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Why do NK cells not destroy bacteria, even though bacteria don't have MHC-I?
Part of the function of NK cells is to destroy cells that are unable to bind their KIR receptors. Or in other words, cells that don't express MHC class I. This is why they can kill MHC supressed infected- or tumor cells, which other immune cells can't.
However bacteria also don't express MHC-I. Yet NK cells are said to have very limited influence one microbial infections. I do not understand why NK cells do not degranulate (kill) bacteria upon finding that they do not have the MHC-I receptor complex.
Could someone elaborate this?

Human cells and bacteria are VERY different. Maybe an analogy would by be a police unit instructed to check in on all houses that don't have letter boxes. If they come across an area with tents, shacks or similar (which obviously don't have letter boxes) they'll still ignore it, just because those aren't houses in the first place.

While you’re correct that NK cells are often activated (in part) by the absence of MHC-I, they require other signaling events to become fully activated:

The Molecular Mechanism of Natural Killer Cells Function and Its Importance in Cancer Immunotherapy. Paul & Lal. Frontiers in Immunology. 2017.
Activating Receptors on NK Cells
Lack of MHC class I on the target cell is not sufficient to trigger NK cell activation. Full NK cell activation also requires recognition of stress-induced molecules by NK cell activating receptors.
Natural cytotoxicity receptors (NCRs) are another immunoglobulin superfamily of activating receptors that utilize extracellular immunoglobulin-like domain for ligand binding. Human NK cells express three distinct types of NCRs... NCRs recognize a wide variety of ligands on target cells ranging from viral, bacterial and parasite proteins to molecules from tumor cells and other host cells.
Role of natural killer cells in antibacterial immunity. Schmidt et al. Expert Review of Hematology. 2016.
6 Bacteria fight back and inhibit NK cell activities
During evolution, many bacteria have developed survival strategies which counteract NK cell activity.
Both Gram-positive bacteria such as Streptococcus pneumoniae and Gram-negative bacteria such as Salmonella spp and Escherichia coli are able to induce prostaglandin E2 (PGE2), which negatively affects NK cell functions at different levels. PGE2 inhibits the cytolytic activities of NK cells by suppressing their responsiveness to cytokines such as IL-12 and IL-15, and suppresses NK cell mediated activation of macrophages by inhibiting the production of IFN-γ. Similarly, PGE2 has a deleterious effect on homing, migration, and survival of NK cells, as it has been shown in Human Herpes Virus 8 (HHV8) infection.
  Thus, bacteria are able to inhibit both cytotoxic and immunoregulatory effects of NK cells in various ways.
8 Conclusions
In conclusion, there is a growing body of evidence that NK cells play an important role in the antibacterial host response. NK cells are able to kill bacteria directly, or to modulate the immune system via cytokines and interferons. Further studies are needed to characterize how NK cells are activated by different bacteria. In addition, the role of NK cells among the other arms of the immune system in the defense against bacteria is poorly understood. Last, bacteria are able to inhibit NK cell activities, and a better understanding of this impairment may be the basis to specifically strengthen the antibacterial host response. Therefore, additional in vitro and in vivo data may open new therapeutic strategies using NK cells to fight bacterial infections.

If you’d like a full-text copy of the Schmidt paper, I can share it with you.


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What is the difference between DNA vs RNA Editing in the context of gene therapy?
As a someone with beginner knowledge on biology, I have come across the terms "RNA editing".
Take this paper for example : RNA Editing with CRISPR-Cas13
From my understanding, DNA -> RNA -> Proteins
If we use a vector for delivering a gene to a cell in-vivo, does it mean that corrections aren't permanent for RNA edits?

There are several differences, both mechanistically and functionally.

DNA edits are heritable by the daughter cells and are therefore permanent whereas RNA edits are not.
The type of Cas protein used in the editing process for DNA and RNA are different.
In the paper that you linked the authors have fused an RNA editing enzyme (ADAR) with dCas13 (a variant that does not cleave the target). So the CRISPR-Cas system directs ADAR to the sites on RNA that need to be edited. Usually when editing the DNA with CRISPR-Cas, people rely on the ability of the complex to cleave the DNA. This double strand break may be then repaired using different pathways (NHEJ and HR) during which editing happens. See these posts for more details:       How is the type of genetic manipulation determined in CRISPR-Cas9?       Mutations/deletions with CRISPR       How does NHEJ cause indels?
It is also possible to edit DNA in a way that does not involve cutting of the DNA. These techniques use similar principle as in the case of RNA editing described in the paper that you linked (see the abstract and introduction of this paper). However, if you cut the RNA, then it will be completely degraded instead of being repaired.

+1 on the answer overall, but should probably clarify that only some DNA edits are heritable (whereas RNA edits are generally not). There’re important conversations about somatic (non-heritable) and germine (heritable) gene editing, and both of those are DNA cuts, I believe.

@CalendarJ By heritable, I meant the daughter cells of a cell, not the entire organism.

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How does isometric contraction work?

What exactly happens to myosin during isometric contraction? I suspect that either myosin heads just "freeze" in the middle of crossbridge cycle, or go through full crossbridge cycles repeatedly at the perfect rate so that the rate of extension becomes equal the rate of contraction (basically, a muscle isn't still, but repeatedly extends by like <1mm, and then myosin immediately contracts to compensate for this extension to keep muscle at static length - and so back'n'forth it goes).
Why isometric contractions spend energy, when physics make it clear that energy is spent only when we change velocity of something? If my second hypothesis is true and the muscle isn't in fact still, then energy is obviously being spent. But if myosin heads freeze in the middle of the cycle glued to actin, there's no reason why energy should be spent.
Say, a person is trying to lift a 10-ton rock with all the strength they got.  It's also an isometric contraction, but in this case, the second hypothesis shouldn't work, because if myosin could finish a crossbridge cycle under such resistance, it would mean that the muscle is strong enough to lift the rock. So in this case, it must get stuck mid-cycle, with the mass of the rock not letting it to finish its conformation change. If so, then why do muscles spend energy then? Myosin is literally stuck in place, and until it finishes a cycle, it won't bind another ATP.

regarding point 3 have a look at this: https://biology.stackexchange.com/questions/44019/doesnt-the-sarcomere-contract-during-isometric-contraction?rq=1 even though if myosin could finish the cycle, it doesn't necessary mean it could lift(the weight) in isometric conditions.

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Liquid that comes out raw mangoes
What is the composition of the liquid that comes out of a raw mango when you break it off from its stem? It oozes out some sort of juicy liquid. Any idea what that is?
Also, is it edible?

It is the sap; you can see the composition of the sap (of Indian mangoes) in this article. Some plants also produce latex from injury sites. The mango sap is not supposed to be eaten as it can irritate the skin; a condition referred to as Mango Dermatitis.


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Does eating hard food really cause wisdom teeth to erupt properly?
According to the article Bad molars? The origins of wisdom teeth, in our evolutionary history, people were eating harder food like nuts and had unimpacted wisdom teeth. Later, that article appears to have jumped to the conclusion that if you eat hard food, that can actually cause your wisdom teeth to erupt properly. I don't see any reason for that conclusion. Maybe they made that mistake because it's a reasonable mistake to make but it's actually not true. I think that in our evolutionary history, people reproduced at the age of about 14. Although at the age of 28, I started getting an infection from an impacted wisdom tooth and had to have it removed, that was probably already nearly grandparent age according to our evolutionary history and that explains why the natural selection against that type of problem at that age was weak. Maybe after we started eating soft food, we had an evolutionary advantage in having a smaller jaw but the evoluionary cost in having a smaller jaw was smaller because we could just evolve to slow down the growth of the wisdom teeth to delay the potential problems it causes to grandparent age. Just because a change in diet affected the way we evolved doesn't mean a person's actions affects the way their own body grows at the individual level. I do realize that it some cases, ones own actions affects the way their body grows.
You may be thinking "Why didn't you ask the question 'Why did we evolve to have impacted wisdom teeth when it sometimes causes a severe infection?' before asking this one? You could have used its answer to help you ask this one better." I could do that but then I would just end up explaining that I Google searched "why did we evolve to have crowded wisdom teeth if it can lead to infection" and then got the article Bad molars? The origins of wisdom teeth as the first search result. That's the very article I linked earlier in this question that I explained why I suspect is inaccurate. I don't think it would have been better to ask that question first and then explain how the first search result didn't answer my question when that search result is in fact inaccurate. If the question I have can be answered, some way of asking a sequence of questions and picking which Stack Exchange website to ask each of them on that will get me an answer to the question I have has to be accepted.

Now I see that they just said chewing hard food can't hurt and science does not yet know if it will actually work. I guess it's fine that I asked this question because I didn't realize at the time I asked it that the article said that and then looked back and saw that it said that but if I had read it carefully in the first place, there would have been no need to ask this question at all. I guess now that I've asked it, it's better to leave it the way it is instead of correcting it to explain what the article really says because if I fix it up in that way, people will just think I'm a jokester

who asks totally useless questions.

This is a good question, questioning your assumptions is a major part of establishing the validity of a hypothesis.

Yes
The relative size and robustness of the jaw does appear to be strongly affected by diet, significantly more so than other parts of the skull. This is not that surprising many developmental pathways interact with physical activity. Bones in particular often rely on a certain amount of stress to develop properly. It is not all that different from low scale bone atrophy.
Size of the jaw of course effects how much space there is for wisdom teeth. As for the evolutionary effect, consider we have only had access to soft processed food on any scale in the last few generation, that is not much time evolutionarily.
Source


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What is the most detailed living-tissue scan available
There are a lot of ways to scan living tissue. What is the most detailed one to date? What kinds of resolutions can it produce? Is there a different answer for 2D vs 3D?

I assume you are asking what is the most high-resolution in vivo imaging that science has performed to date?
I think the best way to answer such questions is to explain the nature of the question.
This depends a lot on what kind of sample you are interested in for the question to address. It also depends on whether we are talking about time (temporal) or space (spatial) resolution, because there is usually a trade-off for imaging methods. Some things we can image with femtosecond resolution, and other things we can with femtometer precision.
What property do you want to look at? Is it a certain staining, such as a fluorescent marker? The topography of a molecule sitting on a membrane? The force generated by a motor protein?
Do you consider a reconstructed image (in 3D) from 2D slices to be a fair comparison with techniques that aim to directly image in 3D? Microscopy and imaging are quite advanced fields and we're only beginning to scratch the surface.
Some more considerations for the questioner: is your sample moving? Are we talking about imaging insects hovering near flowers, or anesthetized flatworms? What scale of the sample is being imaged? What are the requirements for keeping it alive during imaging? For instance, perfusing nutrients or imaging a microbe growing on a substrate normally requires the modification of your microscope in such a way that may limit your optical resolution. Imaging some things necessarily requires long working distance objectives, while other specimen may be visualized at short working distances. These have tremendous impact on resolution!
As a case study: let's say we are interested in looking at the human brain with high resolution. You can do this with high temporal resolution (using EEG) or with high spatial resolution using magnetic resonance! Or are you interested in the resolution of real time activity of the brain, as measured via oxygen delivery to regions? This is not possible with either of the above; you have to rely on functional imaging, e.g. fMRI!

Whew. That is a lot more complex than I had thought. I think you have given me enough info to construct a much better question, though. I may open another one here or perhaps take this over to Quora, since my inquiry may be a bit loose for stack.

Also please know I was a little pendantic in my response, I was hoping others would cover the basics. My two cents: live imaging of cells can go down to single-molecule resolution, if it's a fluorophore. Here's a review for single-molecule imaging methods in neurons. You have stuff like atomic force microscopy which are also feasible for living tissues. Notice that the 'best' spatial resolutions are achieved with electron microscopy and x-crystallography, but these are not performed on living specimen. Good luck! :-)


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Number of DNA strands per chromosome
As I was reading Griffith's Introduction to genetic analysis this evidence was provided for single DNA makes single chromosome.
Eventually geneticists demonstrated directly that certain chromosomes contain single DNA molecules. One strategy was to use pulsed field gel electrophoresis, a specialized electrophoretic technique for separating very long DNA molecules by size. The extracted DNA of an organism with relatively small chromosomes, such as the fungus Neurospora, is subjected to electrophoresis for long periods of time in this apparatus. The number of bands that appear on the gel is equal to the number of chromosomes (seven, for Neurospora).
(Page 86).
This points to the fact that one chromosome has single DNA. What I want to know is that what evidence is there that each chromosome is not made up of multiple similar sized DNA molecules all coiled together to give a single chromosome so that the number of different types of DNA molecules to number of chromosomes have ratio one to one but one type of DNA molecule's multiple copies makes one chromosome.

I don't have a copy of Griffith, so I can't check myself. But are you sure that the experiment he describes is not to demonstrate that each Neurospora chromosome is made of one dsDNA molecule (two strands, incidentally) of length 10 arbitrary units, say, rather than three different dsDNA molecules of length 1 + 3 + 6, say. The question you ask is quite valid, but, I imagine, addressed in earlier in other ways, especially in bacteria.

I think that this and along with some other experiments given in Griffith tries to proves both of these points.

I doubt it. I don’t know the answer for certain, but it seems to me that electron microscopy of bacterial chromosomes (no complications of chromosomal proteins) with size markers might have been a possible approach. Pulse field gel electrophoresis separates chromosomes by size but I don’t think it answers your question. I’d offer to research it for you, but I have other fish to fry at the moment.

What do you mean by "coiled together"? I guess you mean kept together by some non-DNA material, i.e. proteins. Proteins are removed using proteinase k or something similar, so this would break any protein fostered coiling between the molecules and you will see a crazily small chromosome. You can find an example of this kind of experiments ehre (http://www.scielo.br/scielo.php?script=sci_arttext&pid=S1516-89132005000100001) and some reading and exercises here: https://www.ncbi.nlm.nih.gov/books/NBK21330/


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Why are (some) male humans sexually attracted to the breasts of female humans?
Many male humans are sexually attracted to the breasts of female humans. Is there an evolutionary reason for this?

They aren't so much if they are not hidden, i.e. rainforest and old african tribes.

breasts are a signal of fecundity, puberty, age, fitness... plus, if you look at chimp and oprang breasts, they are pretty similar when breastfeeding.

This question is quite misinformed and problematic. 1. It doesn't mean anything to be sexually attracted to a non-reproductive part (like secondary chars. described below). 2. Attraction (perhaps 'mate preference' is better) is not reductionistic, as implied, where the opposite sex is reduced into parts. 3. Sexual selection worked differently across human populations. 4. There is definitely no basis in evolution for the question. As written below, there are evolutionary reasons for breasts and hypotheses as to why they unique in humans, but this is very different than what was asked here.

@Chris Moore How could this question be reworded to make sense? Being outside the field of evolutionary biology, I don't understand your critique. I think this comment could be usefully expanded into a great answer while still addressing the general question being asked even if it is misinformed.

Short answer, we don't know.
There are several competing hypotheses but they are all nearly impossible to test.  Behavior often suffers the same problem as testing, we can come up with a hypothetical reason but since we are the only organism that does it, we have no good testing options. We can't put people in controlled conditions for generations and see if their preferences change. Secondary sexual characteristics in general have problems with testing. Because there is no good way to differentiate reasons for a behavior. We still don't have a great consensus on why secondary sexual characteristics in humans exist, likely because many explanations can be true at the same time, humans have very complex behavior even in out instinctual behavior.  It could just be a quirk of neurochemistry caused X to be attractive, followed by run away selection, and that by itself would create a selective advantage. It can be really hard to test why a preference would arise unless the advantage is obvious because the different hypotheses all behave the same way in practice.
Possible answers include:
-lifting the nipple away from the body to make suckling easier for flat-faced human babies with protruding noses.
-runaway sexual selection (which is also a component of many others as well).
-cryptic signalling of ovulation and/or pregnancy.
-all of the above
Paper reviewing all the different hypotheses

@kmm how is that.

This is a hypothesis that I found in Desmond Morris book, The naked ape.
Basically, humans transit from a rear-penetration position to a frontal-penetration position. In this transition, the sexual clue performs by buttocks was perform now by breast.
In short, according to Morris: breasts are sexual clues because they look like buttocks.

Please, if downvote, explain in a comment why. I understand that this could be a controversial hypothesis, as such, in need to be discussed.

https://www.theguardian.com/science/2017/sep/24/the-naked-ape-at-50-desmond-morris-four-experts-assess-impact

Very good analysis of Morris book. It makes clear that it is loaded of misogynists views. Whit respect for the subject in the discussion, we read: Did boobs replace bums as a sexual signal when we became upright? I don’t know, but the point is that no one does. According to this,  there is no scientific evidence for the hypothesis (nor to confirm or denied it).


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Identify My Spider

I live in Littleton Colorado and caught this spider because I haven't seen it before. Any idea what it is?

That's a male Dysdera crocata, a.k.a, "Woodlouse Hunter". They can be a little aggressive and might try to bite you if handled but they're no more harmful than a common bee sting (even less so actually since they won't potentially cause an allergic reaction).

Awesome, thanks for identifying it for me.


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Question about osmosis

The concentration of water outside potatoes B and C is  more than the concentration of water inside the potatoes. So water will flow inside the potato. Now, since the concentration of water in the hollowed portions is less, water will move inside the hollowed portion and hence fill the hollowed portion of potatoes B and C. I think since potato D is boiled and hence it's cells are dead it can't perform Osmosis and water does not fill inside the hollowed portion of potato D. Is my reasoning correct ? And I can't get why there won't be any water in hollowed portion of potato A. Is it that the hollowed portion of potato A does not contain any solution so no water would go there and if this reasoning is correct then it implies that osmosis is only possible when there are two solutions with different concentrations and not in any other case ?

Please do not post text as images. It is not searchable or indexed, and cannot be read with accessibility devices.

I’m voting to close this question because it is: 1) an (unlabeled) homework question with insufficient research (e.g. looking up a definition of osmosis), 2) contains text as image (despite the OP being advised against this), and 3) would have been best posted in [Chemistry.SE].

Osmosis is actually taking place between the sugar/ salt solution and the cytoplasm inside the potato cells. Or if you want to expand more on this, then water is flowing first from the water in the trough to inside the cells, and then from the cells into the solution present in the hollow of the potato
Osmosis occurs in cup b and c because the sugar or salt makes a concentrated solution which is hypertonic to the cytoplasm, hence water flows out through partially permeable cell membrane by osmosis.
Cup a is an experimental control. It contains no sugar/salt so it can be proven that it was the concentration difference between the solutions that was causing osmosis. No sugar means no solution, just nothing over there(no water , no sugar, no salt, no solution) so osmosis can't occur.
As far as D is concerned, you are wrong that osmosis requires being alive. Osmosis is a natural passive/automatic process, it can happen in dead things too. It's hard to say what can be causing the osmosis to stop. The best guess would be that boiling damages the cell membranes of the potatoes so that aquaporins(water channels in the cell membrane through which water flows naturally by osmosis) are destroyed. Thus the water can't flow through the damages cell membrane.

Oh! So there must be two solutions separated by a semi permeable membrane for osmosis to occur.


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Difference between cerebroside and globoside
I have a general idea about their difference that cerebrosides have a single sugar while globosides have more than one sugars.

This is the structure of a ceramide (syphingosine and a fatty acid linked through amide linkage).
It's not clear to me that do cerebrosides have a single monosaccharide on only one -OH group of the syphingosine, two monosaccharides on each of the two -OH groups, or one oligosaccharide on only one -OH group.
Likewise I am not sure if globosides have a single oligosaccharide on only one - OH group of syphingosine, or two monosaccharides on each of the two -OH groups, or two oligosaccharides on each of the two -OH group.
If you have any knowledge about this, please share. Thanks.

This is Encyclopedia about cerebroside

https://www.guidechem.com/dictionary_keys_cerebroside-p1.html
and this is about globoside

https://www.guidechem.com/dictionary_keys_globoside-p1.html
https://en.wikipedia.org/wiki/Globoside
I hope this can help you.

We're looking for long answers that provide some explanation and context. Don't just give a one-line answer; explain why your answer is right, ideally with citations. Answers that don't include explanations may be removed.


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Frog bloated with pool water
I found a gray tree frog in pool skimmer basket, he seems quite alive but terribly bloated with water. I tried holding it upside down a bit to see if some water would come out but only a few drops. Any ideas if there's anything I can do, or just let nature take it's course maybe he'll survive if given enough time without predators (cats and birds and whatever, around here in Ottawa Ontario).

I have no expertise in this, but it could be the pool chemicals were absorbed and caused this, and if so allowing it access to a large amount of fresh (nonpool) water might give it the best chance to survive.

I'm voting to close this question as off-topic because it is trivial. This site is for academics, researchers and students of biology. It is not an animal rescue society.

I can't say if the question is trivial but there can be multiple possibilities for why the frog is bloated. Unless you provide some additional details providing a conclusive answer would be difficult. However, it seems that the frog is affected by chlorine in water. Nonetheless, we consider personal medical questions and health advice for both humans and animals, as off-topic.

Most frogs die in minutes in chlorinated swimming pool water , after some time they will swell with gas. I have pulled toads out of pools and they have survived ; I assume their dry skin is less permeable to pool chemicals than frogs.

The pool is salt based, i.e. you don't usually smell chlorine after swimming. And the only chemicals in it were a bit of shock a couple weeks ago to kill the algae, and based on the water sample yesterday, that's pretty much dissipated so maybe its not so bad.


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What's the difference between the spindle assembly checkpoint (SAC) and mitotic checkpoint complex (MCC)?
Are the SAC and MCC two separate complexes? Does the SAC activate the MCC? Thanks

It can be helpful look into a few technical articles on the subject to clarify these ideas.
For example, this article has an abstract that lays it out quite nicely in the first 2 sentences of the abstract:

In mitosis, the spindle assembly checkpoint (SAC) ensures genome stability by delaying chromosome segregation until all sister chromatids have achieved bipolar attachment to the mitotic spindle. The SAC is imposed by the mitotic checkpoint complex (MCC), whose assembly is catalysed by unattached chromosomes...

So the SAC is a human conceptual model of how cells prevent the improper onset of anaphase before chromosomes are set up properly for cell division. MCC is the actual protein complex acting as an agent to make the SAC happen in cells.
The SAC could be thought of as containing the MCC and any other agents that prevent improper anaphase until spindle assembly and chromosome bi-orientation is complete, but it is not a protein complex per se in the sense of a bunch of proteins that stick together for a specific molecular function.


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Identification of that red and black bug
Found in France countryside, few hours ago, on a bushlike plant in direct sun light.
There is dozens of individuals, by groups of 5-ish, everywhere on the plant, along aphids, maybe sucking the plant's sap.
Looks like a stink bug, with unexpected colors. Some of them were attached two-by-two by their bottom (mating, probably ?).
Sorry for the bad photo quality.

This looks like Graphosoma italicum (aka G. lineatum; it is a stinkbug):

Graphosoma italicum had been regarded as either a subspecies, or a mere synonym to G. lineatum.
G. italicum can reach a length of 8–12 mm (0.31–0.47 in). The body is almost round, with a large shield. The basic color of the upperside of the body is bright red, with wide black longitudinal stripes. The pronotum has six black bands. The antennae are black. Also the sides of the abdominal segments (connexivum) are red with many small black spots. The legs are black.
Wikipedia

I think you are right that they are mating. Here is another picture of the species mating:

ibid

(Despite it saying that the legs are black, they are clearly striped in some specimens, like in your picture.)
It's found in France, according to Honeyguide.


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Why does one combine PCR and cloning as ways for amplification of sequences?
Why does one combine PCR and cloning as ways for amplification of sequences? Don't they produce the same result? I was reading the paper https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1864885/ and got confused by the following passage:

Cloning and Bisulfite Genomic Sequencing
Each bisulfite-converted DNA
  sample was subjected to PCR by primers that did not discriminate
  between methylated and unmethylated sequences, using a GeneAmp PCR
  core reagent kit (Applied Biosystems). The primer sequences are listed
  in Table 1, and reaction conditions are listed in Supplemental Tables
  1C and 1D (available online at http://ajp.amjpathol.org). Each
  subsequent PCR product was TA-cloned into pGEM-Teasy vector25
  (Promega) for transformation into Escherichia coli strain JM109,
  according to the manufacturer’s instructions. Clones were picked
  randomly and colony PCR was then performed using vector primers T7 and
  SP6 to amplify the cloned inserts. Cycle sequencing was performed
  using BigDye version 1.1 (Applied Biosystems) and an automated
  capillary DNA sequencer Genetic Analyzer 3100 (Applied Biosystems).
  The sequences obtained were aligned and compared using SeqScape
  software (Applied Biosystems). The completeness of bisulfite
  conversion was first confirmed before scoring. The CpG sites sequenced
  as cytosine or thymine residues were scored as methylated or
  unmethylated, respectively. The methylated site frequency was
  calculated for each sample by dividing the total number of methylated
  sites over all cloned CpG sites.

Can someone comment on what purpose the cloning serves when the amplification is already done by PCR?

There are several reasons to clone a PCR product but the main reasons include expressing the product and maintaining the library inexpensively.
In the study you mentioned, the cloning and transformation is apparently done for obtaining single clones (from single colonies).

Clones were picked randomly and colony PCR was then performed using
  vector primers T7 and SP6 to amplify the cloned inserts. Cycle
  sequencing was performed using BigDye version 1.1 (Applied Biosystems)
  and an automated capillary DNA sequencer Genetic Analyzer 3100
  (Applied Biosystems).

Since the original PCR would have a mix of different sequences, cloning is done to separate them out for the ease of studying them by sequencing. If they don't separate the sequences, they would have to use NGS (or more expensive methods like PacBio for longer reads). They have used Sanger sequencing. This article was published in 2007. At that time NGS was not as cheap as it is today and was hence not used by everyone. Also, the NGS machines of that time had even smaller read lengths (~40 for Solexa/Illumina GA and ~75 for GA-II). Considering these, Sanger sequencing may have been preferable to the authors of this paper. However, as I mentioned before, Sanger's method cannot be used for sequencing pooled samples; you need pure templates or else there will be mixed signals and base calling would be inaccurate.
(See the example chromatogram below: look at the position with the Y which has mixed T and C signals. It is not from a pooled sample, though).

Therefore cloning, transformation and colony picking was necessary.
Moreover, in many cases picking individual clones would be necessary for performing functional assays to associate phenotype with genotype.

Thank you for the answer. I am unclear about some points you made.
Why would they need to use PacBio? The initial PCR product is still short enough for any short read sequencing method.
I get the relationship of phenotype to genotype, but this is not the case here. Isn't the cloning just a step adding a bias to the methylation ratio quantification?

@CindyAlmighty You need to sequence single DNA molecules. That can be done using any NGS technology but not Sanger sequencing. However, for many of them the reliable read length is <300nt. With PacBio, you can sequence longer reads. Their reads are indeed smaller so they don't need PacBio. But, note that this article is from 2007. NGS was not that widespread and cheap at that time. There could be an amplification bias between methylated and unmethylated sequences but that would be there in the PCR product stage, itself.

I understand the NGS vs Sanger vs PacBio. I am unsure how it figures in this problem - how is the molecule shortened by inserting cloning between two PCRs.

@CindyAlmighty it is not shortened. This paper is from a time when NGS was not common. Moreover, Sanger sequencing can give you up to 1kb of decent quality read. However, with Sanger, you cannot sequence a pooled sample. It would just cause interference.

Oh, now we are getting on the right track I think. Your help is excellent, as it led me systematically to a solution. I think this is the exact point I was looking for - Sanger cannot sequence pooled samples. But now that I think about it, it is not interference, but we wouldn't be able to phase methylations. Do you agree?

@CindyAlmighty not just methylation. If you have multiple templates in a Sanger reaction then the chromatogram would have mixed up signals and base calling would be inaccurate. In case of same template sequence but dith different methylation, there will be two signals (after bisulfite treatment) at the methylation site (C and T), the intensities of which will depend on the frequency of the two states. However, I guess it would be difficult to calculate the frequencies accurately from the mixed chromatogram peaks (never tried it so can't say conclusively).


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What virus properties affect their airborne contagiousness?
What properties of a virus affect it's ability to be transmitted by air? I assume it must be able to withstand different temperatures and be smallish in size?
For example why is influenza very easily transmitted by air but the ebola virus is not?

Your question is very broad. There are multiple factors that determine the infectivity of a virus.


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Weight of fresh vs frozen tumours
I have some mouse tumours that have been snap frozen in liquid nitrogen following an in vivo study, and I thought it might be interesting to also determine the weight of the tumours. I was wondering if weighing frozen tumours would still be accurate, or if I should have measured them before they were frozen? Would one expect the weight to be significantly altered just by snap freezing samples?

If the tumours were sealed before being frozen, then of course the weight is the same. The temperature of something does not change its mass. However, the frozen ones might be heavier if, during the process, more water (or other substances) got trapped into the tumour. At the end this is a problem of enginneering and about your freezing method and not a question of biology.

I'm voting to close this question as off-topic because it is a question of engineering of the freezing technique and not a question of biology.

I think this is specific enough to a biological technique that it's on topic.

I agree with Bryan; closing this question would be failing to see the forest for the trees.


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Where can I find the list of all tendons in the human body?
https://www.healthcentral.com/article/aging-can-take-major-toll-on-womens-tendons (mirror) claims that:

There are about 4,000 tendons throughout the body.

This claim is echoed by a fair amount of websites but I couldn't find any
decently trustworthy source.
Where can I find the list of all tendons in the human body?
I have only been able to find a list of skeletal muscles of the human body so far. I'm surprised that there are 4000 tendons even though they are only ~640 muscles: most muscles that I am aware of are attached to fewer than six tendons (FYI: Why some muscles have more tendons than others?).

Maybe that article is exaggerating?

@kmm maybe. Having a list would clarify it.

640 muscles should be enough for anybody.

@dotancohen mark my words: after a few decades, every muscular system will have at least 2~8 Gigamuscles, and many will have 16+. Technological advance will not be stopped

Your best bet is the Terminologia Anatomica, which is the international standard for anatomical terminology.
The 1998 edition is freely available. It lists only a few named tendons though, which is consistent with my experience as an anatomist: very few tendons are named separately from the muscles to which they are connected. Central tendon of the diaphragm, conjoint tendon, and calcaneal tendon are a few.
Otherwise, it's just "tendon of biceps brachii" (which actually has 2 tendons at one end and one at the other).
4,000 seems like a too high number to me. 2x the 640ish muscles plus some extra for multi-headed muscles and those with internal tendons or aponeurotic tendons seems like a more reasonable estimate.

The FMA lists 705 tendons, but note that it includes separate terms for left and right instances. As @kmm says, many of these simply shadow the list of skeletal muscles (and is likely incomplete).
You can browse the list on OLS, or if you want to extract a table you can query this SPARQL endpoint, just type in the query here:
SELECT DISTINCT ?x ?v0 WHERE {
   ?x <http://www.w3.org/2000/01/rdf-schema#subClassOf>+
       <http://purl.obolibrary.org/obo/FMA_9721> .
   OPTIONAL {?x <http://www.w3.org/2000/01/rdf-schema#label> ?v0}}


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How many different states can the femur and lower limb be in?
Often the knee can be thought of as a hinge joint. However, when it flexes, the knee permits the lower leg to rotate. So it is not a pure hinge joint in absolute sense because it permits more range of motion then a pure hinge joint.
Since the hip joint is a ball and socket joint, this means that, relative to the pelvis, the femur can also rotate.
In short, both have the capacity to rotate, to some extent independently.
Each leg has one femur and one lower leg. Each can be in one of three states.

Neutral
Inwardly rotated
Outwardly rotated

Basic math tells me that means 3^2 = 9 states
This seems like a small number, but if you then consider both legs that gives you 81 possible states.
I presume not all of these are possible. I assume that, if we exclude deformities, birth defects, or growth defects, in general there must be some kind of consistent patterns that humans tend towards.
What are the most common relative orientations (as defined above) for the femur and lower leg?
For example, if the femur inwardly rotates, does the lower leg automatically rotate inwards?

You have probably meant 18, not 81 states for both legs.

@Jan Stan mean 9^2, that is 81 possible combinations using his argument.

If one leg can be in 9 positions, wouldn't you say that both legs can be in 9 additional positions, so 18 in total? Anyway, if you say that one leg in one position and the other leg in another position make a new combined position, you can say 81.

In anatomy, the term movement usually applies to a specific bone in a specific joint, not to the limb. It is said "the flexion of the femur in the hip," and not "the flexion of the leg." So, if you rotate the femur in the hip inwards, your lower leg will also rotate inwards, but this does not "count" as an additional movement.
Possible movements in the hip joint include (TeachMeAnatomy):

Flexion
Extension
Inward rotation
Outward rotation
Abduction
Adduction

There are known possible movements in the knee joint and in the ankle. After all possible movements in these joints, your feet will be in different positions. It then depend on you what you consider a different position. You can have a flexed hip and flexed foot, or an extended hip and flexed foot - is your foot in the same or different position? From the anatomical viewpoint it is in one (flexed) position in both cases.


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Narcan nasal spray
A recent podcast of Radiolab (time index 3:05) described a person who had overdosed given the nasal spray form of Narcan.  The report indicated the patient was awake seconds after the spray was administered to both nostrils.  If this is true, how does it work so fast?
The limit of my knowledge of biology and of Narcan is it binds with opioid receptors.  As I understand it opioid receptors which are located in the brain, in the spinal cord, on peripheral neurons.  Which receptors does the Narcan spray bind with that it works so fast?
Could this be answered in layman's terms?

Q: The report indicated the patient was awake seconds after the spray was administered to both nostrils. If this is true, how does it work so fast?
This is possibly an exaggeration, although intranasal Narcan can have a rapid clinical response time:

Tania Mieke Robertson, Gregory W. Hendey, Geoff Stroh & Marc Shalit, Intranasal Naloxone Is a Viable Alternative to Intravenous Naloxone for Prehospital Narcotic Overdose, Prehospital Emergency Care, 2009, 13:4,512-515, doi:10.1080/10903120903144866

We included patients with suspected narcotic overdose treated in the prehospital setting over 17 months, between March 2003 and July 2004. Paramedics documented dose, route of administration, and positive response times using an electronic record. Clinical response was defined as an increase in respiratory rate (breaths/min)...
The mean time between naloxone administration and clinical response was longer for the IN group (12.9 vs. 8.1 min, p = 0.02). However, the mean times from patient contact to clinical response were not significantly different between the IN and IV groups (20.3 vs. 20.7 min, p = 0.9).

Since it takes time to establish IV access, there isn't a difference between IN and IV Narcan administration in terms of "time from patient contact to clinical response." That said, IN takes ~5 minutes longer than IV (~13 vs 8 minutes) from administration to onset of action.

Amanda Robinson, Daniel P. Wermeling, Intranasal naloxone administration for treatment of opioid overdose, American Journal of Health-System Pharmacy, 2014 71:24,2129–2135, doi:10.2146/ajhp130798

Case reports
In the department of emergency medicine of Western Hospital in Melbourne, Australia, six cases of acute heroin overdose were successfully reversed using intranasal administration of naloxone hydrochloride, with all patients exhibiting a return of spontaneous respiration within two minutes. The doses used in these cases ranged from 0.8 to 2 mg at the treating physician’s discretion, and the time to spontaneous respiration ranged from 30 seconds to two minutes. While this study only looked at data from six isolated cases of acute heroin overdose, the results were encouraging and led to a larger prospective clinical trial comparing the safety and efficacy of intranasal versus intramuscular naloxone administration.

So, there are reports of IN Narcan responses in less than one minute. The instant response described in the podcast might be artistic license at work, but it's not impossible that a patient could respond on the order of seconds.
Q: Which receptors does the Narcan spray bind with that it works so fast?

Robinson and Wermeling, 2014 (above)

Naloxone is an opioid-receptor antagonist, with evidence indicating high affinity for μ-opioid receptors; it is used in the treatment of opioid overdose to reverse central nervous system (CNS) depression and restore respiration.
Naloxone is a pure opioid antagonist with no agonist activity. Prepared from thebaine, a natural opiate alkaloid, naloxone is a synthetic congener of oxymorphone. While naloxone’s mechanism of action is not fully understood, evidence suggests that the drug works by out-competing other opioids for the μ-, κ-, and σ-opioid receptor sites in the CNS, with a greater affinity for the μ-opioid receptor.
The nasal mucosa has a rich blood supply that contributes to efficient drug absorption and transport to systemic circulation. Administering drugs via this route generally avoids the first-pass hepatic metabolism seen with oral administration and leads to rapid systemic and CNS effects.


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Limbs in synapsids
Within synapsids, there was a change from a lizard-like sprawling posture (like in pelycosaurs) to a more erect stance. Non-eucynodont eutherapsids seem to have had a facultatively erect hindlimb and sprawling or semierect forelimbs. Eucynodonts seem to have had an obligatorily erect hindlimb and semierect forelimbs. Yet so many mammals (especially monotremes) and one tritylodontid seem to have had non-erect hindlimbs. What could have driven them to a non-erect hindlimb? Were there mammals with facultatively erect hindlimbs?

Your main question is unclear to me. Please do not ask multiple questions. I would suggest that you rephrase your question title and the background so that your main question is clear.

Monotremes do not have a sprawling posture, squat posture is not the same as sprawling.Pleas ask only one question per question.

I think you are confused about what erect limbs means, monotremes have erect hindlimbs. Erect is not the same as pillar erect (which is exceedingly rare) Just because a limb is bent or a joint can rotate does not mean it is not an erect limb. More importantly terms like semi-erect don't actually mean much, it is a weak gradation not discrete categories.  Like most things in biology nature does not respect our attempts to pigeon hole. Many animals can in fact switch between locomotive style.
To answer your second question, limb posture is often modified for specialized environments like aquatic living or burrowing. Which is why seal and mole limbs also have odd arrangements.


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What is the typical concentration of Calcineurin (PP2B) in CA1 dendritic spines?
I am trying to find the concentration of CaN (PP2B) in dendritic spines, there is a computational model (doi:10.1073/pnas.0804672105) that uses the quantity of 1uM in the dendritic spine. I think this value is not correct since it was measured long time ago (Goto Brain Res. 1986 Nov 5;397(1):161-72) and was given as Hippocampus 1.45 -+ 0.39 (ug/mg of protein).

Why do you think the data is incorrect simply because it is old? The concentration can be high because the volume of the dendritic spine is very less.

This article says that CamKII concentration (different subunits) is ~60-140µM. Calcineurin should be in similar range, I guess.

I think that this measurement is incorrect for the spine because CaN localization is found in the spine neighborhood, not the whole neuron (that diluted the concentration). Being old is not a problem, sometimes it is gold, like Magee and Johnston (1995) VGCC measurements. A Lisman paper guesses that CaN concentration is maybe 20uM in the spine (CA1), but they don't provide the reference ...

Do you know how CaN and CamKII are correlated? I could not find any article on CaN concentrations but see my previous comment for CamKII concentration. You can at least make an informed guess for your computational model. I do believe, you would do some kind of sensitivity analysis with your model parameters; so a perfect value may not be essential.

How they are correlated? one is a phosphatase that presumably dephosphorylates (CaMKII), an experiment in 2015 is saying that is not the case but they didn't look into the dynamics with enough temporal resolution, as Chang/Yasuda 2017 did. For CaMKII there are several estimations of the spine concentration, which is really good. For CaN, the spine concentration is hard to trust. And there are values in literature from 1uM to 20uM.

Kuno et al., J Neurochem, 1992, PMID 1313851 give 0.96 % total hippocampal protein = calcineurin (both isoforms).
Goto et al., 1986 give ~ 0.15 % total protein = calcineurin
In rat brain, there is ~ 10 % protein / total wet weight (Clouet & Gaitonde, PMID 13398827).
Stefan, PNAS, 2008. 1uM
Lisman and Pi, 2008. 20uM

I don't know how they are correlated; not my area of expertise. I just suggested if you know there is a correlation then you can guess an approximate value.

Thanks! I will let this rest on my head.


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Why do we develop addiction?
Recently, while on the train, I saw a person not holding the handrails on purpose. He decided that playing a game with no outcome whatsoever was more important than his safety. In fact, he bumped into the overhead luggage carrier several times. Twice he almost stumbled and fell, with a possibly very negative outcome for him.
Once he stumbled and bumped so hard into the carrier, it left a red mark on his face, even after facing it earlier.
Still he refused to hold a handrail as that would have prevented him from playing the game.
Clearly his addiction to the game won over any sense of self protection.
Now thinking about it, I think this is the case with most addictions. At the end, they are to some degree, harmful to the addicted person(imho).
Taking this to the time when we were still facing predators, it must have been careless just to think of getting delicious berries whilst not considering the exposure to predators it came with.
These individuals that are addicted (in a way) and don't care of the dangers associated with a problem, are harmed more often.
Thus, making addiction an evolutionary disadvantage.
Therefore, being easily addicted, as a trait, shouldn't have developed much.
Yet addiction is one of the worst problems of humanity and has been so for a long time.
So how could it develop?
Are my conclusions wrong?
Is addiction just a modern phenomenon?
Or are there evolutionary benefits of being addicted?

You are born with several addictions, to food, air, water, sleep, social interaction, reproduction, ect. Being alive is a struggle between desires and self preservation, everything has risks. You could never leave your house and starve to death.

Sorry this is no philosophical question

You misunderstand, a brain that could not function with addiction could not get you to seek food or water or a dozen other things, Addiction is built into how the brain works.

See that's why I say this isn't philosophical. I don't want to discuss if basic needs to survive are an addiction as well...

@steros John's point isn't philosophical, the point is that the behaviors of addiction are the same as the behaviors for obtaining "normal" needs, just taken to a higher degree.

@John has already shown that without a tighter definition, "addiction" includes breathing and eating. I'm slightly less pedantic than that, but I'm struggling with your question all the same. Are you asking why we developed an ability to take a risk and is this linked with addiction? Are you asking if other species have evolved to be susceptible to addictive behaviours? Are you asking for a biologically relevant definition of addiction?

I thought I made it pretty clear that I'm not talking about satisfying basic needs. But when an addiction becomes a danger for the individual. There's clearly a difference to having basic needs to survive and risking your life for something unnecessary. I didn't want to discuss what can still be called addiction though.

You are talking about healthy normal states and aren't talking about clinical addiction. You use a child playing as an example of being "addicted". This is a very soft definition which makes this so hard to answer.

The supposed duplicate doesn't answer the question at all

So how could it [addiction] develop?

Children need to play in order to understand the structure and behaviour of the world around them.
Bumping into things is a byproduct of this.
This behaviour is distinct from clinical addiction.
See this NHS page which covers some examples of addiction

Are my conclusions wrong?

As I understand it, your conclusion is that addiction shouldn't have evolved.
Asking how/why bad traits evolve is a really common question.
Here is the communities answer to why bad traits evolve and good ones don't.

Is addiction just a modern phenomenon?

Clinical addiction is becoming more recognised and diagnosable all the time.
Recently, the WHO started to cover gaming disorder as a form of addiction.
Alcohol abuse has been around since the ancients (Carr, 2011), and I would assume earlier than that.
Animals can exhibit pathological behavious in captivity, but this would be difficult to describe as addiction (see this Bio.SE question linked in comments by @WYSIWYG).

Or are there evolutionary benefits of being addicted?

Addiction is a condition where the normal brain feedback goes wrong and the brain prioritises a task that feels good in the short term at a huge long term cost.
The "reward" system that encourages us to eat and have sex has been hijacked.
Addiction is an advanced neural reward system rewarding itself for behaviours that can be destructive.
Without that same reward system, our drive for survival by means of food and sex may not have been so great.


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What's the name of this spider?
Recently, I was taking a walk down by a riverbank and saw this spider:
Here's all the info I think would be useful

Where? Missoula Montana, United States of America. Specifically, Greenough Park, on the riverbank (as mentioned earlier)
When? today, May 28, 2019
Behavior? They were hard to approach and scuttled away fairly speedily whenever I approached.
Population? They were everywhere, everywhere I looked they seemed to be there, occasionally, I found them in pairs, but never in groups of three.
Additional Info: they were passive until approached, moving rarely if observed from a distance, but when they did move it seemed that their movements were somewhat sporadic, with quick bursts of speed and then stopping and resuming (if they found that necessary)


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Where to download confier (pine) or A. thaliana annotated reference RNA transcriptomes in full .gbk (GeneBank) format?
Where to download confier (pine)  or A. thaliana annotated reference RNA transcriptomes in full .gbk (GeneBank) format?

Annotations are usually provided in GTF format which I personally find more convenient than genbank format. You can download the reference GTFs from NCBI FTP. You can also convert GTF to GB and vice versa. Is there any reason why you would prefer GB over GTF?

You can download the entire set of annotated RefSeq transcripts for a given genome assembly from NCBI Assembly portal.

Go to https://www.ncbi.nlm.nih.gov/assembly and search for Arabidopsis thaliana
Use the 'Download' button to pick 'RNA Genbank format' as the file type and 'RefSeq' as source to download all RefSeq RNAs annotated on this assembly in Genbank format.

Note, however, that the RefSeq transcripts in this file will be the ones that were annotated at the time of the release, June 2018, in this particular case. It is possible that additional RefSeqs have been curated for this species in the mean time, and those will not be a part of this file.


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Mayfly identification - Oregon
Found in a web by a very small, slow moving stream. Douglas-fir forest in Gales Creek area, April 28.

Great picture -- it's reaching for the sky!

Approximate size?


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Database of colors mapped to species
I was wondering about the physics of color, and now am interested in finding out if there are any resources (databases, text files, html tables, or pdf listings) of species and their associated colors or (ideally) color wavelength spectrum.
For example, a rose bush might have a pink (flower) color spectrum and a green (leaf) and brown (stem) color spectrum. A worm might have a brown and pink color spectrum. A lion might have a yellow and brown and gold color spectrum. Wondering (a) if any of this information is captured in any form on the web (such as 1 journal article per species), and (b) if it is aggregated into a database, text file, table, or other sort of list which includes lots of species (animals, plants, fungi, rocks, etc.), so it would say the wavelength of visible light that it emits, or some ranges of it, or even a hex color range.

would be unbelievably difficult as not only do many species have multiple colors in a single individual  or change color over time but many species also vary in color from individual to individual, then you have the species that cn voluntarily change color. You might be able to find a database of pigments but not one of colors.

Pigments would work too.

I have rose bushes with flower colors ranging from white through dark yellow, pale pink to a very dark red, and a couple of rather lavender-ish ones - and that's just in my own garden.  Then there are the multi-hued flowers of e.g. iris, particularly aril iris: https://www.google.com/search?complete=0&q=aril+iris&tbm=isch&source=hp&sa=X&ved=2ahUKEwionsub3sPiAhUpJzQIHaZ9DGYQsAR6BAgHEAE&biw=1311&bih=946

FYI there is a very simple and clear answer to this in regards to minerals - https://earthscience.stackexchange.com/questions/17081/database-of-color-wavelengths-of-minerals


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What is a sequencing artifact?
I'm rather new to bioinformatics, so this might be a rather basic question, but what are sequencing artifacts, in the context of variant calling?

Artifacts are variations introduced by non-biological processes. Sequencing involves a lot of chemical reactions, and changes in nucleotides that can seem like mutations are really introduced somewhere in the processing of the sample. That's what we call "sequencing artifacts". Proper experiment design, with careful replication, should help you clarify which changes in nucleotides are biologically significant.

Some specific artefacts are:
apparent insertions or deletions in the sequence, which are really just skipped base or duplicated base errors during the sequencing
apparent variants which do not exist in the sample but are introduced in the data because of miscalling at individual bases
differences in abundance of variants between the output and the sample due to biases in PCR amplification, or biases in the ability of the sequencer to sequence each variant, or due to stochasticity in abundance of molecules in the sample

I believe an artifact is something that appears in the first analysis but is not actually present in the sample. You would want to sort out all of the artifacts so that your final analysis is accurate.


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Database of plant morphology
Wondering if there are any open databases out there that specify the branching and flowering patterns of plant species, similar to algorithmic botany book.


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Aquatic Snail Identification
I can’t for the life of me find an identification of these snails. They’re thriving in brackish water, but may be freshwater naturally. They’re about .8cm long at their largest. I believe they have live birth due to the lack of eggs but presence of baby snails over the year and a half that I’ve had them.

Hi, Please try to be more specific like where you found this animal. Check the list of the additional info in the species-identification tag: One or more clear Photos.
A Location where the specimen was found (city/region and/or habitat).
An approximate Size (or photo indicating size).
Additional useful info (e.g., behavior, time of day/year, etc...)
Indication of prior research performed by the asker.
A tag for a specific taxanomic group (e.g., botany, entomology, arachnology, ornithology, ichthyology, etc...).

Looks like a Malayan Live Bearing snail , fairly common in the US aquarium trade. I have inadvertently gotten them into all my tanks. Common aquarium fish can't eat them ( unless you crush them on the glass). I did not know they can tolerate brackish water. Yhey will get to 1.5 mm.


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What can be the reason for yellow and dark marks on leaves?
The plant in our office started to have this strange marks, what can be the reason for that kind of marks? how can we cure the lovely plant?

Yellow leaf spots have various shapes, depending on the cause. Downy mildew starts with angular pale yellow spots. In cucumbers (Cucumis sativus) and other cucurbits, powdery mildew causes pale yellow spots followed by powdery white patches.
The location of the yellow spots may help you determine the cause of the symptom. Some diseases, such as powdery mildew, cause spots on older leaves first and then spread to younger leaves. Yellow spots from powdery mildew can occur on upper and lower leaf surfaces. Downy mildew spots occur on the upper sides of leaves between leaf veins that give the spots their angular shape.
Now lets jump into the causes :-

1 -Moisture Stress

Over-watering or under-watering are the most common culprits when a plant's leaves turn yellow.
If plants don't receive enough water, they drop leaves to prevent transpiration (essentially, a plant's way of sweating) and conserve water. Before they drop, though, the leaves will typically turn yellow.
Too much water can be just as damaging to leaves. When the soil doesn't drain well, an overdose of water leaves the soil waterlogged and root systems can literally drown. Without oxygen, roots start to die.

2-Normal Aging

As many plants age, the lower leaves will turn yellow and drop off.
However, to solve this case, don't worry. If the plant becomes too leggy, consider trimming back the main stem to promote new growth and bushiness.

3-Cold Draft

Now let's first understand what a cold draft is. A cold draft is a current of cold air being drawn indoors.
A plant sitting near it is giving off more heat than it receives from the room. Remember, heat travels from places of higher temperature to places of lower temperature.Cold drafts on tropical plants will often cause the leaves to turn yellow and drop.
To solve this problem, particularly If your plant is near an air-conditioner vent in summer or a drafty window in winter, move it to a less turbulent place.It's also a good idea to mist tropicals that you're overwintering to increase the humidity.

4- Lack of Light

A plant that is yellowing from a lack of light will typically yellow on the side that is away from the light source.
To solve this, move the plant to a sunnier location and see how it does. If window light is tough to come by in your home—especially in winter—you might need to rig up an artificial plant light or two.

5- Nutrient Deficiency

This can be caused by too much calcium in the water if you're using hard water, or by a nitrogen deficiency.If this is the problem, the plant's top leaves may be the first to go yellow.
However to solve this issue, since it is species specific, its important to diagnose the problem firstly and them take some remedies.

6-Viral Infection

If your plant has a viral infection, it might show up as blotchy, spreading yellow patches on leaves throughout the plant. This may be accompanied by deformed leaves and stems, as well as discolored flowers.
To solve this , discard any plants that you suspect are infected since viral infections can not be treated.

7- Fungal infection

If caused by a fungus, there is nearly always fungus growth of some type in the spot, particularly in damp weather. This fungus growth may be tiny pimple-like structures, often black in color, or a moldy growth of spores.
To solve this, you can use sulphur(in dust form) and milk.
Sources - https://www.thespruce.com/reasons-for-yellow-leaves-on-houseplants-4150680
https://www.hunker.com/12140067/how-to-diagnose-cause-of-yellow-spots-on-leaves
www.uky.edu/Ag/PAT/cat1/leafdis.htm

Its Chlorosis, degradation of Chlorophyll.
gradually it will lead to necrosis.
it might be due to lack of nutrients, especially manganese, zinc or iron.
it might also be due to poor drainage or root damage.
provide more space for the roots to grow. Treat soil by providing nutrients.
your problem should solve.


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How are testosterone levels distributed among men and women?
Wikipedia tells me that men have 7 to 8 time higher levels of testosterone than women, on average.
Since the hormone is linked with performance in certain athletic events, my hypothesis, which I presented to a disagreeing friend, is that female top athletes in certain fields will have levels above the average male.
I found Why do endocrine profiles in elite athletes differ between sports? (Clinical Diabetes and Endocrinology 2018) which in Figure 10 presented testosterone levels for men and women in a number of olympic athletes:

As you can see in the plot it seems that even in the cohort of olympians there is an overlap, even if small, between men and women. Am I misinterpreting these result? I noticed that the units (nmol/L) are different from those used on Wikipedia (ng/dL), is this somehow important?
So:

Are there information about the distribution of testosterone levels among the general population to help answer the question of the share of women exceeding the average male level?
Am I interpreting the above results correct, are there indeed female olympians with higher testosterone levels than male olympians?

(The mapping between numbers and sport)

Power Lifting (18 M and 1 W)
Basketball (27 M and 14 W)
Football (Soccer; 37 M)
Swimming (100 M and 91 W)
Marathon (1 W)
Canoeing (7 M and 1 W)
Rowing (36 M and 25 W)
Cross Country Skiing (8 m and 9 W)
Alpine Skiing (11 M and 12 W)
Weight Lifting (10 M and 7 W)
Judo (26 M)
Bandy (19 M)
Ice Hockey (38 M)
Handball (23 M and 29 W)
Track and Field (95 M and 49 W)

Did you generate these plots yourself? If not it's good to cite the source. Anyway, if you have the data you can perform a statistical test to see if the differences are significant. Did you try any? Try Mann-Whitney test or student t-test and then you can conclude if the overlap you see is indeed significant.

@WYSIWYG: I attributed the sources, but perhaps not clearly enough (see paragraph before the plot). Thank you for your suggestion, but I think it would be better done with a larger dataset of the general population, this is only for olympic level athletes.

Did the authors of the paper discuss the possibility that some of the athletes  misused testosterone for doping and thus the results might not reflect the "natural" testosterone levels?

As you can clearly see from the data, some women athletes have higher testosterone levels compared to some men even in the same sport. However, this does not negate the statement that a random (or average) female athlete is unlikely to have higher testosterone than a random (or average) male athlete (you can perform a statistical test to check).

To the first question we can look at a paper such as "Estimating age-specific trends in circulating testosterone and sex hormone-binding globulin in males and females across the lifespan" from Handelsman et al.  The figures they provide are:

The top image is of females, the bottom of males.  We can see throughout a lifetime that the top 2.5% of females and bottom 2.5% of males seem to have approximately the same amounts of testosterone.  If we went to the top and bottom 1% there would likely be consistent overlap between the male and female distributions.
I believe you are interpreting the figures correct, although it is important to keep in mind these figures do not include any information on age and are a single point measurement.  To facts that may limit the depth of inference you can make about testosterone levels among the sexes.


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Do trees in a forest generally grow in a lattice formation?
The closest arrangement of trees in which they are at least a certain distance away from each other is a triangular lattice, much like a honeycomb. I wonder if you tend to see this sort of arrangement of trees in the wild?
I guess this would actually not be beneficial to the trees since it would mean they would all be lined up in certain directions which might not be good for sunlight etc.
I wonder if there is much research on the pattern of distribution of trees in a forest?

For most trees and plants, distribution is spatially highly variable. Thinking about the lifecycle of plants—their seeds are non-randomly dispersed, the seedlings and saplings grow in different biotic (neighboring trees, distance to herbivores) and abiotic (different soils, shading, etc.) environments, all the plants are at different life/size stages, and that they are highly plastic in their ability to have fluid morphologies in different conditions—it's really difficult to detect a clean lattice pattern with little variance.
Nevertheless, for some species of plants, where the conditions are right (e.g., very limited and highly sought-after resources, species poor areas, synchronicity of generations, strong antagonism), we see some evidence of regular patterns. Ecologists often analyze spatial distributions to see if they are random, clumped, or uniform/regularly distributed (link). We see some distributional uniformity that does resemble lattice-/tiling-like patterns, which you may find in the references from the link above. There is reference to only 1 tree species in that link :/ I can't say that I see ecologists looking for lattices explicitly, but I would be surprised if there isn't a subfield interested in it. HTH.

Good answer. I was surprised that there are actually plants that have regular distributions. I wonder though whether they are categorised as separate plants or are they in fact a giant super organism with a common root structure. In any case it seems like some form of communication between the different out-growths is needed for this arrangement. Also, I would imagine that such arrangement must grow out from a single plant much like how a snowflake crystal grows from a single seed.

Thanks—good question. Some plants that tend to grow regularly distributed, like creosote (Larrea tridentata) some oaks, can reproduce clonally and through seeds. Clonal propagation ought to lead to more regular distributions. Communication in most plants through root exudates are ubiquitous and very poorly understood, but I think you're right on about stronger patterns arising from sensing and responding to local environments. Animals do this well, and many territories (again, in the right conditions) are lattice-like, such as nesting sites of birds that next at high densities in the open.

It would be closer to an irregular Voronoi pattern.
"A certain distance" is imprecise, it would have to be "regular" intervals to give a lattice/matrix.
For trees that grow at the same rate, a square grid arrangement would give square canopy shapes. A triangle lattice would give triangles and honeycomb would give honeycomb canopy units.
For trees that are different sizes, the regularity would be chaotic. Voronoi:

Voronoi can describe a lot of things in nature, bubbles and animal cells, it's one of the fundamental mathematical patterns in nature just like spirals.
And even some arid clay.
Trees have irregular, not straight sides, that's different from voronoi. The trees are spaced irregularly and chaotically, and so it's a chaos of differently sized and irregular cells, rather than a lattics.

I think it would not quite be veronoi because there's only so close trees can get. And trees would tend to overshadow their neighbours and kill them.

I think you have things backwards.  You can make a Voroni diagram for ANY distribution of points, since it's merely the area that's closer to each point than any of the others: https://en.wikipedia.org/wiki/Voronoi_diagram

@zooby You are correct that the points of any distribution can be joined togeter into triangles... Google "Voronoi Forest" you will find lots of images and mathematics forestry research using voronoi... http://revistas.inia.es/index.php/fs/article/view/8021/2913 lattice is a repeating arrangement, i.e it has a symmetry. mathematics research has used voronoi to define plant spaces: https://pdfs.semanticscholar.org/de5a/1e987457ece17f6512e019e88111530d8d4d.pdf

OK, then what's the point in saying it's veronoi? Why not just say it's an irregular distribution of points? I guess you are trying to show how points can form cell like patterns?

Because you talked about geometry of the canopy... you said triangles, much like a honeycomb, and a lattice, all of which are wrong if you do any geometry. I program geometry so i know the technical words very well. So I replied that it is voronoi cells, and technically not a lattice, or a honeycomb, it's a point and cell distrubution simplified to Voronoi. You didn't specify the positions of the trees, you specified the canopy, which is not triangles. the positions of the trees themsevles have not triangular symmetries. They can be represented by single groups, duos, triangles and quads.

@zooby: Re "only so close trees can get", not really.  It's not uncommon to find two trees growing so close together that their trunks meet and sometimes join: https://en.wikipedia.org/wiki/Inosculation

OK. I see what you mean.


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Why are birds have balls in the form a cork screw i dont have the scientific name
Why do birds have penises in the form of a cork  screw?

Please use a proper vocabulary. "balls" is a slang. Also, balls refer to the testicles, not to the penis.


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Do molecular motors have a life time?
Most of the enzymes have a certain lifetime. I want to know that do molecular motors have a certain lifetime after which they degenerate? Any reference will be appreciated.
Basically, I just want to model a molecular motor with a finite lifetime for that I need a certain numerical age span that they follow or maybe some exponential decay model.
Furthermore, as suggested by WYSIWYG I have got a particular term for the protein lifetime with which I can search. I will try to find the answer myself and post it.

All proteins have turnover. Even if they are not actively degraded they are at least reduced by half because of cell division. Can you please elaborate so that we can understand the rationale of your question better?

@WYSIWYG I just want to model a molecular motor with a finite lifetime for that I need a certain numerical age span that they follow or maybe some exponential decay model.

You should [edit] your question to add all the details instead of replying in comments. Comments are not searchable and even otherwise not easily noticed. Moreover, posts should be self sufficient. Anyway, your question is still very broad. There are several molecular motors in different cell types and there are different ways to model biochemical reactions. Did you try to search the literature (just Google "turnover rate of xxx")?


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Can you design a bacteriophage that attacks the part of the bacteria that makes them antibiotics resistant?
I read in a newspaper about a case where they had found a virus that could attack a specific form of antibiotics-resistant bacteria and managed to save a girl from a certain death by "infecting her" with the virus.
See this article for instance.
I would like to know if it is possible to construct a virus that attacks the part of the bacteria that makes them immune to antibiotics?
I mean if you could combine a certain type of antibiotics with a virus that attacks any bacteria that is immune to that particular type of antibiotics the bacteria is in a bad place.

I have read before, now citing this answer

"Bacteria usually gain resistance mechanisms through horizontal gene
  transfer (such as conjugation and phage infection)."

and that bacteria can be resistent by for instance:

"produce beta-lactamase that inactivate many lactam based antibiotics
  such as penicillin."

then if you can construct a drug that somehow can attack the bacteria because of the specific genetic code that gives the bacteria the ability to produce beta-lactamase then you might be able to attack all bacteria that shares the same genetic code that gives them that ability and the bacteria can not mutate to escape without losing their resistance to penicillin.

Check out phage therapy. For more details check out the reviews by Levin & Bull (2004) and Skurnik & Strauch (2006). The idea was around for quite some time and there is active ongoing research in this field.
However, this idea just involves killing the bacteria using bacteriophages and not reducing their resistance to antibiotics. The bacteria that are immune to antibiotics can be killed by viruses (and vice versa). If you use them in combination then possibly there can be synergistic effects under a certain regime.

Another clinical trial was conducted to evaluate a combination of the
  antibiotic enrofloxacin and intramuscularly administered bacteriophage
  (Huff et al., 2004). Both treatments individually provided effective
  treatments of the E. coli infection, but the synergy between the two
  treatments led to a total protection of the birds, thus suggesting a
  significant value of the combined treatment.

Skurnik & Strauch (2006)

The combined treatment may not always be synergistic; they could also be antagonistic and therefore a good therapeutic strategy should be applied (Chaudhry et al., 2017).

As suggested above for tobramycin, antibiotics can be antagonistic to
  phage because they reduce the density of the bacteria and thus the
  capacity of these viruses to replicate [43]. Worse, antibiotics may
  even interfere with phage replication within the cell, thereby causing
  a reduction in phage numbers [41, 44, 45]. One way to test the effects
  of this possible antagonism is to treat with phage first and
  subsequently treat with the antibiotic, comparing the outcome with the
  case of simultaneous treatment. Here, we used delays of 4 and 24
  hours. Results show substantial effects of delayed treatment with
  phage for some antibiotics but no effect for others (Fig 4). The only
  statistically significant effects of delay are for the 24 hours delay
  using gentamicin and tobramycin, but the magnitude of the effect is
  profound. These are two of the three drugs for which simultaneous
  treatment suppressed phage replication (Fig 4B). The third such drug
  that suppressed phage replication with simultaneous treatment
  (ciprofloxacin) also exhibited greater kill with phage-first
  treatment, but the statistics fail to reject the null hypothesis of no
  effect of delay. This case warrants further investigation.

Unfortunately, bacteriophages are very host-specific and are hence not as broad spectrum as antibiotics. They are just like viruses of animals: the virus that infects a cat would most likely not infect humans. Very few viruses have a broad range of hosts.

For your query:

if you can construct a drug that somehow can attack the bacteria because of the specific genetic code that gives the bacteria the ability to produce beta-lactamase then you might be able to attack all bacteria that shares the same genetic code that gives them that ability and the bacteria can not mutate to escape without losing their resistance to penicillin.

the answer is that it is possible in principle. There are ways to knock out certain genes (CRISPR-Cas is one of the ways). However, the problem is the delivery of these molecules that mediate these knockout, to the bacterial cells. For that, you again have to rely on virus like particles for the delivery which gets us back to square one: how to make delivery machines/viruses that target all pathogenic bacteria. Moreover, the mechanisms of antibiotic resistance are diverse. Considering several other factors (that I am not going to list here), it is very difficult to make an efficient system for targeting antibiotic resistance genes in different bacteria.

It's possible and certain engineered solutions might be even more potent than just phage therapy on its own. For example, imagine if you could deliver CRISPR-Cas with a lysogenic bacteriophage (that is, the phage delivers a CRISPR-Cas payload, and that payload gets integrated into the host genome without immediately killing the bacteria). The CRISPR-Cas system could then activate expression, and maybe not edit genes, but let's say down-regulate specific known antibiotic resistance genes or programs, this is known as CRISPR interference. This regulation could be done to the antibiotic resistance bacteria, and then followed up with antibiotics, resulting in much higher efficacy of treatment. It's like a Trojan horse! Researchers recently have even begun to scale this sort of CRISPRi program to target many genes simultaneously and have demonstrated how this approach could reduce bacteria "survivors" (referred to a persisters by the field) by more than an order of magnitude following treatment of antibiotics such as ampicillin, ofloxacin and cefixime (Reis et al., 2017).


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Could someone identify these microorganisms on microscope?
I'm new in this StackExchange forum, so I don't know if this is an appropriate question.
Can someone please help me recognize these micro-organisms on these photo taken with my phone during my biology lesson using microscope.
Location: Kyjovka river (Czech Republic)
Magnification: 200x

What's the source of the sample? The resolution isn't good enough for me, but the source would be very important.

Unfortunately this is my own photo taken on my smartphone, so there is now way I can give you a better photo. Anyways thank you for your reply. I do not really need the exact name of specific species, anything would help me I think.

Are you asking about the wormy things? These are most likely some type of nematode (identification of nematode species is usually only achievable biochemically). If you mean something smaller in this sample, I doubt we can help you out (microorganisms are not easily or confidently identifiable by eye)


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Cracking sounds made by glowing plankton
Recently I had opportunity to swim in place with glowing plankton, it was amazing experience and it as well gave birth to few questions in my head.
I manged to google that they can glow thanks to chemical reaction called Bioluminescence.
Once submerged I could hear a cracking sounds, are these sounds as well effect of said chemical reaction?
Few more questions I am wondering:
How often can the plankton light up? Do they need to recharge or something?
Do they light up during the day as well but we can't see them because of daylight or do they act depending on how much light is there around them?


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What insect is this? Found in Russia
Found in Russia in the kitchen. Its about 15 mm long.

As you know Russia is a very large country, it would make sense to mention the exact part of Russia where you have taken this picture. It would also be good if you briefly describe the current climatic/weather conditions of your place.

Common name: Stonefly completely harmless!
(the terrestrial adult does not have mouthparts) and is an indication that the stream nearby is somewhat healthy.
Below is great info from online site. I just now joined Biology Stack so not sure if we can post links but I’ll try it at the end.

Neither a stone nor a fly, the stonefly is in an order of insects called "Plecoptera," which means "braided-wing", due to the prominent network of veins in its wings. The common name “stonefly” refers to the fact that the larvae live among stones in rivers and streams, and the adults fly.
Like most insects, the larvae and adults live radically different lives.
By far the majority of the stonefly’s life, two to four years, is spent as a larvae or naiad (the term for larvae that live in water). The naiads are entirely aquatic, living secretive lives in cool streams where they feed on plants, algae and decaying matter.
Giant stoneflies are the largest stonefly species, with adults reaching nearly two inches long. They emerge from the water in late May to early July and live only a few days — just long enough to mate and lay eggs. To attract a mate, the males drum their abdomen on the substrate or surface on which they're resting. The female feels these vibrations and moves towards it, sometimes drumming a response call. Adults have no mouthparts so they do not eat or bite. As large and imposing-looking as giant stoneflies are, they're completely harmless.
While most people would find the giant stonefly to be an interesting-looking insect, fisherpeople get particularly excited about them because they indicate good water quality — and possibly trout. Like trout, stoneflies need fairly cool, stable water temperatures and a high amount of dissolved oxygen. Stoneflies are also a favorite food of trout, so they can be used as lures. Finding these critters in the Mississippi River is another indicator of how water pollution has greatly improved from historical conditions in the early and mid-1900’s.

https://www.fmr.org/news/2017/12/27/nature-notes-its-sign-giant-stonefly-found-downtown-st-paul

Aaand this is about as good an answer as we'll get given the information we have ... Russia is home to hundreds of species of stoneflies, and the size given and visible cerci (the two threadlike appendages visible at the bottom of the animal as seen in the photo) eliminate perhaps a third of these (cerci in the families Leuctridae, Nemouridae, and Taeniopterygidae would not be visible past the wings in fully-winged species -- which this animal is; members of the families Perlidae, Perlodidae and Pteronarcyidae average MUCH larger than the 15mm given by Matt).


text:
How are haplotype blocks different from genes?
According to Cardon et al. 2003, a haplotype block is

A discrete chromosome region of high linkage disequilibrium and low
  haplotype diversity. It is expected that all pairs of polymorphisms
  within a block will be in strong linkage disequilibrium, whereas other
  pairs will show much weaker association. Blocks are hypothesized to be
  regions of low recombination flanked by recombination hotspots.

It seems obvious that the parts of the genome that compose genes will have a somewhat similar behavior.
So what are the differences between haplotype blocks and genes? Are genes a kind of haplotype block?
Cardon, L. R., and G. R. Abecasis. 2003. Using haplotype blocks to map human complex trait loci. Trends in Genetics 19:135–140.

Haplotype blocks may cover more than just one gene.
While positions within a gene are also in high linkage disequilbrium (or well correlated) with each other, this phenomena of high LD may extend beyond the gene body and overlap with the next gene.  A good visual representation of this comes from Jeffreys et al. in the figure below:

Red means more LD, black means zero LD.  Each point in the heatmap is essentially a pairwise correlation between two points in the genome.  Therefore regions of red represent regions of high LD or haplotype blocks.  Going from left to right we can see that each gene appears to be in its own block of high LD.  However, the genes PSMB9 and TAP1 appear to be in the same block.  Other examples exist as well, a great source is this review.

OK! Cool! But in the end, is a gene a haplotype block? I guess there are cases where there are haplotype blocks that span many genes, but genes themselves seem to have the same characteristics of a haplotype block.

Yes genes could likely be considered haplotype blocks, although this distinction does not add any understanding about genes.  Perhaps similar to calling a square a rectangle, the distinction is true but rather redundant.


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Do human genes get affected by irregular sleep and other factors
I'm new here so please go easy on me.
Do our genes-the ones that carry our appearance, intelligence and other traits get destroyed or lost due to irregular sleep, excessive body heat, smoking, drinking and other factors?
Asking cause, I have some relatives of mine with really good genes that are worth passing down but afraid that their children wouldn't get it because of the abovementioned habits.

Personal medical questions and health advice are off-topic on Biology. We cannot safely answer questions for your specific situation and you should always consult a doctor for medical advice. In this site, we just answer academic queries about biological principles. You should reformat the question to remove all the references of health advice if you don't want your question to be put on hold. Moreover, try to put in some research effort from your side. We would really appreciate it.

This is a good opportunity to correct some major misconceptions. I'll be brief and avoid being technical because this is introductory biology.
First, genes are present on DNA, and "store instructions" on building proteins, among other things. Poor diet, lifestyle and sleeplessness do not primarily affect the DNA itself, but rather the reading of it and the production of the proteins. Genes seldom get lost or damaged in a way that affects the next generation, at least in modern humans. Analogy: genes are the recipe in the cookbook, not the prepared dish. Lifestyle choices affect the dish.
This is because the aforementioned "bad habits" must affect cells responsible for the next generation (sex cells) - which is unlikely - unless the effects of the "bad habits" are strong enough to influence the entire system and cause damage to the production or maintenance of sex cells or their DNA. Sex cells are well isolated from the rest of the body. The other foreseeable way these habits can affect the next generation is to affect pregnancy itself. Poor sleep or smoking during pregnancy is obviously not advised. Gestation is a critical period in development.
In short, the expression and action of genes is certainly affected by sleep, diet, and so on, but the genes themselves are much less affected. Mutations may build in the body and contribute to the formation of cancer and other disease, but the sex cells specifically are very likely to remain mostly unaffected; it is these cells' DNA that is passed down to children.
As for the I have some relatives of mine with really good genes that are worth passing down* statement... That's a matter of eugenics and short-sighted opinion, which is strictly not scientific. Let's not address that!

There can be epigenetic effects on the gametes; see this. Moreover, lifestyle can affect the mutation rates and germ cell differentiation all of which can affect the quality of the gametes.

At least age is shown to be correlated with increased de novo mutations in the sperm.

@S Pr sorry, I never meant to come out as a racist person. Apologies, but I really didn't mean it. Although I do understand why it can be misinterpreted.


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Can creatures that can see color in completely different visible spectrum exists?
From wikipedia - "The visible spectrum is the portion of the electromagnetic spectrum that is visible to the human eye."
So humans can see the light from 400-700 nm and this is because our eyes can interpret/sense this little portion of the electromagnetic spectrum.
I wonder - could somewhere out there exist a creature which is possible to see different part of the spectrum ? I know that on Earth a creature can have a different visual spectrum "flavour" but I do not know whether it is possible the visible spectrum to be completely different - e.g. on some other planet can creatures exist that can say to see light in lets say  1500-2000 nm ?

maybe [this] (https://biology.stackexchange.com/questions/58005/are-there-animal-species-that-sense-infrared-light-with-their-eyes) can answer your question. They show animals on Earth that uses different molecules to transduce the visual stimuli, which is the key element to sense different portions of the electromagnetic spectrum, here on Earth, and in any planet as long as I can tell.

See also https://biology.stackexchange.com/questions/57708/what-is-the-biological-potential-for-vision-of-wavelengths-outside-the-human-vis/57710 - may be considered a duplicate. Note that speculation about completely foreign biology is not on-topic here, questions have to be about real biology that can be studied.

From what I have read so far - asking this question about life vision on other planets - is an on the edge on sci-fi and assumptive. As we haven't found complex life on other worlds - we can guess. However as far as what I read - based on the conditions the life live (e.g. their star type, distance from it etc.) and their chemistry - maybe life could be completely different - their vision could theoretically be different as well - sensing their world in different spectrum of light.

Maybe this question is similar with asking - could vehicles engines be completely different from what we have now on Earth. I suppose yes.


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Why does histamine cause bronchoconstriction?
What purpose does histamine-caused constriction serve in lungs during allergies and such, since it's vasodilator in other parts of body. Wouldn't it be more practical to vasodilate lungs so that white blood cells can arrive and toxins can be flushed more quickly.  Thanks in advance

You can think of it as a mechanism of preventing more toxins from getting in. Also note that bronchoconstriction is different from vasoconstriction.

You should think about bronchoconstriction as the constriction of bronchi (airways), not lung arteries.

Basics first: Crash Course
We will be introducing:
Autonomic divisions, Histamine and Vasoactivity (or Broncho-)
Starring: Innervation of the Lower Respiratory Tract
Lower respiratory tract is mostly innervated by the parasympathetic division, it has only scarce sympathetic-receptors there.
So, why it matters?

Autonomic divisions serve as fight-or-flight and rest-and-digest mechanism for the body as to respond for sudden changes.
You are having a good picnic, your body is in a state of rest. Your body is absorbing nutrient and enjoying your day. Blood isn't needed so much on your hands, or skin, or muscle.
This is the Parasympathetic Division
Suddenly a snake appeared in front of you, you scream, you panicked, and you flight away (or fight?). Your eyes dilate (where is that snake!), your muscles work, your respiratory tract dilates, as to prepare to avoid being killed by the snake. Blood rushs in to your muscles, but shunts on your digestion part, as what every you eat doesn't matter.
This is the Sympathetic Division
What matters?

Parasympathetic division only knows how to lock down things.
Sympathetic division can lock things, open things, and so, and so, and so.

How does sympathetic division work with so many things?
It has different receptors which reacts differently on input
Imagine people when reacting to clown: NOOOO and YAYYY
Histamine serves as modulation to outputs of autonomic division, directly or indirectly
Histamine is a broad-response chemical used to respond against an infection. As different cells have different ratio of autonomic division, it can cause dilation or constriction on different places.
One thing to note that, in a nutshell, histamine serves to buffer the work of autonomic innervation. It is entirely up to the regular function of the "autonomics" there to do their business.
Vasoactivity (or Broncho-) is achieved by state of balance between innervation by the autonomic division and local signals
Local signals play a part. A balance of signal determines the effect of innervation.
For bronchi, when histamine puddles, local signal sends stronger input than global innervation. Hence, the parasympathetic takes over.

histamine-caused constriction serve in lungs during allergies

Histamine serves as to protect the lower respiratory tract from inhaled irritants. The lower respiratory tract is innervated by parasympathetic stimulation. Parasympathetic stimulation only knows one command: constrict and strike.
When histamine buffs up the signal, it constricts.

vasodilator in other parts of body

Indeed it is. The vasodilation effect is achieved by GPCR-mediated sympathetic innervation.
Histamine buffs a diverse response of sympathetic division, hence dilates the blood vessels.

Wouldn't it be more practical to vasodilate lungs so that white blood cells can arrive and toxins can be flushed more quickly

In line with WYSIGYG, vasodilation is different from bronchodilation (or constriction). We have noted above that the operators are different, and they serve different functions.
As a note, white blood cells can't just come anywhere they want. Ever seen your nasal mucus being very viscous? That will happen your lung when white blood cells arrive.
White blood cells also cause fibrillation, which succumbs people when does.
It has been a reason why pneumonia and lung-infection related diseases, tend to succumb people by drowning them in "their own mucus".
Another part of sending much things down your lower respiratory part is...
How could you clean the mess up?
The upper respiratory part is the defense capable of trapping irritants by mucus and send the mucus to your stomach.
Bronchus? Not so much. More mucus will eventually drown your lungs.

I invested 50 minutes for this.