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allogeneic organ transplant and the immune response
What happens when an allogeneic organ transplant is performed on an immunocompetent recipient vs. when it is performed on an immunosuppresed recipient using a donated organ with immunocompetent cells?

Is this a homework question?

No, it's a question I saw when reviewing organ transplant

The situation is just as you'd imagine. In an immunocompetant recipient, a host-versus-graft reaction occurs. This is called transplant rejection. Single episodes (acute rejection) are easy to treat and rarely lead to organ failure. Chronic rejection is the leading cause of organ transplant failure. The organ slowly loses its function and symptoms start to appear. This type of rejection cannot be effectively treated with immunosuppressants. Some people may need another transplant.[1]
In bone marrow and other transplants, T cells in the allografts reconstitute T-cell immunity in the recipient. Unfortunately, these T cells recognize the recipient as 'non-self' and employ a wide range of immune mechanisms to attack recipient tissues in a process known as graft-versus-host disease (GVHD).[2]

Acute GVHD describes a distinctive syndrome of dermatitis, hepatitis, and enteritis developing within 100 days after allogeneic hematopoietic-cell transplantation (HCT). Chronic GVHD describes a more diverse syndrome developing after day 100. In addition to allogeneic HCT, procedures associated with high risk of GVHD include transplantation of solid organs containing lymphoid tissue and transfusion of unirradiated blood products.[3]

GVHD is increasing due to the increasing number of allogeneic hematopoietic cell transplantations (HCT). More than 25,000 allogeneic transplantations performed annually. Given current trends, the number of transplants from unrelated donors is expected to double within the next five years, significantly increasing the population of patients with GVHD.[4] Yet the major complication, GVHD, remains lethal and limits the use of this important therapy.
Long-term immunosuppressants are usually the treatment regimen for chronic GVHD. Fungal, bacterial, and viral infections are a major risk with this treatment since the immune system will be suppressed for a very long time.[5]
[1] Transplant rejection
[2] Graft-versus-host disease
[3] Graft Versus Host Disease
[4] Graft-versus-Host Disease
[5] Graft vs Host Disease: An Overview in Bone Marrow Transplant


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Need clarification on a sentence regarding vesicle-mediated translocation
I've chanced upon a passage that is not entirely clear to me:

In addition to conjugation, transformation and transduction, other less well recognised mechanisms of DNA uptake occur in nature, while other mechanisms of HGT are probably yet to be elucidated, in particular, DNA uptake by eukaryotes:
Vesicle-mediated translocation by a range of gram-negative bacteria such as Neisseria gonorrheae, E. coli and Pseudomonas aeruginosa, which can bud off vesicle structures that contain genetic material (e.g.antibiotic resistance and virulence genes) and then fuse with another bacterium (Dorward et al., 1989; Kadurugamuwa and Beveridge, 1997; Yaron et al., 2000).

(From "Risks from GMOs due to Horizontal Gene Transfer", by Paul Keese)
Is it the bacteria that fuse with another bacterium, or is it the vesicles that fuse another bacterium? I'm not sure.
I thought the vesicles were budded off in the first place so that they could carry gene material to another bacteria.

(asked a parallel question at ELL SE)

If you looked at the PubMed page that you linked to you will see in the right hand column a list of similar articles. The first is a review or HGT from plant to bacteria, so if you read that, you will likely find a better explanation of the process than the article you are referencing.

@AMR - thank you! Got it.

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Which word is used to indicate that a vessel is "blood-filled" during a necropsy?
I'm translating a necropsy report, and one sentence says:

Синусоиды полнокровные. Портальные тракты сохранены, сосуды умеренно полнокровные.
The sinusoids are plethoric. The portal tracts are intact, with moderately plethoric blood vessels.

The meaning of the Russian word is "full of blood". There are three words in English: plethoric, congested, hyperemic. Which one is used more often in necropsy reports when describing the "blood-filledness" of blood vessels and tissues?
Per the comment below left by Bryan Krause: in my text, this feature, "full-bloodedness" of vessels, is clearly not pathological, because each of the several dozen animals has this "plethora of blood" in vessels in many instances across the document, and in the end the researchers come to the conclusion that the animals did not display any negative effects from the treatment.
I googled in Google Books using "congested vessels autopsy", "plethoric vessels autopsy" and "hyperemic vessels autopsy" and found all terms in use:

Those words aren't necessarily synonyms so it isn't as simple as which is more often used, it would depend on what condition the Russian pathologist was referring to.

@BryanKrause - is there a good description of the difference between these three terms in postmortem pathology? It looks like there's only one word in Russian for this, "full-blooded" (polnokrovny). It looks like in English the word "congested" might be used to refer not only to blood (judging by my Google Books search)

I'm not a pathologist so I'm hesitant to say much more because I'm not sure what common practice is for reporting "normal full-bloodedness" - my impression is that all three words are referring to an over filling of blood - in the examples you provided this is certainly the case - but that may be inaccurate. "Blood-filled" might be a safer translation even. And yes, "congested" has many other meanings, such as 'nasal congestion' when the nose is full of mucus or "traffic congestion" when a lot of vehicles are on the road. It is a generic term, not at all specific to blood.

congestion implies increase blood filling on account of a passive process such as congestive heart failure, hyperemic an active process such as inflammation and plethora doesn't assign a cause to the excess blood content of the vessels.  I wouldn't use any of these terms to describe a normal vessel filling at post mortem. But I'm also not a pathologist.

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How do you accurately measure anguiliform (eel) locomotion?
In one of my courses, we were discussing a paper by Muller and van Leeuwen (2006) which made a lot of comparisons the differences between carangiform (mullet) and anguilliform (eel) locomotion. While reading the text, one of the passages stood out to me:

When comparing the estimates of vortex ring height with those of ring width, mullet and mackerel shed approximately round vortex rings, whereas eel vortex ring are almost twice as wide as they are tall. Such distorted rings are less likely to form and once formed, they are more likely to break up, all of which results in a different vortex pattern in the wake.
The time-resolved flow fields of eels indeed support the notion that the vortices in its wake break up: two independent studies, visualizing horizontal cross-sections through the eel’s wake, observed that individual vortex cores elongate and split into two (Muller et al. 2001; Tytell 2004a). We can therefore conclude that the shape of the propeller, and hence implicitly the propulsion mechanism, might affect wake shape. This observation also implies that a propeller shape that promotes the formation of a suboptimal wake is less efficient, and therefore the absence or presence of a wake that is predicted to maximize efficiency is a valuable indicator for the hydrodynamic efficiency of a fish’s swimming design.

So, essentially during carangiform locomotion the body of the fish moves 1/2 wavelength whereas anguiliform swimmers make 1 wavelength. My questions are how can they make such a statement when particle image velocimetry (PIV) does not adequately measure the movements of anguiliform swimmers, let alone their efficiency, when they are essentially swimming through their own vortexes? Are there any studies that address this issue in anguiliforms?

Can you elaborate on why PIV is inadequate for studying anguilliform swimmers?

Just to add to @kmm , what are your qualms with the application of PIV here? ( I work in one of the labs cited, and don't understand your question)


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How would cloning affect conservation of rare species?
Many species are at risk of extinction, and cloning could be seen as a relatively quick method to produce large numbers of members of the species to aid in conservation efforts, especially if the species involved has low fecundity (such as the giant panda).
However, cloning results in the reduction of genetic diversity, which may lead to significant issues due to inbreeding and susceptibility to diseases. This can most clearly be observed in the Gros Michel banana cultivar, which was nearly wiped out by Panama disease due to the cloned banana cultivar not having any resistance to the disease.
What are the main positive and negative aspects of cloning when applied to conservation of rare species?
(This question is based in part on this question, which was closed for having not done any research, but has an interesting premise that I wish to see answered on this site.)

Cloning become an important method for conservation genetics. However, it is not a magical solution and doesn't solve all of the the problems. There are two key considerations with conservation: short term issues which are causing the immediate threat such as poaching, habitat destruction etc. and long term issues of genetic variation. Genetic variation is critical to the long term survival of a species because low genetic variation results in inbreeding depression (reduced ability to survive and reproduce resulting from higher expression frequencies of deleterious mutations) and reduced potential for adaptation. The rate of adaptation is determined by the strength of selection and the volume of genetic variation; without genetic variation there can be no adaptive evolution. Therefore, genetic variation is key to the long term success of a species.
Where cloning can come in is it can be used to increase the gene pool, sometimes quite substantially. Consider the meta-population of a species, this could be allowed to include all of the wild sub-populations and all captive or managed (semi-captive) populations. For example, there are ~3900 wild tigers in the world, and ~5000 in captivity. Among all of those, only a subset contribute offspring to the next generation of wild animals, reducing the effective population size, and increase rates of inbreeding and genetic drift. For example, often very few males fertilise the females of a population with strong effects on the effective population size. What cloning could be used for (to various levels, depending on the specifics of the method) is to allow other individuals to contribute. For example, by cloning the members of a wild population that were unable to secure mates during a reproductive season (there is often high variance in mating success which reduces effective population), conservation managers can artificially re-inflate the effective population size to more closely resemble the census population size. In other cases, conservation managers may chose to clone particularly viable/fertile individuals that are approaching old age or nearing death, and are therefore at risk of being lost from the population. Conservation programs could use cloning of (semi-)captive individuals and introducing clones from (semi-)captive populations in to wild populations allowing genetic variation to be drawn from the gene pool of (semi-)captives in to the wild populations. Increasing the variance in the gene pool will increase the adaptive potential of the wild population. Another option is to clone wild animals in threatened areas (e.g. where populations are in decline as a result of poaching) and to put the clones in to safer areas such as national parks, or even zoos, to preserve genetic variation while conservation managers try to bring the other issues under control. Effectively this would act a bit like a seed bank.
However, there are some issues to consider, and this is a non-exhaustive overview. What if there was a good reason for some individuals not mating? The action of selection, which causes adaptation, is to induce variance in reproductive success as a result of the genes an individual carries: in principle selection reduces genetic variation and allows the "better" variants to prosper. So if we clone a wild individual that produced no offspring in the reproductive season we may just be maintaining genes in the population that selection would otherwise be removing. In other words, cloning efforts could be counter-productive to the long-term success of the species and make conservation more difficult. What if we reintroduce bad genetic variance to the wild population? Captive populations have adapted to some degree to the environment that they are in, this may have selected genes out of those populations that are more beneficial in the wild. For an extreme example, dogs are descended from wolves and have adapted to an enormously different environment, so it would probably be very counter-productive to start cloning chihuahuas and introducing them to wild wolf populations as a conservation strategy to get genetic variation from captive "wolf" populations (but maybe the chihuahuas would be a good food source at least). Can clones be effectively, and efficiently, reared and introduced to wild populations? It will be extremely hard to actually get to the point where clones can be successfully introduced to wild populations. Resources (including money), are extremely limited in conservation, so there may be better ways to use those resources. Are populations under remaining threat from short term issues such as poaching and habitat loss? If there is continued extrinsic threat to the wild population then there is not much use in cloning, because clones will also be threatened by the same issues. Many places are still under serious threat from poaching. Adding some clones would be like trying to stop a ship from sinking and using a tiny bucket to bail out the water; you need to plug the hole first or use a really big bucket (can cloning be a big enough bucket?).
Bonus: You could read here about the issues faced in the Isle Royale system of wolves and moose, where wolves are on the verge of extinction, and the impacts it will have on the ecolsystem.

The Isle Royale wolf conservation paper is really interesting, thanks for the great read.


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What is the biggest facultative anaerobic metazoan known to science?
Related: What's the biggest obligate anaerobic organism discovered till now?
I had always assumed that the Riftia tube worms were obligately anaerobic since they lived next to anoxic volcanic vents, but a quick literature search showed it to be a facultative anaerobe, being able to survive at least 60 hours without oxygen.
If "facultative anaerobe" is defined as being able to survive at least 24 hours in the absence of molecular oxygen in an otherwise normal environment, are there any metazoal organisms larger than Riftia (which are up to 1.5m long)?

The answer to your question is going to be some plant or fungus. You might want to stick the word "metazoan" somewhere in your question.

Tapeworms? They can grow much longer. Are you specifically interested in free living metazoans?

I didn't specifically ask for free-living metazoans, so tapeworms would be a good answer.

@MarchHo am not able to find a reliable evidence for the anaerobic metabolism in large cestodes.

I think a tapeworm is your best bet. For tapeworms specifically, I found this textbook, Animal Physiology: From Genes to Organisms, which claims:

Active facultative anaerobes include some parasitic worms such as tapeworms that can survive without oxygen indefinitely...

I was not able to find any primary research on the subject either @WYSIWYG (other than a paper from 1951 that doesn't seem to be available anywhere), but if the textbook's claim holds, I can't think of anything larger than a tapeworm.


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What are the survival limitations of alcohol?
This question was inspired by watching one of the Pirates of the Caribbean movies; particularly where Jack Sparrow allegedly survives on a desert island by finding an unlimited supply of rum. I've heard alcoholic drinks dehydrate you more than hydrate you, so this seems like an unsustainable strategy.
My question is threefold.

How long can a human survive by drinking hard liquor (40%
alcohol by volume) for their sole water intake (ignoring food)?
If it's unsustainable, what will finally take you down?
If the hard-liquor approach isn't viable, what % alcohol can
keep you hydrated (beer, wine, etc.)?

Related:
1. Question on dehydration studies
2. Question on what dehydrates

I would say that the main problem with high percentage alcohol is that it is a cytotoxic substance which will not do good.

There are a lot many things that can happen because of excessive alcohol consumption. First of all the gut will be affected. Excessive drinking can also cause palpitations

One reason this is too broad is there are many ways of drinking alcohol - three tots in a row, spaced out over an hour, etc. - and these things matter when you're dealing with a toxin.  Also, the rum he was drinking was probably greater than 40%, especially if it lasted that long.

I commented above that it will depend heavily on at what pace you drink your rum, but in short, no, no you cannot.  If you do it quickly, you'll die of alcohol poisoning, and if you drink it slowly, you'll probably die of dehydration[1].
io9 summed up some research a few years ago, the majority of which is largely bunk.  One study (ncbi, free pdf) however, from 1996, claimed to find that:

These results suggest that alcohol has a negligible diuretic effect
  when consumed in dilute solution after a moderate level of
  hypohydration induced by exercise in the heat. There appears to be no
  difference in recovery from dehydration whether the rehydration
  beverage is alcohol free or contains up to 2% alcohol, but drinks
  containing 4% alcohol tend to delay the recovery process.

So stick to (American) beer.
Sidenote: In Belgium, they divide their (truly excellent) beer into two categories: special, which are stronger and often bottled, and thirst-quenching, which have a lower alcohol content and are often had with lunch.
[1]: Citation: Personal experience and the story of Johnny Tarr.

Interestingly enough, the mainstay drink in the Middle Ages (medieval times) was "small beer" (cheap low-quality beer with low alcohol content). Back then there was no concept of water purification and treatment - most of the water in a town or city back then would be loaded with pathogens and considered unsafe/unsuitable for drinking. The alcohol in "small beer" was enough to eliminate most of these pathogens while dilute enough to be used almost like water.
However, health problems quickly start as the amount of alcohol increases. As Amory mentioned, 4% alcohol weighs on dehydration recovery. There's no way anyone could survive on a desert island drinking only 40% alcohol hard-liquor or similar.
No matter if the rum is spaced out over time or consumed like water, it's a non-solution. Spacing it out over time and allowing proper detoxification over time will be insufficient to keep up with regular water needs; drinking it like water will quickly cause lethal alcohol poisoning.

Beer contains roughly 5% alcohol. This isn't anywhere near the concentration to kill most of the pathogens possibly present. Beer was interesting, because it is boiled in the process and is thus less likely to be spoiled than pure water at that time. Additionally it would be great if you could add sources to all of your answers.


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What is the "Spandrels" debate about?
In a former question, as a side question, I asked a clarification about the "Spandrels" paper. Being not a biologist, it was the first time I encoutered it.
Subsequently I tried to collect some information, because I read that the paper is debated and deemed "wrong" by at least a part of the community.
Despite my efforts I have not fully grasped what the issue is:

is the incorrect reference to the architectural element? (i.e., the paper is wrong because it uses a not fully agreeable comparison)
are some (or all) the claims in it wrong? if yes, are there any suggested reading to understand why?

I ask specifically because the first reference I encountered points to Dawkins, and I would like to understand if this paper is a mere pawn in the big "gradualists versus punctuationists" debate or if it has merits on his own.

While spandrels might not have been a suitable metaphor, that doesn't change the primary argument made by Gould and Lewontin. I'll write up an answer later this afternoon.

Short version
The paper has nothing to do with punctuated equilibrum vs. gradualism (see also here), which was published a few years earlier. This debate is much different (but equally important, I think).
The authors of the Spandrels paper criticized evolutionary biologists of taking a very narrow view of the evolutionary process. They claiming (wrongly) that evolutionary biologists believed that every single trait on an organism was an adaptation that resulted from natural selection. The trait would not be present unless it was an adaptation. The authors claimed (rightly) that traits could not be considered independently. Instead, the traits had to be considered in light of the evolutionary history and developmental biology of the organism. To your specific questions:

The architectural metaphor was wrong. Does it make their entire argument wrong? No. They did not understand architecture. That does not mean they did not understand evolutionary biology.
Are some of their claims wrong? I think yes and no, but the full answer requires more nuance than can really be given here so read the long answer below if interested. I don't know of a single reference that supports/rebuts the Spandrels paper but consider Why Evolution is True by Jerry Coyne, The Greatest Show in Earth by Richard Dawkins, and Endless Forms Most Beautiful by Sean Carroll. None of these address directly the charges lodged by the Spandrels paper but they do show how evolutionary biology is integrative of many ideas instead of isolating each trait without considering the biology of the entire organism. (I have no commerical interest in any of these books. I simply support the ideas presented.)

Long version from my perspective.
In 1979, Stephen J. Gould and Richard C. Lewontin (hereafter, G&L) published a paper, "The Spandrels of San Marco and the Panglossian Paradigm: A Critique of the Adaptationist Programme", in the Proceedings of the Royal Society of London, Series B.  The title of the paper mixes two metaphors. The first is the character Dr. Pangloss from Voltaire's "Candide." Dr. Pangloss is a bit of an optimist, who says,

It is demonstrable ... that things cannot be otherwise than as they are; for as all things have been created for some end, they must necessarily be created for the best end. Observe, for instance, the nose is formed for spectacles, therefore we wear spectacles. The legs are visibly designed for stockings, accordingly we wear stockings. ... [A]nd they, who assert that everything is right, do not express themselves correctly; they should say that everything is best." - Dr. Pangloss

Dr. Pangloss is saying that everything has a purpose, and each thing is designed specifically for that purpose. G&L extend this metaphor to evolutionary biologists.  G&L claim that evolutionary biologists (at least to the time of their publication) tended to make claims similar to Dr. Pangloss: every trait that could be found on an organism results from natural selection and adaptation.  G&L write,

An adaptationist programme has dominated evolutionary thought in England and the United States during the past forty years. It is based on faith in the power of natural selection as an optimizing agent. It proceeds by breaking an organism into unitary "traits" and proposing an adaptive story for each considered separately. - G&L

Hence, the Panglossian paradigm. Every trait has an adaptive purpose and is necessarily the "best" that it can be. G&L then argue that evolutionary biologists of the time failed to consider the entire organism when assigning adaptive value to each trait separately.

We criticize this approach and attempt to reassert a competing notion ... that organisms must be analyzed as integrated wholes, with bauplane so constrained by phyletic heritage, pathways of development, and general architecture that the constraints themselves become more interesting and more important in delimiting pathways of change than the selective force that may mediate change when it occurs. - G&L

G&L are saying that the many organismal traits are functions of evolutionary history, developmental pathways, and other structural contraints.  G&L argue that most evolutionary biologists of the time did not consider the entire organism when ascribing adaptive value to any one trait. In G&L Panglossian metaphoric terms, evolutionary biologists had decided that the adaptive value of the nose was to support glasses, but they had failed to consider that the nose may have evolved for other reasons (e.g., smell) and that the supportive value of the nose was an evolutionar by-product instead of an evolutionary cause.
This brings us to the second metaphor, the architectural spandrels. Spandrels are triangular spaces that form when two arches meet, or when an arch meets a rectangle.  According to G&L, spandrels are a necessary by-product of the architectural joining of the two shapes. The spandrel itself serves no purpose. In evolutionary terms, spandrels have no adaptive significance that resulted from natural selection. Instead, they are an evolutionary by-product that resulted from selection on other traits (arches and rectangles).
While the architectural metaphor apparently fails, their primary argument does not change.  Traits cannot be considered individually. Traits of an organisms must be evaluated as one part of the entire organism, together with it's developmental biology and its evolutionary history.
Here are two examples to represent their argument, written for a general audience. The first example is based on the human hand.  Our hand has five fingers. Each finger except the thumb has three bones (called phalanges), which you can see easily when you curl your finger. The thumb has only two phalanges. What is the adaptive value of having four fingers with three bones each, and a thumb with two bones? You might say that such a structure imparts excellent manual dexterity, from grasping to manipulating objects. But, would we not have that same dexterity if we had four fingers, or six? Why does the thumb have only two bones and not three? How could that be adaptive? These specific traits may not be the direct result of natural selection.
The structure of our hand is explained by our evolutionary history. Our primate ancestors had five fingers. So did our earliest mammalian ancestors, as did our earliest reptilian ancestors. However, some of the earliest amphibian ancestors, such as Acanthostega, had more than five digits (toes, fingers). Somewhere in early amphibian evolutionary history, our ancestral lineage converged on five digits, and most descendant vertebrates retain that five digit pattern. Even those vertebrates today without five digits usually display five digits during development, such as the ostrich (scroll down to image of blue-stained bones). If we assigned an adaptive purpose to the  human hand independently of its evolutionary history, we might very well be wrong.  Science doesn't like wrong.
Think about the five toes of your foot. Each toe has three bones except for the big toe, which has two bones. Manual dexterity? No. Evolutionary history? Yes.
The second example is the groove in your upper lip below your nose. This groove is called the philtrum. Can you think of an adaptive function for the philtrum? You might think that it helps to direct odors towards our nostrils, or hypothesize some other adaptive purpose. However, it appears that the philtrum is a by-product of the development of our embryonic face (YouTube video). The trait of our philtrum may not have adaptive significance. It is a by-product our face formation when the two sides meet in the middle.
G&L's publication produced quite an uproar. It's easy to find criticisms of the paper. Some have criticized the architectural metaphor. A bad metaphor does not necessarily make a bad scientific argument. Others have criticized the scientific rigor of their arugments. This blog entry, associated with the respected ecology journal Oikos, dislikes the paper and identifies several problems. The Oikos blog also links to several other sites that either support or dislike the G&L article. Most evolutionary biologists disliked the claim that they did not see the "whole organism."
Rightfully so, I think. I do not know of one evolutionary biologist (myself included) that has ever considered a particular trait without considering the broader evolutionary history of an organism. Indeed, considerable effort is spent by evolutionary biologists to determine how the evolutionary history of an organism influences its trait. The same applies for evolutionary developmental biology and other biological processes. For example, Martin et al. (1993) related evolutionary rate to body size, metabolic rate, and generation time of various animals, a very integrative (not isolating) approach.
To be fair, I think the G&L paper needs to be considered in the context of its time. Remember that i was published in 1979. Reread the first G&L quote above. They say, "during the past forty years."  The G&L paper was published in 1979. Forty years before this paper was published was during the "modern evolutionary synthesis." Without going into details (ask another question on Biology.SE!) the modern evolutionary synthesis provided the genetic mechanism (and so much more) that explaiend how Darwin's concept of natural selection could actually work. Once the relationship between Mendelian genetic inheritance and natural selection was proposed, many evolutionary biologists tested this connection. It is not surprising to me that G&L perceived this strong "bias" towards a selectionist (Panglossian) paradigm because many biologists of the time were trying to understand how Mendelian genetics contributed to natural selection.
At the time of the modern synthesis, the structure of DNA was not yet known.  The structure was finally realized by Watson and Crick (and Franklin!) in 1953, only 26 years before G&L's paper. Today we think nothing about the DNA structure but molecular genetics has advanced so much since G&L's publication that we have a much greater understanding of evolution and natural selection at the genetic level. Today, you can't study the evolution of a trait without considering its underlying genetic architecture.
In my opinion, one of the most, and perhaps the most, important development in the field of evolutionary biology is the field of evolutionary developmental biology (evo-devo). This field did not really mature as a discipline until about 2000, when the Proceedings of the National Academy of Sciences in the US devoted an entire issue to the topic. Developmental biology was a discpline that G&L had argued was important to consider. I'd bet that even they had no idea how important the evo-devo discipline would become to understanding evolutionary change. Still, recognition of the relationship between evolution and development was recognized as long ago as the mid-1800s by Ernst Haeckel. Evolutionary biologists were not necessarily considering traits in isolation from evolutionary history or developmental biology.
In the end, G&L used broad brush strokes to paint evolutionary biologists into a small canvas, claiming that biologists had a narrow evolutionary viewpoint. The evolutionary biologists responded (then and now) that their perspective was wide, even when focused on a particular trait.
The G&L paper continues to prompt considerable debate, which I think is the value of their paper. Every young graduate student should be required to read the paper. Even jaded scientists need a refreshing jolt to an established way of thinking. Our thought processes will alway benefit when we are reminded that evolutionary biology is a broad discipline that must embrace many other disciplines to arrive at a full understanding of the history of life on Earth.

may I point out that at the This [blog entry] seems to be missing a link?

@Federico Fixed.


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The evolutionary process in bird wings, especially with regard to winglets
In this answer on aviation.SE a comparison is made between the shapes of airplanes wings and the shapes of birds wings. It concludes with the following remark:

After all, no bird has winglets. Not a single one.

In addition to be a disputable assertion (the wing tips such as the eagle's could be considered akin to a "winglet" of the fanned type) this has stricken me as based on a quite wrong assumption of how evolution works.
I tried to make my point in the comments only to reach this point:

So you consider evolved wings as not mature. The winglet modification is just waiting to happen? Nature never tried it, in >100 million years of biological flight? Could be, yes. But is extremely unlikely. That settles it for me.

Am I correct in identifying this in a wrong interpretation of the evolutionary process?
As I understand the evolutionary process, the current bird wings are not necessarily perfect, are simply the version that so far has given the best advantage. The lack of "winglets" in birds cannot then be explained simply by assuming that they do not improve the wing, but it could also be that there has never been an evolutionary pressure to evolve them or that since birds flap their wings they would be detrimental instead of beneficial or whatever other reason.
Is my understanding of the evolutionary process correct? if not, where am I at fault?

As a small addendum, another user cited the "Spandrels" in comparison to the above debate, could someone explain what could have been the meaning of the comparison?

Planes have wing dimensions and velocity at least an order of magnitude greater than birds, so the physics is different. In order to make a like-for like comparison, the plane wing would have to be placed in a wind tunnel with a fluid of much higher kinematic viscosity than air, which would supress wingtip vortices considerably. For more info google Reynolds Number.

there is always a evolutionary need, there is competition for food, escaping from predators quicker etc. if its advantageous and there is any natural selection, theres a evolutionary need.

I looked up winglets so I had context for this answer. I'm interpreting winglets as the vertical tips at the end of airplane wings. If so, then you are correct. The spread primary feathers of soaring birds like eagles function as winglets (Tucker 1993). Airbus has a biomimicry web page devoted to some of the biological designs, including winglets, they incorporated into their airplane designs. Some studies suggest airplant winglets do increase efficiency (e.g., Hossain et al. 2011), but there is still some debate.
From the aviation.se answer:

Look at birds: They use two different wingtip designs. I guess we will both agree that those designs are mature after millions of years of evolution. And still there are two distinct wing tip shapes: One is the "fingered" wingtip with large, spread-out feathers, and one is the pointed tip you find from seagulls to albatrosses. Why is there not one, mature design?
This has to do with the environment they are used in. Seabirds fly in an unobstructed environment with steady winds and need to stay aloft for longer duration. All other birds have to cope with trees obstructing a straight flight path and gusts from hills, or those trees. They need to maneuver quickly and cope with gusty winds. This is helped by a reduced span and the possibility to fold the outer wing in or fan it out in an instance. Hence the fingered wingtip.

Although bird wings do tend to match his descriptions, he is not correct that these correspond entirely to ocean-going birds vs all other birds. Many inland birds have pointed wings, including swallows, nightjars, swifts, and falcons.  Some seagoing birds have winglets, such as pelicans and cormorants.  While wing type is shaped by natural selection in a given environment, it also reflects the evolutionary history of the birds.
There is not "one, mature design" because wings many different shapes and sizeshave evolved under varying selective pressures. For example, the long pointed wings of ocean-going albatrosses are excellent for gliding with little energy expenditure but they are lousy for taking flight or for landing. Other wings are shorter and broader, providing greater maneuverability in the woods. In this sense, there is no perfect wing. Each has evolved for different evolutionary reasons.
The main question
From the aviation.SE thread:

the fact that no random mutation has produced a winglet* in birds is in no way a demonstration that airplanes do not benefit from them, there is no logical relationship. [*even though the "fanned" design you refer, such as the eagle's, can be considered a form of optimum winglet] –  Federico

followed by this response:

So you consider evolved wings as not mature. The winglet modification is just waiting to happen? Nature never tried it, in >100 million years of biological flight? Could be, yes. But is extremely unlikely. That settles it for me...

Federico is correct. The basic wing type was set long ago as birds evolved from non-avian dinosaurs. Comparisons of modern bird wings with fossils suggest that the basic structure of bird wings has not changed very much since then. The current structure may be the best that has evolved by natural selection so far but that does not mean the wing cannot be improved further. As you noted, mutations could occur in existing genes that lead to further improvements of the structure and function of the wings. If those mutations never occur, then the improvements won't occur. This is one constraint of the evolutionary process (Hoffman 2014). Natural selection can only work with existing traits, using existing genes and genetic variation.
Another consideration is that wings for powered flight have evolved independently at least four times (birds, bats, insects, pterosaurs). Each time, a different type of wing evolved. Is one better than another? Bat wings have aerodynamic properties very different from birds but function very well for bats (Hedenstrom et al. 2009). Along the lines of your argument above, each wing type perhaps is (or was for pterosaurs) optimum given the environmental circumstances and evolutionary constraints. That doesn't mean they could not be improved.  If a wing evolves again in some organismal group in the distant evolutionary future, odds are very good that the structure will be different from those that have evolved so far. Perhaps that wing will be even more efficient than current wings.
Spandrels

Another user cited the "Spandrels" in comparison to the above debate, could someone explain what could have been the meaning of the comparison?

The use of "spandrels" in evolutionary biology stems back to a well-known paper by Stephen Jay Gould and Richard C. Lewontin called "The spandrels of San Marco and the Panglossian paradigm: a critique of the adaptionist programme", published in 1979 (Gould and Lewontin 1979). A spandrel is the space that forms between two adjacent arches or between an arch and a rectangular shape.  The spandrel emerges as a result of putting two arches next to each other and filling the space. It results from the joining of two arches. It was not specifically designed as part of the arch. Gould and Lewontin claim that evolutionary biologists are too quick to assign adaptive value to every trait on an organism, and argue that not every trait results directly from adaptation. Instead, they say, the trait may be a "spandrel" that emerged as a by-product of other traits. The "spandrel trait" has no adaptive value in and of itself.
The use of spandrels in the comments of the aviation discussion is not clear to me. Clearly, the person intended the evolutionary meaning, mentioning the paper by name. But I cannot tell at all the person's intent.
Edits: Incorporated comments by @Federico and @Andrew - thanks. I corrected horrendous typos and attempted to add clarity.
Citations
Hedenstrom, A. et al. 2009. Bird or bat: comparing airframe design and flight performance. Bioinspiration & Biomimetics 4 015001. doi:10.1088/1748-3182/4/1/015001
Hoffmann, A.A. 2014. Evolutionary limits and constraints. Pp. 247-252. In: The Princeton Guide to Evolution, Princeton University Press, USA.
Hossain et al. 2011. Drag analysis of an aircraft wing model with and without bird feather like winglet. International Journal of Mechanical, Aerospace, Industrial and Mechatronics Engineering 5: 30-35.
Tucker, V.A. 1993. Gliding birds: Reducion of induced drag by wing tip slots between the primary feathers. Journal of Experimental Biology 180: 285-310.

thanks for the answer. As for the efficiency of the winglets, it severely depends on the constraints and is debated. And turbulence is an unavoidable byproduct of lift generation, so I guess birds will neve fly "wake-free".

@Federico I certainly don't pretend to understand the intricacies of aerodynamics. :) It's interesting how geese have evolved flying in a V formation to take advantage of lift provided from individuals closer to the front of the formation.

I was not pretending you to, I simply pointed that out so that you can eventually review your answer to remove debatable points. I am aware of the formation flying of migrating birds, but the question/dabate was more focused on solitary ones. As for the "mature" remark, I guess it uses it in lieu of "whatever will happen, the shape won't change much" or "the current wing shape is the best possible one".

"...the long pointed wings of ocean-going albatrosses are excellent for gliding with little energy expenditure but they are lousy for taking flight".   ...and landing, apparently.

@Federico I've modified my answer in light of your (and other) comments. I've also tried to add clarity and remove redundancy.

One point you never mention is that birds are different to airplanes in how they are propelled. Airplane wings are completely fixed and don't flap. Would airplane-style winglets work on "flappy" wings? I suspect not.

@romkyns I agree that a fixed airplane winglet would not function well on a bird wing. It doesn't matter because birds achieve the same effect with the spread primary feathers at the wing tip. Besides, anything more than a stork with a jet engine is a scary prospect! :)

The logical assertion "winglets have not happened in a long time, therefore they are not advantageous" is incorrect.
It is possible for an advantageous trait not to evolve even when advantageous, if there is no "path" to it. The trait only occurs gradually, in small incremental steps. If intermediary steps are harmful, the trait will not occur, even if the end result would be beneficial.
(now, this does not say anything specific about winglets, just about the general argument)

One famous example of an "imperfection" that keeps existing despite a better solution being available can be seen here: https://www.youtube.com/watch?v=cO1a1Ek-HD0 (beware, video features dissection of a giraffe)
There is a nerve that connects the brain to the larinx. In fish, this nerve is somewhat short, but in the giraffe, it is enormous. The interesting thing is: the points this nerve connects are very near, even on the giraffe.
What happened was the the nerve passes below an artery. For fish, this is irrelevant. But, as larger mammals evolved, the nerve had to gradually grow to a bigger path. Evolution could not do the "reengeneering" to have a smaller nerve, because there was no immediately advantageous way to do it.

thanks, this is also the kind of review I was looking for.

It is also possible that airplane-style winglets hinder more than they help on wings that need to be flapped.

There are two possibilites with evolutionary processes: The development either never went into this direction or it brought no advantages. Besides this two possibilities the claims from the other forum are wrong. Birds (not all of them though) do have winglet-like structures. If you look at big birds, you can see feathers on the end of the wings looking like this:

These feather fulfill exactly the same purpose here. Some more information can be found here and also in the Wikipedia.

The Harun Yahya site is not the best site for reference. While his overview is correct, he has very strong creationist beliefs and very strong anti-evolutionary beliefs. He attributes to the design of bird wings to his god, not evolution.

Ups. Thanks for noticing. I will look up another one.

For the sake of openness, Chris, I did not intend to tell you what you should or should not include in your answer. That is up to you. I have strong opinions about including creationist ideas in evolutionary discussions though and that slipped through. I hope you accepted my comment in the positive spirit intended and not as a criticism.

@MikeTaylor Don't worry. I welcome critic to my answers and comments - I don't see this as something negative but as a chance to get answers better or learn something. And I don't like to include creationism in evolution either as it is simply unscientific. So yes, your comment was very welcome since this simply slipped through.


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What is the female equivalent of the morning erection that some men experience?
There was question about what causes "morning wood." It was answered that the erection in the morning is caused by decline of norepinephrine during REM sleep. Which in part allows to prevent uncontrolled urination.
My question is: How does the decline in norepinephrine affect women? They obviously don't get erection.

This question is protected to prevent "thanks!", "me too!"... - that's quite funny protection :)

Women have erections too! These erections are called clitoral erection. Clitoral erections are usually accompanied with vaginal lubrification.
Just like men (see here), the absence of norepinephrine during the REM phase of the sleep causes erections. In women, this phenomenon is called Nocturnal clitoral tumescence while it is called Nocturnal penile tumescence in men. In women, not only the clitoris get engorged with blood but the vagina too.

You sure? Because I have only had 1 typical sign of a female orgasm and only once. And I haven't been sexually active in my life. What I felt was a vaginal contraction. For a few seconds it felt like I could control menstrual flow. I myself have never had a clitoral erection though I have had noticeable vaginal discharge increase related to my menstrual cycle.

@Caters It is not a sign of orgasm just like discharge isn't. Both can be signs of arousal. Clitoral (and vaginal) erection possibly results in outer (closer to the entrance) vaginal tightening and as far as I am aware (I don't have a vagina, so I can only rely to womens' reports) if one touches clitoris when there is no erection it is not as pleasant (or even unpleasant) feeling than when there is an erection. But it might be the case that not every woman has these.

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


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Did the Britons 100 years ago have different intestinal flora and fauna?
Note: this is not a question about history, but about human digestive system over time :)
I know a lot of colleagues who traveled for business trips to India. All of them caught  terrible diarrhea there, in spite of keeping all the rules related to use of reboiled or canned water only, eating only peeled fruits, not eating the street food etc.
My question is: how did the millions (or hundred thousands, I am not sure with the amount) of Britons survived in India during the time of the British Raj 1858-1947?
Did they have to keep the same safety dietary rules as the contemporary Westerners all the time? (I cannot see this as technically possible...)
Were our intestinal flora and fauna different one hundred years ago?
Was the hygiene level and quality of water much lower in Europe then so coming to India was not such a biological shock? (Well, I would believe this in the 1800s but not in the 1900s...)
Or did just some of them die and the rest got accustomed?
EDIT:
I am aware that there is an initial shock for your body when travelling to a very different area generally. However, the Indians (and other Asians) can easily drink the tap water in most of the EU countries and eat the street food, which is not valid vice-versa. So there must be some difference.

Its true for any place in the world.. When you shift initially, in most cases, your body would need time to get adjusted to the food there. Not only the food but the weather is also a cause for diarrhea in many places. When I was visiting Britain, the initial few days played havoc with my bodily functions too which I attributed to a couple of pork sausages..

Who said they did not have the same problems? I'm sure they did and I'm sure most of them had horrible diarrhea.
A quick google search brought up Man and Microbes: Disease and Plagues in History and Modern Times, by Arno Karlen which states that

In 1817, when the first cholera pandemic began [...]. In Calcutta and Jessore, cholera killed 5,000 British soldiers within weeks

However, those who survived would get used to it eventually. Cholera is much more serious than simple dysentery of course but its main symptom is also diarrhea.
The locals of wherever you happen to be are used to the pathogens that are common in the drinking water. If I am not from a place and drink water with new pathogens, I will be sick. I will also, however, eventually get over it and my body will be used to them. Depending on the details, either because I have developed an immunity or because I have developed the necessary intestinal fauna to deal with it.
So while the intestinal fauna may indeed have changed over time, this has absolutely nothing to do with what you're asking. First because your assumption is wrong (the British were subjected to the same health issues as modern Europeans visiting Asia) and second because people adapt.

terdon, do you have any reference proving your statement "the British were subjected to the same health issues as modern Europeans visiting Asia"? And also - we have had many Indians visiting the company I work for, they have drunk tap water and have eaten everything and they have not caught diarrhea!


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Is there any knowledge of physics can be applied in to evolution?
I have asked a similar question in Biology.SE (What physics knowledge can be applied to biology of organisms and ecosystems?), but it just about organisms and ecosystems, not evolution. After watching a clip that Richard Dawkin talks about applying Darwinian evolution to physics, I would like to ask a vice versa question: is there any knowledge of physics can be applied in to evolution?

Are you wanting to know about the biophysical interactions of nucleic acids driving evolution, or applying brownian motion to evolving population models?

@GoodGravy I want to know both to have a good start to google better

Related question on Physics.

@HDE226868 I agree that it's a related question, but it's not a duplicate one.

@Ooker No, I didn't mean that! I just put it here because it's relevant to the question, just as you linked the other question in your question here. I didn't think it was a duplicate.

Meteors an such are part of astrophysics. Meteors can cause extinction, which is related to evolution. So I would say yes.

There's some. The basic idea is that entropy, as rigorously defined in statistical physics, can be equated to complexity. This is an idea that has been around since at least the 1957 paper by Jaynes. In a fairly hand-wavey way, one can then say that a system that is being fed a large quantity of free energy (as the earth is by the sun) tends to become more complex over time (i.e. evolve).
Thinking this through a bit, the above argument applies as easily to weather patterns as it does to living creatures. Recently, with the rise of computers and modeling there have been attempts to apply these kinds of general ideas (increasing free energy leading to increasing complexity) to living creatures in a more systematic way. Jeremy England is one researcher working on this problem, and this link goes to a pretty good pop-science-style writeup of his work on the topic.

your answer is indeed what I'm looking for. Thank you so much.


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How can CI repressor both activate and repress $P_{RM}$ promoter found in $\lambda$ phage?
I'm reading a paper where the authors constructed a toggle switch that uses bidirectional $P_R/P_{RM}$ promoter found in the $\lambda$ phage. There are 3 binding sites - $O_{R1}$, $O_{R2}$, $O_{R3}$ - located between the two promoters. CI is expressed by $P_{RM}$ and CI dimers bind to these binding sites:

What I don't get is that CI seems to function as both an activator and a repressor of $P_{RM}$.
First, my understanding was that $P_{RM}$ is an inducible promoter activated by CI which also represses a constitutive promoter $P_R$:

CI is a transcriptional activator of $P_{RM}$, thus producing positive feedback.
CI preferentially binds to $O_{R1}$ and $O_{R2}$, repressing the constitutive promoter, $P_R$.

However, it is also stated:

In high concentrations, CI binds to $O_{R3}$ and acts as a repressor to $P_{RM}$.

This seems to suggest that the CI can function either as an activator or as a repressor depending on the binding site bound; specifically, CI dimer binding to $O_{R1}$ and $O_{R2}$ will repress $P_R$ and at the same time activate $P_{RM}$, while CI dimer binding to $O_{R3}$ will repress $P_{RM}$. Is this correct?
I (a computer scientist by training) was always given the impression that a transcription factor is either inherently a repressor or an activator of a promoter, but this doesn't seem to be the case here. I would expect that e.g. CI would act as a repressor to $P_R$ and an activator to $P_{RM}$ regardless of the binding site. So why does CI binding to $O_{R2}$ (and $O_{R1}$ as well?) activate $P_{RM}$, while binding to $O_{R3}$ represses it - why the inconsistency? Note that I'm primarily interested in this from the modeling perspective.
What I also don't understand is whether or not $P_{RM}$ promoter is inducible or constitutive (e.g. in the absence of bound transcription factors, how leaky is it)?

many DNA binding proteins have more than one role... ;)

There's no rule that says a transcription factor must be either a repressor or an activator. The lambda repressor (CI) is in fact a repressor and activator of transcription, depending on where it is bound and to what promoter you are referring to. I know your question isn't directly about lambda phage, but I think this mechanism may be best explained in the context of where it was first invented: nature. So, I will try to briefly explain how the lambda repressor's dual role allows regulation of its own expression and controls lysogenic induction.
The cI gene is under the control of the PRM promoter. The PRM promoter is weak because the sigma factor of RNA polymerase (RNAP) holoenzyme has low affinity for it. Binding of RNAP to PRM, and thus transcription from there, at a reasonable level requires an activator. There is another protein involved in this process as well, called Cro, that can also bind the OR operators. The cro gene is under the control of the PR promoter. PRM is not a constitutive promoter because it requires an activator. I have heard PR called constitutive because it is a strong promoter and can bind RNAP without an activator. But, at the same time, it is under the control of the lambda repressor. I suppose it depends on which definition of 'constitutive promoter' you use.
The OR operators are not identical and thus CI and Cro bind them with different affinities: CI has the highest affinity for OR1, followed distantly by OR2 and OR3, while Cro binds OR3 with highest affinity. Binding (of any two molecules) is dependent on both their affinity to each other as well as their effective concentration. At lower concentrations, CI can only bind OR1 and OR2 cooperatively. That is, each lambda repressor dimer binds to another, forming a tetramer, with one half binding OR1 and the other binding OR2. Binding both operators as tetramer allows for a stronger interaction. At higher concentrations, CI can bind OR3. Furthermore, OR1 and OR2 are located in the PR promoter, while OR3 is located in the PRM promoter.*
Most lambda genes are under the control, directly or indirectly, of the PR and PL promoters (PL is similar to PR, but the promoter itself is not directly involved in cI regulation). When lambda exists as a prophage, its DNA is integrated into the host genome and most of its gene expression is repressed. This requires CI repression of PL and PR. When the viral DNA is first integrated, there is no CI in the cell (because it is a phage gene). Expression of cI is initially dependent on a different promoter (PRE), but I won't get into this here. Once CI concentration is high enough, it can bind to OR1 and OR2 as a tetramer. Binding here physically blocks the PR promoter and prevents expression of cro (CI acts as a repressor of PR here). It also interacts with RNAP (actually the sigma factor) and facilitates is binding to the PRM promoter, which leads to further cI expression. This process is commonly called recruitment: since CI is bound tightly to the DNA and has some affinity for RNAP, it can create a stronger interaction between the DNA and the RNAP-CI complex. Simply put, it induces the PRM promoter and is thus functioning as an activator of cI transcription. As CI concentration increases, it will bind OR3 more (which is located in the PRM promoter) and repress the PRM promoter by physically blocking RNAP from binding. In these ways, cI can autoregulate its expression level, both positively and negatively.
When the lysogen is in some kind of stressful condition, normal host processes will result in proteolysis of CI and its DNA/sigma binding domain is cleaved from the dimer- and tetramerization domains. This means that CI can no longer oligomerize and is no longer able to bind cooperatively to OR1 and OR2. The result is loss of PRM activation (leading to vastly reduced cI expression) and also a loss of PR repression (leading to cro expression). Cro can then bind OR3 and represses PRM. Lack of PR repression also allows expression of early phage genes (which are under the control of PR).
Note that a similar situation occurs at the PL promoter region, and binding of CI to both OR and OL as well as CI octomerization is important in prophage regulation, but that seems even further out of the scope of your question. Hopefully you can see how he lambda "repressor" actually functions as both a repressor and activator of transcription. If this kind of stuff interests you, I highly recommend a textbook called Molecular Biology of the Gene by Watson et al.
*See comments. Upon further research, the PRM and PR promoters both overlap OR2 (Autoregulation and Function of a Repressor in Bacteriophage Lambda, Ptashne et al.), as the diagram in the OP shows. It appears that the -35 region of both PRM and PR overlap OR2 by 2 and 3 base pairs, respectively. That led me to wonder that if CI binds to OR2, which is in PRM, wouldn't it physically inhibit RNAP binding and thus repress transcription? Well it appears that CI interacts with the same region of sigma that is responsible for binding the -35 region of PRM (Amino acid substitutions in the -35 recognition motif of sigma 70 that result in defects in phage lambda repressor-stimulated transcription, Kuldell and Hochschild). So instead of blocking sigma binding here, it enhances it.

I wish I could accept both answers, and upvote answers like this more than once. I'm accepting this one for its very clear description of the process, particularly the physical blocking of PR and CI interacting with the sigma factor. The only thing I'm confused about is that the paper I linked shows OR2 as located (?) or - rather - shared by both the PR and the PRM promoter (judging by the picture), while you wrote "OR1 and OR2 are located in the PR promoter, while OR3 is located in the PRM promoter".

The schematic I was looking at showed it that way, but perhaps I shouldn't have said it so definitively given the contradiction. Upon further research, you were right and I have updated the answer to reflect this. Thanks for pointing it out!

I'm tempted to say, "It's complicated."
CI does indeed act as both a repressor and activator. Transcription regulation in the lambda bacteriophage is quite complex for such a small system, so some confusion is understandable. Lewis et al. gives a rough description in a relatively recent paper (1):

The CI protein autoregulates its synthesis. At low cellular CI concentration, CI enhances its own synthesis from PRM; when high, CI
  represses PRM (1, 8, 9). It was originally believed that both positive
  and negative autoregulations are achieved exclusively by the action of
  CI dimers at the PRM-OR-PR sequence of the phage genome (1, 10) (Fig.
  1A), based on the following observations. (i) There is a hierarchy of
  intrinsic binding affinities of a CI dimer to individual operators
  sites: OR1 > OR2 > OR3 (11–17); (ii) CI bound to the intrinsically
  weak OR2 site is strengthened by cooperative interactions with CI
  bound to the stronger adjacent OR1 site, and the ensemble of two CI
  dimers at the OR1 ∼ OR2 sites represses PR and activates PRM (13, 16)
  (Fig. 1A); (iii) at high CI concentrations, a CI dimer can bind to the
  weakest operator site, OR3, repressing PRM (1, 2) (Fig. 1C).
  Incidentally, a second pair of CI dimers binds cooperatively to OL1 ∼
  OL2, and represses PL (7).

CI binding affects transcription of Lambda phage DNA through several mechanisms, including DNA looping between the OR operator sites at the Prm/Pr promoters and OL operator sites at the Pl promoter. The behaviour of an engineered transcription system derived from Lambda phage thus depends on whether the possibility of DNA looping between these sites are retained.
The discussion section gives addditional exposition:

Our study confirmed several predictions of previous investigators
  discussed above about the mechanism of autoactivation and
  autorepression of PRM by measuring in vitro transcription on
  supercoiled DNA templates containing different combinations of
  operator mutations. Our transcription data support the model that
  autoactivation requires CI binding to OR2, and that activation is
  stimulated by cooperative dimer–dimer and tetramer– tetramer
  interactions between CI molecules at OR2 and those bound to other
  operator subsites. First, cooperative interactions of CI not only
  occur between OR1 and OR2 in cis, as reported previously, but also
  between OR1 ∼ OR2 and OL1 ∼ OL2 in trans, resulting in individual site
  occupancies at lower CI concentrations as judged by their effects on
  PRM activation. The trans-cooperativity by octamer formation requires
  adjacent CI binding sites between OR1 ∼ OR2∕OL1 ∼ OL2 or OR1 ∼ OR2∕OL2
  ∼ OL3 and not OR1 ∼ OR2 and OL1 ∼ OL3 (Fig. S3 F and J). Similar
  trans-cooperativity between OR3 and OL3 is inferred from PRM
  repression at lower CI concentrations. Cooperative interactions lead
  to DNA looping when they occur between CI at OL and OR sites. PRM is
  autorepressed by the binding of CI to OR3 as reported previously
  (1–3), and this is stimulated by dimer–dimer and tetramer–tetramer
  interactions that occur through DNA looping. Our results are in
  agreement with Revet et al. (18) that looping per se strengthens the
  binding of CI to the suboperators (Fig. 5). Our work provided
  quantitative evaluation of the contribution of each operator to
  autoregulation.

Phew!
If you wish to accurately model the system described by Huang et al., I would look very closely at the circuit sequence and determine which parts of the lambda phage system are actually present. They may not have taken into account the latest knowledge about regulation of the Pr and Prm promoters when discussing their system.
On to the second question: When isolated and with no CI present, the Prm promoter may be used as a constitutive promoter (2). Under such conditions, the Prm promoter showed similar rates of transcription as the constitutive promoter ptet.

Great answer! Just one more thing: if the Prm promoter can be used as a constitutive promoter, why would it require CI for activation in the first place? Is the constitutive expression level too low without activation?

CI is just one component in the "gene circuit" that determines the lifecycle transitions in the Lamba phage. Expression from the different promoters need to be regulated for the circuit to operate properly, and if the promoter was "always on", it couldn't perform its function in that circuit. Consider an analogy to a computer: Transistors work by turning electrical current on and off, corresponding to 1s and 0s. You can't do any computing with constant current, and likewise a constitutive promoter is not very useful for creating a "genetic circuit".


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How can calcium be a kept as a local signal in the cytoplasm?
We went through this in my class last week and it doesn't make sense to me at all.
It's small and it diffuses in and out so easily so wouldn't it diffuse out quickly and thus not be a local signal? Or where it's stored in the RER does that change things?

Diffuse out of where? Ions cannot pass through the membrane.

I may try to write up a full answer later, but for a quick answer: calcium does not diffuse out of a cell ever, it actually takes a lot of effort for cells to keep their calcium concentrations so low. Instead, cells have a lot of calcium buffering capacity, so when calcium comes in it only stays free temporarily. That's when it has the opportunity to have influence. As it lingers and diffuses away from where it influxes, it is constantly being picked up by chelators, so it doesn't have a chance to diffuse away from a local signal at any high concentration.

Ions can only pass through channels in lipid membranes, such as voltage gated calcium channels at presynaptic membranes. That might clear up a bit of the confusion. Chelators bind free calcium ions, preventing them from interacting with other signalling molecules.

@BryanKrause — Please follow the injunction you read when you click on the comment box: do not use comments for answers. It breaks the SE model.

As @BryanKrause says in his comment, net flux of calcium would not ever be from inside the cell to outside the cell. There is a large gradient the other direction. Per Berg, the cytosolic concentration of calcium in a resting cell is on the order of 100nM, while extracellular concentration is in the mM range.
Signalling occurs when channels open up and allow $Ca^{2+}$ to diffuse down that very steep electrochemical gradient (from extracellular or topologically similar sources, e.g., the endoplasmic reticulum).
At least part of your question seems to involve a concern that the signal would not be very long lived. Though your concern about it diffusing out of the cell isn't warranted, the question about the time dynamics of calcium signalling is interesting. Calcium signals are, in fact, often very brief (though in other cases they last much longer). This is actually a benefit, and is one reason these signals can have very localized, very brief effects. For localized membrane fusion events, e.g., exocytosis, the signal lasts on the order of microseconds. The control of the time and position of a calcium signal involves a large number of players, including sequestering proteins, various compartments and stores, and tight control of the balance between calcium on and calcium off signals. It is discussed in this nature review, and summarized in this simplified figure:

You might also be interested in looking at some videos of calcium signalling. There are a number on youtube. This is one example

Calcium ions hold a +2 charge, and thus are unable to diffuse through lipid membranes. It is stored in the ER, and released to act as a signaling molecule in the cytoplasm. Being unable to cross membranes it remains in the cytoplasm until it is actively transported back into the ER.

Overall, decent answer, please add some references though.


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Is the worm brain understood?
Is the relationship between worm (C. elegans nematode or any worm) behavior and the worm brain understood? Is the learning technology within the worm brain understood? If so, what's a summary of the mathematical processes and biological implementations used? If not, what is the impediment to understanding?

Hi! This is an interesting question but you might have more success if you narrow it down to a specific question about worm or C. elegans brain function. It's also helpful to show you've done some research by summarizing what you already know so that answerers know where to begin with an explanation.

"Understood" is also incredibly broad and nearly impossible to actually obtain: you can read about the Dunning-Kruger effect. Or this image, which I happened to find just now unsourced on a LinkedIn blog but it is definitely not the original, there are dozens and dozens of variants on the same idea.


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How are oncogenes targeted for therapy?
How would oncogenes be targeted for therapy and are there any examples of existing therapies for such cancers if the gene was upregulated (i) as a result of copy number variation and (ii) due to increased promoter activity?

You mean by targeting the mutated gene in the cells or by targeting the gene product of the mutation?


text:
Neuston vs pleuston
I was recently reading about the wonderful chondrophores, and came across the terms "neuston" and "pleuston".  According to Wikipedia, "neuston" are "the organisms that float on the top of water ... or live right under the surface", while "pleuston" are "the organisms that live in the thin surface layer existing at the air-water interface of a body of water".
How are these terms used in the scientific literature?  Are pleuston considered a subset of neuston?  Some examples of organisms in one category but not the other would be helpful.


text:
Changing time and rpm of centifuge
Inspired by this question, I want to ask a question about centrifugation.
Suppose a protocol says : 10 min at 2500 rpm . Can we instead centifuge for 5 min at 5000 rpm or 20 min at 1250 rpm ?

No, it isn't that simple, because centrifugal force varies with the square of the rotor speed. Have a look at the Wikipedia page for clearing factor.
Those equations are usually used to determine what you need to do if you are going to use a different rotor, but they can also be used to solve your question.
Because you are looking at a situation where the same particles are being centrifuged, the sedimentation coefficient s is the same in both centrifuge runs. Also all of the factors relating to the rotor properties are the same (rmax etc.). So, if you have a set of conditions that work, t1 and RPM1, and you want to choose new conditions t2 and RPM2, you can use the equation:
RPM2 = SQRT(t1/t2) x RPM1
For the example you mention t1 = 10 min and RPM1 = 2500 rpm. If you change the time to 5 min:
RPM2 = SQRT(10/5) x 2500 = 3536 rpm
Because the centrifugal force varies with the square of the rotor speed you don't need to double the speed if you halve the time.

So what if it was RCF instead of RPM in the question, i.e.,10 min at 2500 x g? Thank you.


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What is the essence of difference of how different chemicals affect the same receptor?
It is known that various chemicals can bind to the same receptor type, producing different effects. Be these chemicals agonists or antagonists, there are more variations in how they influence the receptor than just sending an activation or inhibition signal. There seem to be various flavours of activation (not sure about inhibition), where, for example, a psychedelic drug binding to a serotonin receptor produces a different result than serotonin itself.
For a more clear representation, I have split the question into logical parts:

What is the essense of this difference? Does it come from the chemicals molecule properties like shape and electron configurations of the atoms?
If we were to draw two comparative pictures of how two such different chemicals affect a receptor, how would we picture that? What would we chose to be the characteristic figure(s) on our pictures? What qualities of the connection (probably changing over time) would we consider to display on the picture?

Does this question make sense or are there any false assumptions?
UPDATE:
Response to the comment by WYSIWYG: I cannot cite any source saying so. It is that I got this question at some point: is ligand-receptor activation a binary function, which can only give either 0 (no interaction or inhibition) or 1 (activation) values, or it is something more varied?
Taking into account that ligand-receptor interaction is molecule-molecule, it is logical to assume that the resulting complex can put the receptor molecule in a variety of states, depending on the ligand molecule structure. Here the Ionic Bonds and Hydrogen Bonds sections shed some light on this - the described interaction patterns seem like they can produce quite different results. Like, for example, they put receptors molecules electron cloud configurations in different states. But does in reality such interaction always result in either 0 or 1 state of the receptor?
The pdf paper refered from this question leaves the reader to guess: are the varying effects of the chemicals produced solely by their profile of different affinity to different groups of receptors, or do they also interact with each receptor type differently. In other words, is the drug effect produced by a certain amount of 1s being fired by the receptors, or is it changing the quality of their firing signal itself, i.e. making the receptor to initiate different, non-typical processes inside the cells?
Or, in the cited Wikipedia article, under section The specificity of drugs it is said that muscarine and nicotine can selectively activate specific subtypes of acetylcholine receptors. Is the result of these chemicals activating these receptors exactly the same as of acetylcholine? If we deliver both muscarine and nicotine to their sites, will they produce the same effect as if we deliver acetylcholine to both of them?
Also, I cannot really find much information on what lies beyond the receptor, namely - how does it send the signal somewhere else.. but I guess that's molecule-molecule again, so here we get the chance of varying result too. Or don't we?

Agonists primarily act by mimicking the actual ligand (molecular homology). They basically elicit the same effect as the actual molecule. Can you cite an example where two ligands binding to the same receptor elicit different responses. This seems theoretically possible depending on the signalling network downstream of the receptor.

@WYSIWYG: I have replied to your question in the update to the original question.

Search term you are looking for is "promiscuous". GPCR are very promiscuous. Look at these articles 1, 2, 3, 4. Similary you will find many explaining this common phenomenon.


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What does "cell type composition" mean?
I am reading an article about detection of differential methylation. They use the term "cell type composition" in the following context:
"Researchers need to carefully design studies that associate phenotypes with DNA methylation. Some aspects, such as cell type composition, cannot be readily controlled by design; patients and therefore individual DNA samples simply differ in their cell type composition." (Robinson, MD., 2014)
I would like to know to what "cell type composition" refers?
Does it refer to the composition of a specific cell-type in terms of its methylation pattern (or can it refer to something more general outside this context)? It makes sense to me that different cell-types should have different methylation patterns, that's why there are different cell-types in the first place. But is it that even within one specific cell-type, the composition of methylation pattern is different across different individuals?

The problem is that for most sequencing operations you nowadays still need more than one cell - even though this will change soon.
Accordingly, you have to sample cells from a tissue which often, if not usually, contains more than one cell type, see e.g. this picture from a lung tissue from the Wikipedia article on tissues linked above:

It is not always easy to pick cells of one type only (think of trying it with blood, which is a tissue as well). So what you then get is a mixture of different cell types which probably differ in methylation patterns.

Does it refer to the composition of a specific cell-type in terms of its methylation pattern (or can it refer to something more general outside this context)?

No, it means that you have cells of different types within your sample.

It makes sense to me that different cell-types should have different methylation patterns, that's why there are different cell-types in the first place.

At least one of the reasons, there are more, e.g. other modifications and mutations.

But is it that even within one specific cell-type, the composition of methylation pattern is different across different individuals?

That is a different problem and may also be true. But this is not what your quotation, as I understand it, refers to. They refer to the problem that you might sample the same tissue across patients but still get a different composition of cells from different types due to sampling error.


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Genetics - Ancestry DNA relationships
If my uncle and I both got our DNA tested and compared ancestry results, should we have 50% or 25% similarity? I get normally it would be 25% but since the mitochondrial DNA and Y chromosome are (mainly) used to figure this out using the test we did, shouldn't we share the same exact maternal DNA since it's my mom's brother and that doesn't recombine or anything and they got it from their mother? I just want to know if this is a different genetics problem than normal. Thanks!

This question would probably be better asked on Genealogy & Family HIstory SE.

The coefficient of relationship between you and your uncle is 25% (see wiki > coefficient of relationship for more info).
However, the percentage of similarity depends on the genetic diversity in the population of interest. If you were studying a population of fully homozygous clones (no genetic diversity), then no matter what the coefficient of relationship is between any two individuals, they would still be clones and therefore perfectly similar.

Usually relatedness is described via the coefficient of relationship because it is natural, relatively simple to calculate, and corresponds well to the actual amount of DNA likely to be inherited.  In this system, you are 50% related to your mother, and your mother is 50% related to her full brother (your uncle), so you are 50% $\times$ 50% $=$ 25% related to your uncle.
This measure is an expected value, the average amount of DNA inherited across a large number of instances.  A particular instance can vary from the measure due to randomness in the biological process.  Although the percentage from parent to child is always the same, more distant relationships are affected by genetic recombination resulting in a bell-curve distribution around the expected value.
The coefficient of relationship matches the biological behavior of the autosomes (nuclear chromosomes other than the sex chromosomes, X and Y), which contain the vast majority of the cell's DNA.  The behavior of the X and Y chromosomes and the mitochondrial chromosome differ, however, so this measure does not provide an exactly accurate expected value for all inherited DNA.

"... got our DNA tested and compared ancestry results ... since the mitochondrial DNA and Y chromosome are (mainly) used to
  figure this out using the test we did ..."

The above pieces of the question suggest a misunderstanding of DNA testing.  There are three main kinds of consumer DNA tests: one tests only a few characteristics of the Y chromosome, one a few characteristics of the mitochondrial chromosome, and one tests many characteristics of all the autosomes (and optionally the other chromosomes).  The first two are older and not used so much today.  The last is what is usually done today to indicate ancestry, and it provides results consistent with the coefficient of relationship measure.

Just a note regarding your last paragraph – Y-DNA testing is still a very popular test in genetic genealogy, especially surname studies.


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Umbrella term for "parts of the brain"
I am looking for an umbrella term for general "parts of the brain", esp. for (somehow arbitrary) "subsets of neurons".
For the tree of life there is an umbrella term for all kinds of taxonomic groups all down the tree. They are called taxa.
Domains, kingdoms, phylums all down to families, genus, and species are taxa:

In brain sciences there seems to be no such umbrella term which is generally agreed upon.
Which term would best include all of the following?

brain hemispheres
coarse brain subdivisions (cerebellum, cerebrum, ...)
cerebral lobes (frontal, parietal, ...)
the thalamus („a large mass of gray matter“)
nuclei (thalamic, ...)
Brodman areas
cortical layers
cortical columns
the limbic system
regions of interest (in fMRI)

All of these immediate suggestions don't fit perfectly:

(brain) region
(brain) division
(brain) area
(brain) volume
(neural) group
(functional) system

When you just want to list the components of the brain, that is to say what the brain consists of from the gross anatomy perspective, you can say that the main parts of the brain are:

cerebrum
cerebellum
brainstem

You can also say that the parts of the brain are some smaller, but anatomically well defined components, such as the pineal gland and pituitary gland.
When you intend to describe the functions of anatomically well defined brain areas, you can say that the brain structures are cerebral lobes, thalamus, hypothalamus, hypocampus, amygdala, putamen, corpus callosum, cyngulate gyrus, etc.
A part is "a portion or division of a whole that is separate or distinct; piece. A structure is "mode of building, construction, or organization; arrangement of parts, elements, or constituents." So, it's not about what "it is," but about how you look at it. A thalamus is a part of brain and is a structure made of several nuclei...
You can see these terms used very differently in various texts, but a short overview of brain anatomy by Mayfield clinic use them in the same way as I did. These terms are not a part of any official classification in neurology.

This fits perfectly, for the moment. So, to call a cortical column a (anatomical) "part" would be OK, but also to call it a (functional) "structure"? I can go on with this, thanks for your "opinion", which surely is not an arbitrary one.

It's nothing written in stone here. My impression is that "parts" are used to describe anatomy and "structures" to describe physiology.  To me, it sounds fine if you say that a hemisphere is a part; saying it's a structure sounds awkward, because a hemisphere as such does not really "do" anything. Thalamus can be both a part and a structure if you want.

And what about cortical columns being a part? How does this sound in your ears?

Interesting enough, thank you for the clarification - even though it still might be not written in stone, right? And why do you say cortical columns are not "(functional) structures". At least they are considered "functional units", aren't they?

OK, particular cortical columns can be associated with particular functions, so if you insist, they could be brain structures. A "part" is a "piece" in the sense that you can disassemble a complex thing, lie a car, into clearly defined pieces. When it comes to brain, you can say something is a part when you just want to mention it as part of the bigger brain. If you want to describe it from inside, you can say a structure. It's about the perspective not what "it is."

Gerstner et al. in their splendid book Neuronal Dynamics use the term neuronal populations as a synonym for "groups of neurons", e.g. in chapter 12:

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


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This strange spiral creature grew up in my cup of water after night
This grew up in my water cup over night!

Length ~ 12mm
Form - spiral made of dark dots
It does not move
Growing slowly

Can some one help identify it?

I would guess these are eggs of some animal. Just a wild guess.

Can you give us a location as well?

Yes, of course! https://www.google.com/maps/@46.3494507,48.0312648,332m/data=!3m1!1e3

Wow, what a precise location :D I didn't know that there was a city with such a name, only knew the fur with this name! For how much time that speak would grow? Did it happen something afterwards?

It was expanding for 20-30 hours, then almost completely disappeared in water.

See my comment on this question

Definitely eggs since it appeared so quickly. Caddisflies (Trichoptera) lay their eggs in spirals within a slimy blob, but some searching made me see that other animals do too. Like this https://bugguide.net/node/view/641162 that apparantly comes from midges. Perhaps someone else can come closer!

@picapicaThank you! We have a lot of Caddisflies and Chironominaes here, great guess!

It appears like the egg mass of some Chironominae species. At least searching "Chironomus eggs" returns visually similar images. @picapica can you post an answer?

See this SO question for an answer to a related question, which points to Chironomous egg masses.


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What is the name of this injured species?
Location: South India
Size: 2-3cm
looks like injured species, unable to stand.

It's a sort of scarab, though which will be hard to pinpoint. It's not injured, they're just clumsy.

Well, after a lot of research, I hardy believe that it is a Rhizotrogus aestivus. First of all, the size (2-3cm) you mentioned fits exactly. Secondly, the colour matches fair enough. Finally the antennas and the body shape, may not be seen very well in the picture but I assume that they match. The only thing that I am not sure is the "laziness" of that insect, beacause they are only lazy or clumsy and not active, only when they are about to die.
For more informations check here: https://inpn.mnhn.fr/espece/cd_nom/10907?lg=en


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What kind of ribes is this?
I have a plant in my USDA zone 5 garden that appears to be in the ribes genus.

Details:

The location is east of Toronto (Ontario, Canada).
The plant is currently flowering (today is May 18th, 2019).
It is approx 4 feet tall.
The plant flowers every year, but does not set fruit (not self-fruitful).

More photos here:

https://i.sstatic.net/coEp5.jpg
https://i.sstatic.net/wv0TA.jpg
https://i.sstatic.net/pFmtk.jpg
https://i.sstatic.net/KvjGe.jpg

What species is it?

I think this is Ribes americanum or wild black currant.
I'm basing this on page 306 of Newcomb's Wildflower Guide, an excellent source for the Eastern US and some of Canada.  On that page we have two main choices:

Base of flowers prickly or bristly... or

Base of flowers not prickly or bristly...

Your excellent pictures suggest that your specimen is in category 2.
From there, we have:

a. Flowers solitary or 2-3 in a cluster; branches bearing a few thorns. or
b. Flowers 5 or more in racemes.

Your specimen looks to have quite a few flowers, so in category 2b we have a choice of Ribes americanum:

Whitish or yellowish flowers, longer than wide (and fruit black, you can check later I guess),

or Ribes sativum:

Greenish flowers, wider than long (and fruit red).

Color in the white/green/yellow range is a bit subjective, but your flowers look longer than wide, hence Ribes americanum.
Of course, with this in mind you might re-inspect the plant and refine this a bit.

I'm glad the photos worked out. I was just using an old phone camera. The key seemed to be to take lots of photos; one of them was bound to be in focus. :)


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Extremely Scientific Sexual Education Material?
I'm trying to prepare material for 'the talk' about sex and reproduction. I know there's plenty of great books and resources out there for young readers, which I'll use to start with, but I'm also looking for something overbearingly scientific.
Essentially, I'm looking for an academic-level resource that is as close as possible to a literal play-by-play second-by-second explanation of puberty and the entire reproductive cycle. This is partly to polish my understanding, and to prepare myself for unexpected questions.
For example, it should explain the mechanics that sperm/egg cell(s) use to get around, how sperm penetrates the ovum, the process of breast development, and how they become lactation-ready, how the milk is made, what controls where adult body hair grows, the chemical process leading to feelings of lust, etc.
I was mentally reviewing my knowledge of this the other day and realized I know a lot of 'what' but not 'how' or 'why', so here I am.
Multiple books/resources is fine.


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Help with molar ratio
What is meant when asked write molar ratios in 3 parts? For example I am currently assembling a vector that requires annealing several oligos to two pcr fragments prior to ligating them into my vector; which will be used for future transformations. I was told to "assemble the annealed oligos with the 2 pcr fragments. Use a 100:1:1 molar ratio of annealed oligos:each pcr fragment." I'm thinking this means- concentrated oligos:diluted pcr frag #1:diluted pcr fragment #2. I am confused about how to determine the final concentrations of my pcr fragments in relation to the concentrated/undiluted annealed oligos. Why? Because I only know their concentrations as ng/uL not as 5x, 2x or 1x. Should I calculate it as 1(part) divided by 102 (whole) for each fragment? Then multiply that number by the actual concentration of my pcr fragments.
I am sure the answer to this is probably simple but I'm sorry I don't understand it and am hoping someone helps me with understanding calculations of this sort. Thanks.

The whole point of this problem is that for each 100 molecules of annealed oligos, you need to have one molecule of each fragment.
You need to take into account the following:
The MW of each fragment is approximately proportional to the length of the fragment. Thus if you divide the concentration by the length of each fragment, you can get a value that simulates the molarity, meaning that you can use these values to fix to the ratio that you are asked between the different fragments.
For example, if the fragment1 is 100 bp and you have 10ng/µl, fragment2 is 200 bp with the same concentration, then you need to add 1 volume of fragment1 and 2 volumes of fragment2 to get the 1:1 molar ration.
In a similar way, you can calculate the amount of oligos added to have 100x more (of the ratio of concentration to bp length) than the respective fragments.


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what is the difference between pituitary dwarfism and thyroid dwarfism?
My book (Comprehensive Biology class XI, by J P Sharma ) mentions of two kinds of dwarfism- "Pituitary Dwarfism" and "Thyroid Dwarfism" but does not provide any details about the matter. so please help me.

Did you do and searches of your own (what did you find when you Googled the terms?) Please share what you found, then someone might fill in the details which are missing.

How can this be a homework question? The matter is quite confusing so I asked that. :O :(

Pituitary Dwarfism is a condition where less amount of growth hormone results in abnormally slow growth and short stature. Growth hormone is released under the influence of hypothalamic growth hormone-releasing hormone(GHRH), and is inhibited by hypothalamic somatostatin. Growth hormone deficiency has different negative effects if happens according to age it manifests;  in newborn, the primary manifestations may be hypoglycemia, while in later infancy and childhood, growth failure is more likely. Growth hormone deficiency can be congenital or acquired. It is usually permanent, sometimes transient.
Thyroid dwarfism is a condition arising from the deficiency of a thyroid hormone. It happens when there is lesser thyroid hormone secretion (defect of manufacturing or lesser supply of Iodine) before attaining the full development congenitally. It causes retarded growth and development of bones with disproportionate body proportions (that's dwarfism ).


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How does P-protein (phloem) help in sealing of wounds?
While I was reading a book I found that "P-proteins in the sieve elements of phloem help in sealing  of wounds along with callose".
So how does p-protein do that, moreover how can it reach to other parts of plant body in order to seal the wounds?

The endoplasmic reticulum produces phloem proteins, also known as p-proteins, which are situated next to the inner surface of the plasma membrane of sieve tube elements (together with organelles). When it comes to the question "How do they reach the wounded area," the answer is as follows: once sieve tube members are injured, phloem sap seeps out of the sieve tube and begins to leak. This causes a drag on the p-proteins (perhaps due to increased pressure).   These p-proteins are filamentous, so as they migrate to the wounded sieve tube member, they aggregate on the sieve pores, blocking the transport of phloem sap to the injured cell and preventing leakage.
Source: https://www.toppr.com/ask/question/what-is-the-function-of-pprotein-and-callose-protein-in-the-conduction-of-food-from/
And:
https://link.springer.com/chapter/10.1007/978-3-642-74445-7_13 with some modification for clarification.
If you still didn't get it, I will explain it in a more detail.

Welcome. Please correct the language use (punctuation is lacking, capitals are missing etc etc) and add some links to your answer to credible sources so people can background read on your post

I have edited it but there is still no comment or up voting on my answer at least say something


text:
is there a constant leakage current across axon even in absence of stimuli?
because of resting potential is their a constant leakage current across membrane due to resistance of membrane and ion pumps continuously pump restore the resting potential ?

yes - and now I have to fill up the minimal amount of characters

Have a look here  -  http://biology.stackexchange.com/questions/36123/if-the-average-resting-potential-of-a-neuron-is-70-mv-why-is-there-such-a-high/36127#36127


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Plants that are siblings: How does this impact pollination?
A friend has two cherry bushes (prunus tomentosa). Prunus tomentosa is said to be partially self-fertile, but benefits from cross-pollination.
The two cherry bushes set fruit, and so my friend saves me two seeds. I plant the seeds at my house, which is miles away from his, and now have two bushes of my own. They are in bloom.
My cherry bushes are siblings. How will this impact their ability to pollinate?

I've used a specific species in my example, but that doesn't mean the answer needs to be species-specific. An answer about plants in general would be fine.

You might get better results on the gardening site for your specific situation. @Remi.b's answer is good for the general biology but going into all the possibilities might be a little too broad. For example, for apples, it is common to add a granny smith tree since it crosses well with a lot of the other varieties people grow. However, if your friends' two bushes were either self-fertile or cross-fertile enough to set fruit I think you are likely in good shape. Another alternative would be if your friend is willing to give you cuttings from their bushes.

In your case, your two bushes might well be half sib (the pollen might come from different donor) and one (or maybe even both) bush might result from selfing event. In any case, if the species is able to self, I don't see why full sib mating would cause any trouble.
Many species protect themselves from selfing. These plants are said to be self-incompatible. The evolution of the genetic mechanism underlying such self-incompatibility has been highly studied and is fascinating. The wikipedia article offers a good overview.


text:
Mystery rodent in Winnipeg
I spotted this rodent in Winnipeg, Manitoba, Canada on September 6, 2020.
It is about 10 inches long.

What is it?

That is a Franklin's Ground Squirrel

Winnipeg is part of its range:

Have a look at a gallery of such photos here: https://inaturalist.ca/taxa/179937-Poliocitellus-franklinii/browse_photos


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Shrub in open gravel field

Location: Gravelly open field. East of Toronto.
Date: August 4, 2022
Description: Shrub; alternating leaves; 8 feet tall; trunk is 1.5 inches wide at the base.
Tip: It's possible to zoom in on the photos by clicking them a couple of times

Almost certainly Hawthorn (Crataegus) genus. This is a fairly common genus of flowering and fruiting shrubs to small trees that produce white flowers in the spring and small red apple-shaped (pome) fruit in autumn. Species are found wild all over the Northern Hemisphere and are invasive in a number of countries in the Southern Hemisphere.
They are characteristically quite thorny (as you can see in your photos 2 and 3), with the spikes being actually short stems. Leaves arise from the short spurs off stems and several species have deeply lobed and/or serrated leaves (leaves have both in your photos).
There are quite a few species, but which one this is, I don't know.