, thus the longer a niche exists, the more stable the form of animals living in it will become.

Looking at adapting to niches from the other side, we could ask why dolphins look so much like ichthyosaurs.

I particularly like your first paragraph in your "better answer" - it's a good clear and simple summary of the effect of constant selection! (+1) Do you he any references and links to external material to add so people can follow it up with further reading if they want?

@rg255 Unfortunately I didn't have any particular papers in mind when writing that answer, I could probably dig out my old uni notes and find the lecturers references if you were really interested?

I think in the case of crocodiles in particular, this is a question of body type. Crocodiles have fixed jaws, meaning that they have lost the mechanism used to move their lower jaw from side to side. This simplification means that they can exert a huge amount of power, making it a great adaptation for their particular strategy of hiding in water and ambushing large land mammals that drink from it.
However, it also means that it's very hard for them to adapt to any other niche. Anything that would require eating smaller prey, or eating on land, would be untenable, because crocodiles can't chew. (Instead they close their mouth and rotate their whole body in the water to rip chunks of flesh off.) They can't easily re-evolve the ability to chew, because the mechanism needed to do that is pretty complicated, so their fixed jaw is more or less "locked in" evolutionarily.
So crocodiles have remained constant because they are very well adapted to a particular niche; because they've lost features that would allow them to adapt to other niches; and because the niche they occupy has been around for a very long time.
Personally I think these are the primary reasons. The low mutation rate mentioned in the other answers seems to me more likely to be effect than cause. If you are very tightly adapted to a particular niche then there is less advantage in genetically exploring other possibilities, so the descendants of individuals with lower mutation rates would have an advantage over those with higher mutation rates. This would provide an evolutionary pressure for a low mutation rate, which might explain the observation. (But this last paragraph is speculation on my part. I work on modelling evolution and I know that this kind of selection on mutation rates can occur, but I have no evidence at all about whether it happens in crocodiles.)

I think the "fixed jaws" argument is a weak one: if they evolved jaws which are more fixed then they can evolve ones that are less fixed, and you're whole answer hinges on that argument. You also have no sources and say nothing direct about genetic drift or consistent/variable selection (niche stability). As it stands this is a very opinion based answer and has questionable scientific content.

@rg255 to answer your first point, it's typically much easier to lose complex features than to evolve them in the first place. E.g. vertebrate eyes evolved only once but have been lost but have been lost many times. (I don't know if a species exists that is known to have lost its eyes and then un-lost them, but I very much doubt it exists.) If the developmental pathways responsible for the jaw hinge mechanism have been lost they are very unlikely to reappear. On your second point I can only plead guilty to the lack of references, but I did mention the other two things, albeit briefly.

(The reason I only covered them briefly is that you already covered them in your answer. This was only intended as a complement to yours.)

Well, two things.
First the assumption that creatures that are living fossils are strong as a species isn't strictly true. Evolution; especially in relatively long-lived animals like crocodiles and sharks (compared to dogs, houseflies, j-walkers, etc.) is such a long process. It isn't factually verifiable that they are doing well as a species, only that they are in a stable food chain.
Second; and User23715 raises all these point, animals that aren't exposed to evolutionary motivators (mutagens, predation, and habitant change) won't have as much genetic divergence. A crocodile won't benefit from a Darwinian advantage if it doesn't provide enough of a survival advantage to eventually fuel a divergent evolution. Any dominant trait needs to be aggressive enough to stay dominant. In a simple dominant-recessive model it would need to be twice as potent for hundreds of generations (close to 2000 years for crocodilian life spans and birth rates).

Welcome to Bio. Could you add sources to your claims?


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amount of tRNA and its extra arm
How much of the total RNAs is tRNA? Some say 15% and some 20%. Those percentages came from my different teachers. Which is correct? And what are the functions of the extra arm (variable loop) of tRNA? My teacher said it was just for classification but an international textbook says its function is unknown.

could you post sources for the claims of 20 and 15%

Total RNA of what? The species? What species? The cell? What cell? Total in terms of what? The number of genes coding for it? Molecular mass? RNA moieties? Please [edit] your question and clarify.

With respect to at least two sources I could find, tRNA is commonly reported as encompassing 15% total RNA in both rapidly-dividing mammalian cells such as HeLa, and in S. cerevisiae (1, 2). To give you an interesting tool to look it up in the same way I did, I used Harvards' Bionumbers webpage to search tRNA.
As for the function of the variable loop, it would seem that it serves to stabilize the tRNA overall structure through three-base interactions, and somehow interfaces with the type II tRNA synthetase (3). I'll try to find more on this interaction.


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Lentivector biosafety
Lentivectors are widely used in molecular biology, most commonly to transduce in a stable way a desired gene. These vector system takes advantage from the ability of viruses to introduce their own genome in the host cell. Thus the lentivectors are transfected to a producer cell line (typically HEK) and there viruses are produced with the desired insert. Eventually this viruses will be harvested and the desired cell lines transduced.
For bio-safety reasons, this system is engineered in a way that that the risk posed by the "virus system" is reduced. Thus the viruses produced by this system are incapable of replication, meaning with this that, as far as I understood, the viruses that are formed are then unable to form more in the second host as the genes in charge are not recruited. Yet, apparently the plasmids used can recombine and pose a possibility to create a replicating capable virus. Yet as far as I found in the literature this has never been detected and stands as a theoretical possibility.
My first question, in actual numbers, what is the probability that such event would take place (the number of recombinations in the specific locations). In the case that this would happen, the lentivector system would be potentially dangerous, as this system is based in HIV most of the times. Additionally, this vectors use not the endogenous HIV envelope protein but rather VSV/G from vesicular stomatitis virus, in order to increase the tropism and stability.
Additionally, even though HIV derived, most of the HIV genes are taken away from the lentivectors, yet in my opinion the most important ones are there. Second question, taking into consideration all of this, this theoretical "created" virus would be able to eventually cause AIDS or other whatever adverse effect? it is noteworthy that now is able to infect almost all human cells due to the VSV protein, then is it correct to think that the disease would be much worse, and much more contagious than the original HIV? note that even the stability is increased.
Yet, I can additionally think that this recombinant new virus may be indeed destroyed by the immune system, despite the increased tropism, due to the fact that vesicular stomatitis virus does not cause pathologies in humans, and possibly this protein works as an antigen and can induce an enough immune response.
Last, would theoretical recombinant virus be detected by a standard HIV test?
To simplify things, I am referring to third generation lentivectors

I'm not sure what you mean by "the plasmids used can recombine", there is no plasmid containing the viral genome, only the envelope and a few receptor proteins. The rest of the viral genome is not even present, it has been replaced with the gene of interest that you added. Therefore it would be nigh impossible to create an active virus using only three or four genes even if we where trying. Perhaps I misunderstood your above statement, correct me if I did.

I would say it's more likely for a lentiviral vector to be used on a patient who has an active HIV infection. This could also hypothetically allow the recombinant gene to be incorporated into a functional virus. This probably hasn't happened yet because the number of people receiving lentiviral vectors so far is really low (maybe zero? I haven't heard of lentiviral clinical trials, but I haven't looked either)

CDB> the envelope (VSVg), plus gag gene (polyprotein), the pol gene (integrase, reverse transcriptase, RNAse H ,HIV protease), rev gene (viral mRNA export from nucleus) found in the lentivectors transfected can recombine multiple times in order to produce a "proviral" DNA piece capable to code all this genes in the posterior generations.

Luigi> thanks for your answer
user137> I dont get you point. to begin with, how do you want to stably transduce the already existing HIV viruses with this system? besides even if so, you would get a transgenic HIV, but its beyond reason to think that you would target every HIV particle in the body as such, so these would continue perpetuating the infection + disease. Besides, what gene do you want to transduce to the virus in order to kill it? and yes I think there are such studies, but double check.

@Katz I'm saying that you could accidentally use a lentiviral vector in an AIDS patient, or that someone who receives the lentiviral vector could later get HIV. If both viruses happened to hit the same cell, the recombinant DNA delivered by the lentivirus might be transcribed into a viral RNA, packaged into a capsid and sent out into the body to infect new cells or maybe other people. While this new virus would probably be replication deficient, it could cause trouble. This and other reasons are why I don't like viral gene therapy.

as long as it is not replication capable I would not bother for the replication incompetent virus generation, they cannot produce any disease and the only risk they pose is insertional mutagenesis, which I do not think its too bad in terms of statistics (correct me otherwise), the only issue I think is that in case the lentivector produced viruses have an oncogene as an insert then yes this poses a higher risk. Regarding to viral pathogeneicity, the real issue is that even the replication incompetent virus can become replicative due to genetic rearrangements

I want to know the actual risk of this to happen, if happened, the actual chances to generate disease, and also if this theoretical virus would be detectable> if we are totally blind to verify any accidental event that might happen when handling lentivectors or not

How many recombinations are required to achieve an active virus?
The FDA has recognised the likelihood that lentivectors can be converted into actively replicating lentivirus if they undergo recombination with wild type HIV in a HIV positive patient. In this case, two recombination events are required to transfer the lentivector sequence into the HIV sequence (the mechanism of transfer is identical to the case of first-generation lentivectors).
This article from VCU describes another mechanism through which this can occur in first generation lentivector systems, which consists of two recombination events between the lentivector and the helper plasmid. Note that the 3 genes gag, pol and env are present on the same plasmid, and that plasmid is flanked by LTRs. Second generation lentivectors, such as the pLKO system, do not suffer from this problem and require wild type HIV to produce actively replicating lentivirus.

To reduce the likelihood of this happening, second and third-generation lentivector systems split the genes into multiple plasmids, which then requires more recombination events to produce replication competent viruses. Additionally, the polyA tail of the 3' LTR is replaced to reduce likelihood of recombination events occurring.

According to Addgene's article on lentivector biosafety, the gene of interest's transfer plasmid (both 2nd and 3rd generations) has a deletion in the 3' LTR region which prevents it from becoming replicatively active. Therefore, the only likelihood for the recombination to occur is for the cell line expressing the virus to undergo replication with an active, wild-type HIV strain. An example is this pLKO transfer plasmid, which contains a truncated 3' LTR, preventing the sequence from replicating outside of E. coli, which replicates it not using the LTR but instead using the plasmid origin of replication.
Are the active viruses produced by recombinations more dangerous in the wild than wild type HIV?
This is difficult to answer, since recombination only allows an active virus to form, but it does not guarantee that the virus will be dangerous. Dangerous viruses are theoretically possible, but require far more recombinations than the minimal 2 for replication competency in 2nd generation lentivector systems.
For example, lentivector systems generally do not encode for the viral proteins vpr, vif, nef and vpu. These proteins are necessary for increasing the infectivity of HIV in different types of tissues (but not cultured cells such as HEK293). The lack of these proteins in a hypothetical replication competent lentivector would significantly hamper its spread in the wild. Incorporation of these proteins is plausible but extremely unlikely, since more crossover recombination events will be required.
To use your example, the env protein coding for the VSV protein coat resides in the envelope plasmid. Since the replication competent lentivector formed by 2 recombination events will be a pseudotype containing only the HIV env proteins, it will need to further acquire the VSV gene to replace its env proteins, since these genes are not present on the same regions. There is no homology between the two DNA strands, which would significantly hamper the likelihood of the VSV gene somehow being incorporated into active HIV.
The addition of various chimeric proteins and LTR regions in 3rd generation lentivectors only complicates the matter.
Overall, I was unable to find any sources comparing the infectivity of these theoretical transgenic HIV versus the wild type. However, even though it is theoretically possible that a transgenic replication competent lentivector can have better tropism than HIV by acquiring the VSV gene, the likelihood of that occurring is far lower than that of it being produced in the first place.
Can a lentivector be detected by a HIV test?
Regarding the final question of whether a lentivector can be detected by a standard HIV test, the answer is that the detection is possible if the person who was infected with lentivectors, has obtained an immune response to the lentivector gag proteins, and the lentivector loads are high enough.
HIV tests are specific to different parts of the virus, but most of them target the viral protein p24, which is a component of the gag polyprotein.
PCR based HIV tests also exist, but these tests would depend on the specific primers produced and whether the RT-PCR would produce an amplicon given the specific sequence of the plasmids.
Since gag genes are encoded for in most lentivector systems, it is therefore very likely that anyone infected with a lentivector would therefore express antibodies towards p24, and therefore result in a positive for the ELISA as well as the Western blot tests assuming that the p24 and antibody quantities are high enough to reach the cutoff point.
I was unable to find publicly available cutoff levels for the ELISA and Western blot levels, but if (hypothetically speaking) a person was injected with a load of lentivectors, they would likely test positive for HIV. However, since the lentivector is not actively reproducing, it would quickly be cleared out by the immune system.

from your answer, is it correct to think that there MUST be wild type HIV1 present? because if it so, then of course I can guess its no good at all, but if you already have HIV maybe it is not that "important"? I was asking for the possibility of forming replication competent viruses in the conditions in which lentivectors are produced> transfect 293T cells with the plasmids, which I guess do not contain HIV sequences.

additionally there is a third question in the text, which was not somehow highlighted, but related to the infectability and disease outcome that this theoretical virus might have

Updated to clarify some issues, most notably the erroneous description of the vector in the VCU article @Katz

thereby, cannot non-homologous recombination occur between the transfected packaging/envelope/construct plasmids in order to create a replication competent virus without any HIV sequence present? I would say yes.
incidence?
and, the immune response for the VSV/G enveloped recombinant virus? can VSV/G protein act as an antigen? would it be enough to prevent pathology?

@Katz There doesn't seem to be any wild type 3' LTR present in any of the 2nd or 3rd generation plasmids according to the plasmid maps, so even non-homologous recombination will not result in viruses being produced. In healthy individuals, there is no reason why the VSV protein will not be targeted, since they are clearly non-self viral proteins.

sorry to reopen this but, could you specify what functions does the HIV 3 LTR have and what possible effects could this deletions found in the lentivectors have in a mechanistical way on the virus life cycle? i reopen this because I found that LTRs function as regulatory sequences, specifically 3LTR in polyadenilation, but the genes in the lentivector systems ARE indeed expressed, and the insert gene that ussually goes between the LTR is SUPPOSED to be working, thats the whole point,  so I really wonder how fatal this really is.

@Katz The genes in the lentivector are not expressed by the LTR promoter, but by the gene's own promoter. The truncated LTR prevents the transcription of the entire sequence including the LTRs.

I made some research and found that the mechanism of action of the truncated 3LTR is that it produces what is called in the literature "self inactivation". Yet after reading the papers still I do not get the mechanism implied to work, I think I am potentially missing some important part on LTR biology and the role it plays.

@Katz http://www.pnas.org/content/83/10/3194.full.pdf seems to describe the mechanism quite clearly.

ok, the trick was on the RT mechanism which works in a jumping way

yet, as the retroviral LTRs are both identical I could bring the argument of recombination and say that the 3LTR could recombine with a correct one. Additionally I can guess that the homologies this time might actually serve..