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Species Identification and Care
We've had this plant for a while as one of two. And both have grown incredibly over the last year. We actually know very little about these beyond watering when they look a little sad and would like to look after them better.
We can see that the plant has a 'trunk' of sorts now. Should this be under the soil? Are the plants large enough to repot? Should I change the soil?
The pot is 28cm wide at the widest and the plant is 32 cm high from the soil.

This is one of the many Yucca species, probably Yucca gigantea as this appears to be the spineless form with floppy leaves.
The trunk should protrude from the soil, indeed this species can get quite large with several trunks/branches, each with a cluster of leaves on the tip.
They are hardy indoor and outdoor plants which grow best in full sunshine and dry warm conditions. They are not particularly frost tolerant, but will survive light frosts with maybe some damage to the leaves if in a sheltered spot.
They do best in free-draining soil which retain some water and nutrients (so don't go to cactus extremes), something like 1/3 peat with 2/3 sand should do fine. They are drought tolerant and have generally low water requirements. You should be able to re-pot this plant without any problems every second year. Just water the day before, remove from the pot and replace some of the soil. Alternatively they will do well with a feeding roughly monthly of a balanced liquid feed.


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What is this plant with yellow large fruit?
Found this in a garden in San Francisco. Can't decide if it's pomelo, capri lemon or something else, ideas?

How large are the fruit? It is definitely citrus.

Also, is it fruiting now?  (Mid April.)  It looks rather like a quince, but that fruits in the fall.

@jamesqf - quince have the opposite shape - pear-like; larger at bottom than top, rather than larger at top, smaller at bottom like these ones. Quince also have obtuse, thin paler green leaves, not glossy dark green ovate leaves. Also note spines on stems - definitely citrus.

@bob1: You're welcome to come look at my quince tree next fall :-)  And I don't see any spines on the stems.

@jamesqf - I am well aware of the shape of quince. Check out the ~horizontal branch just below middle of the pic. Look where the stalk of the leaf joins the branch. Also see the branch passing in front of wall on lower right of pic; see the spikes sticking out...

@bob1: There are a number of varieties of quince.  This is the variety I have: https://onegreenworld.com/product/aromatnaya-2/  As you can see, the fruit is not noticably pear-shaped, and the leaves are dark green and glossy.

@jamesqf: {Doyenne du comice] (https://commons.wikimedia.org/wiki/File:Pyrus_communis_%27Doyenn%C3%A9_du_Comice%27.jpg) pear is similar. Turn the quince leaves over and they will be paler and slightly fuzzy, also on a reddish/brown stalk and brown bark cf. green stalks and green young (1-2 year) branches on citrus. Still note the fruit in the picture is smaller at bottom than top - opposite of quince. Actually most of the fruit in the pic are squashed spheres. All of them lack the bracts you see on the bottom of quince

source: Stack Exchange

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

sort: votes


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What was the evolutionary advantage of having seeds so large that they could only be dispersed by megafauna?
I understand that fruits like the avocado and the osange orange are so large and unwieldy that their evolutionary "intent" was to be consumed whole by megafauna that are now extinct. What I don't understand is why there was selection pressure for such a relationship to develop. Wouldn't it be to the plant's advantage if its seeds could be dispersed by more types of animals? What advantage does the plant get by limiting seed dispersal to a small set of large animals?

There are a few advantages to megafauna:

they travel large distances and are hence are likely to be able to
spread your seeds widely.
They also eat large amounts, so can carry a lot of seeds and
distribute those around widely.
Large fruit capable of being eaten only by the largest fauna might have the seeds survive by not being eaten and destroyed by smaller animals
Large animals have large guts, so the more of the seeds might survive undamaged

Another significant factor is that a megafauna animal also produces mega-feces, literally a large pile of nice warm fertilizer for the new plants to grow in.

You may be focusing too much on the megafauna. If there are selective advantages to making a big seed, some seeds at least will get bigger and bigger until there is no animal that will disperse them. If you've ever sprouted an avocado seed, its shoot and first leaves grow very high very quickly. Smaller seeds may have more dispersal routes, but if they end up near an avocado seed, they will have to grow in its shade.
Seeds may continue to get bigger past the point that they can be swallowed whole by an animal, if simply dropping the seeds is viable (Quercus insignis acorns can be up to 8 cm in diameter), but then there will be selective pressure to reduce the energy spent on the fruit coating the seed.

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


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Is this also a carpenter ant?
I live in Dayton, Ohio.  I've found large-ish ants in my kitchen, and I'm wondering if they're carpenter ants.
I realize there's been a few questions about carpenter ant identification, but in my defense, this one comes with video: https://youtu.be/HGWertws0oo
Picture, with penny for reference:

See the video for better shots (mixed in with bad shots, haha).
Is this a carpenter ant, or something more benign?

It is a carpenter worker ant. They usually live in outdoors , If they build a colony inside your house,then it will be a huge trouble to you to patch the walls since, they are capable of creating larger holes and cracks in the wall .I don't know what exactly is your doubt? If you can you can elaborate your specific point.


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Does N-methylcocaine exist in nature?
N-methylcocaine cation (pictured) is a cocaine analog that blocks HERG intracellularly, if somehow it were able to get into a cell.  A review of tropane alkaloids in Erythroxylum does not include it, or any N,N-dimethyl derivative, but this might be attributed to the issue that a quaternary ammonium salt, though it might be technically considered an alkaloid, would not be isolated (or removed from a soft drink flavoring?) by acid-base extraction.  But before we let paranoia overtake us ... is there any indication the compound exists as a natural product?  (You don't need to look beyond Erythroxylum.  An answer just for E. coca or E. novogranatense would be welcome.)

HERG? It may make you paranoid, but please keep the rest of the list out of it.

I'm not sure which list you mean, but here's one.  The way this article tells it, anything in your kitchen probably messes with the channel. True, this makes me less sure that this was a meaningful observation about the compound in this question, but I'm still curious.

the question of whether it can exist or not is not answerable. rather i would ask can it not exist and why?. Nature encompasses the entire universe. just because humans haven't seen it or synthesized doesn't mean there isn't a planet out there full of it.  or a bacterium it there that makes it.

I admit, I wasn't literally thinking Mars. An answer from Erythroxylum or even just E. coca would be quite welcome.

My comment was an oblique way of suggesting you define HERG, and, if you must personalize please do not use the first person plural, as it suggests the reader shares your emotions. However, on a less oblique note,  may I suggest that you move your post to Chemistry SE. Not only is it a little more likely that someone there will know the answer, but, more to the point, someone there is more likely to know how to find the answer. I imagine there are books and electronic sources for information about natural products, because of their vast numbers and pharmaceutical importance.


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How does a frog separate blood in its ventricle?
Since a frog has two atria and one ventricle, how does it separate oxygenated blood from deoxygenated blood when both are mixed in the ventricle? Or does a frog simply pump a mixture of both to the heart and the lungs? I checked a few videos and sites for this, but was unable to find an answer.
https://www.youtube.com/watch?v=MhOCzvA4KhM&ab_channel=iWorxSystems%2CInc.
My best guess, based on the above linked simulation, is that it has to do with a difference in densities of oxygenated and deoxygenated blood, but I am not sure.

In older books, I read about various theories about blood separation in amphibians, but newer books, such as Solomon - Biology (at least 6th Edition onward), mention:

Oxygen-rich and oxygen-poor blood are kept somewhat separate. The amphibian heart has two atria and one ventricle. A sinus venosus collects oxygen-poor blood returning from the veins and pumps it into the right atrium. Blood returning from the lungs passes directly into the left atrium. Both atria pump into the single ventricle, but oxygen-poor blood is pumped out of the ventricle before oxygen-rich blood enters it. Blood passes into an artery, the conus arteriosus, equipped with a fold that helps keep the blood separate. Much of the oxygen-poor blood is directed into the pulmonary circulation, which delivers it to the lungs and skin, where it is recharged with oxygen. The systemic circulation delivers oxygen-rich blood into arteries that conduct it to the various tissues of the body.

I would add to this my notes from when I was a biochem student (but studied Zoology), mentioning the arterial cone and a spiral valve. This is better described in Britannica:

The conus arteriosus is muscular and contains a spiral valve. Again, as in lungfishes, this has an important role in directing blood into the correct arterial arches. In the frog, Rana, venous blood is driven into the right atrium of the heart by contraction of the sinus venosus, and it flows into the left atrium from the lungs. A wave of contraction then spreads over the whole atrium and drives blood into the ventricle, where blood from the two sources tends to remain separate. Separation is maintained in the spiral valve, and the result is similar to the situation in lungfishes. Blood from the body, entering the right atrium, tends to pass to the lungs and skin for oxygenation; that from the lungs, entering the left atrium, tends to go to the head. Some mixing does occur, and this blood tends to be directed by the spiral valve into the arterial arch leading to the body.


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Why is the chordate nerve cord described as hollow when it appears to be solid?

My textbook says arthropods have a double, ventral, solid nerve cord. And chordates have a single, dorsal, hollow nerve cord.
What is hollow exactly in a cord that looks like this?

Your book is talking about an embryonic structure, the neural tube. This structure forms from an invagination of the neural plate, a collection of cells on the dorsal surface of the early embryo. The process forms a hollow neural tube that will eventually develop not only into the spinal cord but also into the entire CNS.

(image from https://commons.wikimedia.org/wiki/File:Neural_Crest.png)
There is still a lot of development to happen at this point: the cells making up the neural tube will divide many times and proliferate to create the central nervous system. Within the section that becomes the spinal cord, hollow part remains and becomes the central canal, contiguous with the fourth ventricle in the brain and containing cerebro-spinal fluid:

(image from https://commons.wikimedia.org/wiki/File:1313_Spinal_Cord_Cross_Section.jpg)
(note: I had a bit of trouble finding an image showing stages of spinal cord development with a license suitable for posting here, but you can find a bunch if you image search for "spinal cord development". Some examples: https://www.medicalimages.com/stock-photo-illustration-of-spinal-cord-development-within-the-embryo-atweeks-five-a-eight-b-and-ten-c-image22427030.html https://www.brainkart.com/article/Development-of-the-Spinal-Cord_18920/ )


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Maximum Allometry of aquatic mammals omitting Kleiber's Law
As far as I understand, blue whales cannot get any physically larger due to the extremely demanding caloric intake it has on consuming large quantities of krill, not due to any other physiological reasons, as it for what limits a land animals's, being their bones not being able to support their own weight.
Be that the case, how big can an aquatic mammal be, in terms of volume and/or mass?
Would other organism's, such as Hydrozoa, to name one example, display any difference in this regard?
For reference on the Blue Whale size being limited by caloric consumption, here is a link on a study:
https://science.sciencemag.org/content/366/6471/1367.abstract
Goldbogen, J. A., et al. "Why whales are big but not bigger: Physiological drivers and ecological limits in the age of ocean giants." Science 366.6471 (2019): 1367-1372.
APA

Welcome to the site! "As far as I understand" is really insufficient... please source your claim, and demonstrate what research you have done so far.  Thanks!

Thank you! Yes, I will post a link to what I am referencing about.
I am not studying biology as my main career, that being Material Science, but I have always have had a fascination with marine biology, so pardon if sometimes my knowledge isn’t up to standard.


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What are these needle-like plants growing in the ground?
I was outside and noticed some strange, needle-like plants growing on the ground. I managed to search for "needlegrass" but couldn't find it.
Here is the photo taken on April 20, 2021 in Long Beach, California; these red circles point at what the strange plants look like:

What you have here is a Filaree/heron's bill/stork's bill (Erodium species). These are widespread in California, being plants of disturbed and unmanaged soils - farms, dunes, roadsides, etc.
Note that I'm not Californian, or even from North America, all I did was google "weed species california" (without the quotes) and hit the first link that looked reputable, then used a small bit of knowledge of plant forms (rosette in this case...) to follow the links inside - and found the species at the link I supplied.


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What does T and the numbers mean in T coliphages?
I have searched a number of websites and articles relating to nomenclatures or phages but never found anything explaining what T in T-4,5,6.. Phages mean in the Coliphages. Also, what does the number mean? I have seen that many times, the T - even are grouped as one, why is it so?
Thank you.

The "T" stands for "Type" as in type 1, type 2 etc. To quote Wikipedia on Escherichia virus T4 (emphasis mine):

Bacteriophages were first discovered by the English scientist Frederick Twort in 1915 and Félix d'Hérelle in 1917. In the late 1930s, T. L. Rakieten proposed either a mixture of raw sewerage or a lysate from E. coli infected with raw sewerage to the two researchers Milislav Demerec and Ugo Fano. These two researchers isolated T3, T4, T5, and T6 from E.coli. Also, in 1932, the researcher J. Bronfenbrenner had studied and worked on the T2 phage, at which the T2 phage was isolated from the virus.[39] This isolation was made from a fecal material rather than from sewerage. At any rate, Max Delbrück was involved in the discovery of the T even phages. His part was naming the bacteriophages into Type 1(T1), Type 2 (T2), Type 3 (T3), etc.

It turns out Wikipedia is incorrect: The original use of Type as a designation for these viruses comes from a paper published in 1945 (PDF) by M Demeric and U Fano: BACTERIOPHAGE-RESISTANT MUTANTS IN ESCHERICHIA COLI Genetics 30:119. In this paper they collected phages from Luria (of LB/Luria Broth (actually properly known as lysogeny broth)) and Delbruck amongst others and collated them all for comparison. Delbruck references them in his review article (PDF, possible paywall, summary here), also from 1945.
I could find no evidence for why the phages were numbered as they were, though strains from Luria (actually previously from his supervisor as P28 and PC) were labeled T1 (Luria alpha) and T2 (Luria gamma), so it is possible that it was simply in order that they were received or possibly in order of discovery amongst the several groups working on these viruses.
The T-even phages were grouped because of structural similarities, and are now strains of the species escherichia virus T4 in the genus Tequatrovirus (see link for taxonomy).

Was the numbering done chronologically or based on some observation?

@Karthik, no idea, see revised post.


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Why does bicep activate during dead hang?
Hanging from a bar causes my bicep to feel much harder than when simply holding my arm straight above my head relaxed, without a bar.
This was slightly surprising to me: I used to assume that since the arms are straight during a dead hang, the biceps don't have to do work.
Are they under static contraction just to hang from a bar? Is it an effect of having to grip the bar, or would I observe the same tension in my bicep from being suspended at the wrists?
Why does this happen?

It doesn't contract, it tensions. Contract means it gets shorter, which would mean your are pulling your bicep. I just tested what you said, with one hand on a bycep, and hanging by one arm. The bicep doesn't contract. perhaps you should ask people on a bodybuilding or physio forum, reddit is easy perhaps.

@aliential thanks for pointing out the correct terminology. I thought this was considered static contraction

I didn't notice that it contracted though... even when you hold the arm straight, without clasping something, it does the same, it tensions, and it doesn't tension fully when you have all your weight on one arm, it depends how much you manage to relax the shoulder at the same time.

@DwayneDeSouza when I hold my arm straight without clasping anything, my bicep still feels very soft as if it's completely relaxed. When I am hanging from straight arms, my bicep feels very hard.


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Why do we use word prime with base pairing in DNA such as 5-3 prime.. prime stand for?
I was reading base pairing sequence in DNA and found 5-3 direction but my question is why we are using word prime with 5 or 3 such as 5 prime 3prime. Prime stand for?

The answer to this requires a proper chemical representation of the sugar and base rings, which is not present in the answer to " What does 5' and 3' mean in DNA and RNA strands?", but can be found in the custom diagram in my answer to another question.

It comes from Lagrange's notation in math, where "prime" denotes a derivative. So if you have a function x and then a derivative function of x, you'd call it x' (x primer) and if you have another one then it's x'' (x prime prime). So basically you are adding prime to say "another one of x". In DNA this refers to Carbons. DNA is composed of nucleotides which are composed themselves of a sugar + a nitrogenous base (or nucleobase) + a phosphate. Both the sugar and the nucleobase have Carbons and those carbons are called with numbers. The nucleobase gets the first "round" of names: Carbon 1, Carbon 2, etc. while the sugar gets the prime ones: Carbon 1 prime (that is, another Carbon 1), Carbon 2 prime (another Carbon 2), etc. So the 5' means Carbon 5 from the sugar in the nucleotide.

Welcome to Biology.SE! Please provide references supporting your assertion that this use in Chemistry is derived from Lagrange's notation — in general, on this site we expect answers to be backed up by supporting references. Thanks!

"Prime" is how you enunciate '.
e.g. "five prime" is the enunciation of the written 5'.


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What is this insect? 6 legs and red body
I'm in Brazil, southeast region, urban area. I've found these 6 legged insects with red bodies and black heads. They have long antennae (about as long as their limbs) and they walk around like ants, but slower. Their bodies are about 1.5mm in length.
I have also found a cluster of what I imagine are eggs they laid or got out from (there were 5 or so next to them last night).
Can someone identify them?

Welcome to Biology.SE! If possible please try to get clearer pictures and then [edit] them] into your question — closeups from multiple angles will improve your chances of getting a definitive answer.

These appear to be the nymphs of the red-shouldered bug (Jadera hematoloma), which eat the seeds of the Sapindaceae family (Soapberry family) throughout South America, Central America and the southern parts of North America.
There is a close-up picture of one of these at bugguide.net, and further images here on the same website.


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Nutrient agar as the medium for antibiotic susceptibility testing
I couldn't get Mueller Hinton agar to conduct antibiotic susceptibility testing. I'm thinking of just choosing nutrient agar as the growth medium for the bacteria Staphylococcus epidermidis. Will there be any major issue in choosing nutrient agar as the growth medium?
Thanks in advance

The standard breakpoints used in clinical susceptibility testing (Kirby-Bauer/disc diffusion assay) are considered reliable when every part of the testing method is standardized. If you change any part of that standardized method without properly validating those changes, it may or may not affect the outcomes and there would be no way of knowing without some sort of comparison study for validation.
Difficulty obtaining the proper media would seem common enough that this exact problem has been studied. This study did a head-to-head comparison of nutrient agar (NA) and Mueller-Hinton agar (MHA) for susceptibility testing on 149 clinical isolates along with a few QC reference strains. They found that NA agar did not produce acceptable results for the QC strains according to the relevant Clinical & Laboratory Standards Institute (CLSI) guidelines. Use of NA also resulted in many errant determinations among their clinical isolates (including many isolates of Staphylococcus aureus).
Given the error rates in this study, I would say that you should not rely on susceptibility testing results using nutrient agar in any sort of clinical context.
Reference:
Nassar, M.S.M., Hazzah, W.A. & Bakr, W.M.K. Evaluation of antibiotic susceptibility test results: how guilty a laboratory could be?. J. Egypt. Public. Health. Assoc. 94, 4 (2019). https://doi.org/10.1186/s42506-018-0006-1


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Is there a scale suitable for continuous tracking and recording of plant weight?
I want to measure water transpiration and evaporation in a bonsai tree, and measuring the weight of the tree in its pot is my proxy for water usage.  This has worked well with manual measurements, but I want to go to the next level.
I would like to monitor the weight of something continuously (e.g. once a minute) and access the data easily via a phone app.  Is there something like that?
There are numerous options for similar devices if you want to measure ambient temperature and humidity (e.g. https://www.amazon.com/SensorPush-Wireless-Thermometer-Hygrometer-Android/dp/B01AEQ9X9I).
But all my searching for balances with similar functionality have failed.  I've found many lab balances and kitchen scales, and body weight scales.  Only the body weight scales interact with apps on your phone, but they do not record continuously.
If you know of one, or just have better google-fu than me and can suggest a more precise search term, any pointers would be appreciated.

I'm afraid this has absoultely nothing to do with biology... please take the [tour] and check out the [help] for details on what is on-topic here.  Thanks!

I’m also voting to close this question as it isn't about a biological mechanism or process.

Fair enough.  Moderators, feel free to delete, too.  I didn't because there is a penalty for deleting an answered question.

In my defense, I thought the application, trying to measure plant water use, was biology related, and this seems like a community that might use similar equipment to what I am looking for.  But if you think it is off-topic, I don't object.

maybe this company  https://www.industrial-needs.com/scales-and-balances/recording-scales.htm

Our scale software allows a real-time measurement on a computer and
depending on the weighing data, they can also be saved with a date
stamp as a TXT file on the computer


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Are there any organisms that perform photosynthesis-like processes with thermal energy alone?
The closest I can find are thermophiles, but it seems they use the chemicals present in the hot environment for energy, not the heat itself.

Welcome. Photosynthesis means synthesis fueled by photons. As a consequence, thermally driven 'photosynthesis' is technically impossible. Can you elaborate on your Q, add relevant considerations and your own findings so far? One-liners are discouraged.

@AliceD - heat(infra-red radiation) is composed of photons too, just longer wavelength than visible light, so it isn't technically impossible. You can certainly generate fluorescence from IR range, and fluorescence uses similar electron stimulation to photosynthesis

@bob1 - Heat isn't the same as IR; objects can release IR and more so when their temperature rises. Objects can absorb IR and increase in temperature. Heat in itself is a vague term; it describes perceptually high temperatures. But that's subjective - what is high?

@AliceD, my understanding is that anything above 0K will emit IR. Conceptually IR is how a potential thermoautotroph could work, not that we know of any organisms that do work this way.

Thermophiles are organisms that are capable of surviving high temperatures. It doesn't mean they use or harvest the thermal energy in any way. Normally proteins start to unfold and degrade at temperatures above about 41 °C and all other organisms have a hard time coping with the effects.
Usually biology uses chemical energy. Photosynthesis is the one exception of a biological system converting the energy of photons directly into chemical energy stored in complex biomolecules for all others to use as nutrition.
Organisms that do not rely on those complex biomolecules but can support themselves are called autotroph. So photosynthetic organisms are  photoautotroph and micro organisms that use chemical energy from inorganic compounds are chemoautotroph. The inorganic compounds used can be as simple as decomposed water by radioactive decay.

Welcome. OP asks for thermally-fueled 'photo'synthesis (thermosynthesis?), not for a definition of thermophiles.

OP wrote "it seems they use the chemicals present in the hot environment for energy" and OP is right about this. OP asks for "photosynthesis-like processes" and not for miraculous "thermally-fueled 'photo'synthesis". There is nothing wrong with asking if life is known that directly converts thermal energy. An to my knowledge the answer is: No!

@AliceD Heat is certainly not a "vague term" but directionless energy not able to perform work.


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Conservation Law in Gene Regulatory Network modelling
I was going through the GRN modelling from Chemical and enzyme kinetics
by D. Gonze & M. Kaufman (PDF). The gene has 2 sites for activator/repressor. It say the DNA $D_0$ combines with activator/repressor at one of the sites leading to $D_1$ and then $D_1$ combines with $X$ again leading to $D_2$. It says then then total DNA is conserved in the reaction leading to $D_{Total} = D_0 + 2D_1 + D_2$. I want to ask why is there "2" with $D_1$ shouldn't it be $D_{Total} = D_0 + D_1 + D_2$. What I am talking about is given on page 49 of the document.
$$D_0 + X \leftrightarrow D_1$$ $$D_1 + X \leftrightarrow D_2$$
For first chemical reaction the rates are $k_1$ and $k_{-1}$. For the second reaction the chemical reaction rates are $\alpha k_1$ and $k_{-1}$.
Also, what will be the rate of the reaction for $D_2+X\rightarrow D_3$ when the DNA has 3 sites instead of 2.


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Does the false positive covid-19 PCR % referred to by Surkova & Nikolayevskyy in The Lancet mean % of all tests, or % of positive tests?
In False-positive COVID-19 results: hidden problems and costs it is said:

The current rate of operational false-positive swab tests in the UK is
unknown; preliminary estimates show it could be somewhere between 0·8%
and 4·0%

My questions:

Are there any more accurate estimates or research done on the real false positive rate than what Surkova & Nikolayevskyy are referring to?
Is Surkova & Nikolayevskyy referring to a percentage of total tests done, or a percentage of positive tests?

To clarify. Let us, for the sake of example, say that the false positive rate they are talking about is 1%, and one day we test 100.000 people, and that we get 5000 positive results. Will that mean that:
A: 1% of the 100.000 are false positives, therefore there are 1000 false positives?
or that
B: 1% of the 5000 that tested positive are false positives. Therefore, 50 are false positives?

Check the references supplied for those numbers in the article - they explain how the numbers are derived.

I’m voting to close this question because it requires one to read a specific external source to assess and possibly answer. This site is for general problems in biology, not for interpreting particular papers.

Actually, neither A nor B in the example are a correct interpretation of a false positive rate, because there isn't enough information provided to determine a false positive rate. In the terminology of clinical diagnostic testing evaluation, testing outcomes can be classified into one of four fundamental categories: True positive, false positive, true negative, or false negative.
While there are four possible outcomes, any given patient only has two possible test results, positive or negative. And the assessment of that result depends on whether they have the disease or not. So patients with the disease can only have a true positive or a false negative, and patients without the disease can only have a false positive or a true negative.
Since it's not possible for a patient with the disease to have a false positive, we get to ignore them in calculating a false positive rate. So a false positive rate would be the number of false positives out of the total number of possible false positives (or the percentage of patients without the disease who test positive). With an ideal data set in which you knew both the test result and true infection status of each patient, you could calculate it like this:
$$ FPR = \frac {False\ Positives}{False\ Positives + True\ Negatives}$$
The thing is, we don't usually use this in evaluating clinical diagnostics, but rather it's complementary value, which is called "specificity" (for some reason), and is essentially true negative rate.
$$ Specificity = \frac {True\ Negatives}{False\ Positives + True\ Negatives}$$
But note that neither of these values can give you the number of false positives in your example without more information. If you assumed that all 100,000 people tested did not have the disease, then you'd expect 1000 false positives (given your 1% false positive rate). But it gets more complicated when you have a non-zero rate of infection in the tested population. The greater the underlying infection rate, the fewer false positives you expect to see (and vice versa, with a lower infection rate, you expect a greater proportion of positives to be false, which I think is pointed out in the article you linked). Basically, it's really hard to determine something like a false positive rate on the fly and even harder to estimate it's impact in the real word, especially when the test you're trying to evaluate is also the best means you have for determining true infection.
Another consideration is that, for a well designed PCR diagnostic test (most COVID tests are), the majority of false positive results will come from technical errors (i.e. cross contamination, mislabeled specimens, etc.), rather than randomly from the test itself. And the rates of those kinds of errors can vary with the underlying rate of infection, the number of tests being processed by a given lab, the level of training those lab workers have, the number of hours they're putting in (tired people make more mistakes), and probably other factors I'm not considering.


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Can hunting of large specimens of a species make the size and weight of the species tend to be smaller?
Siberian tigers in the wild don't grow as much as they used to be in past (in the 1900s).
Their average weight was measured 176 kg in 2005 study. But it was also said that those tigers observed in study were sick and in conflict to humans.
I think their smaller size is because of low prey density because at that time, hunting of animals that come as tigers' prey was high.
Could it also be because all the large specimens were shot?

Welcome to Biology.SE! Please add a reference for the study you are citing — this is both expected practice in science (and on this site) and helpful for providing context for your question. Thanks!

I don't know of any research about this on tigers or any other terrestrial predators, but this is a well-known phenomenon in "trophy" animals1 (i.e. big game hunted for sport) and wild-caught fish1-4.
1: Allendorf, F. W., & Hard, J. J. (2009). Human-induced evolution caused by unnatural selection through harvest of wild animals. Proceedings of the National Academy of Sciences, 106(Supplement 1), 9987-9994.
2: Heino, M., Pauli, B. D., & Dieckmann, U. (2015). Fisheries-induced evolution. Annual review of ecology, evolution, and systematics, 46.
3: Monk, C. T., Bekkevold, D., Klefoth, T., Pagel, T., Palmer, M., & Arlinghaus, R. (2021). The battle between harvest and natural selection creates small and shy fish. Proceedings of the National Academy of Sciences, 118(9).
4: Bowles, E., Marin, K., Mogensen, S., MacLeod, P., & Fraser, D. J. (2020). Size reductions and genomic changes within two generations in wild walleye populations: associated with harvest?. Evolutionary applications, 13(6), 1128-1144.


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How do APCs find their specific T-cells in the lymph nodes?
My understanding is that when an APC (more specifically a dendritic cell) encounters an antigen in the periphery, it ingests it and presents it on its surface. It then migrates to lymph nodes to activate the T-cell that has the specific receptor for this antigen.
Now, I know that T-cells circulate throughout the body, but given the amount of the cells in a lymph node, and the fact that only a few T-cells are specific for a given antigen, it seems to me highly improbable for the APC to meet the specific T-cell.
Is it really that the APCs randomly check every T-cell there? If so, do we know how long would that take? Or is there a way to quickly locate the specific T-cell?

Can you give some link to Janeway's which is available online or any other reference? - I think it might be some misunderstanding to assume that ther is only one singel (stem) T o B cell that fits. I think it's a "bunch" of stem cells that shares one specifity, so chances are not that bad, to meet.  What's more, there might be polymorphy, i.e. several affinities that fit. Wonder if  you ever came across such or similar argument.


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Where can I find a list of trees in the world?
I want to make an app for smartphones that list most common trees in the world.
Where can I find a list?
I would like to include if the tree is deciduous or perennial and geography/climatic location.
I can buy a book if it is complete, preferably with photos of tree leaves. If I had only the list I may find the rest of information on wikipedia or other sites.

I suggest the Audubon society books, Ideally you want something with a dichotomous key, like https://gobotany.nativeplanttrust.org/simple/ Note I believe that legally if you are using their images and information for a salable app from any source you need that sources permission.

@John Thanks! I did something similar for minerals and I wrote a site to use their images with the agreement of including advertising of their website in the application. I will ask the authors for permission if I use this site.

Are you aware that the leaves are not necessarily the only thing you need for identification - you also often (usually) need flowers, fruits, size, branching patterns, and bark colour and texture. For instance could you tell the difference between bitternut hickory and pecan on leaf alone? Hint - pecan is slightly curved.

@bob I will include in my guide that info if I find it. I think I will buy Audubon society books. I guess they include that info.

Possibly, but there are some 60,000 species of trees in the world, so you aren't likely to find that in a single source. The Audubon guides only cover North America, and even then will only cover most of the trees. Comprehensive guides are often called a "flora", but this will include all species, though usually divided into volumes of monocots, dicots, algae,  bryophytes etc. rather than trees and not-trees. Flora don't always have pictures.

@bob1 I may try to make a guide about North America trees, make other for british trees with John's sugested site and search something else for my country Spain. Thanks, 60.000 wow!


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Probably a moth larvae but better to confirm

What I know,
It reacts to light
the red seems to be blood but can't say for sure
1 to 10 mm
it has a casing of something soft fabric possibly
it grabs to walls

That's what I thought, but I still have some doubt because it only has one black spot.

This is probably a larvae of Tinea pellionella, the case-bearing clothes moth.
T. pellionella is a species of tineoid moth in the family Tineidae (i.e. the fungus moths).


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Why is fructolysis independent of glycolysis?
In glycolysis, glucose is converted to fructose-6-phosphate before further breakdown. However fructose, instead of being phosphoryated to fructose-6-phosphate by glucokinase (and thereafter to pyruvate via glycolysis), yields fructose-1-phosphate in the reaction catalysed by fructokinase.
Why is this so?
It should be just as easy to phosphorylate fructose to both compounds. Wouldn’t it be more economical to use a single reaction, so everything would be easier to regulate? As there are several disorders that arise from the deficiency of enzymes used in fructolysis, wouldn’t there be a selection pressure against two separate metabolic pathways?
Edit:
Thanks for David's criticism; I see the confusion, I actually meant that it is mainly metabolized in the liver. I don't really have any real sources as I do not have access to much and quite a large portion of online resources is behind paywall. After a bit of digging I was able to find an overview that reiterates most of my claims. Sorry for not being able to provide more.

In the liver, fructose is rapidly converted to
fructose 1-phosphate via fructokinase. Fructose 1-phosphate is then converted into the trioses dihydroxyacetone
phosphate and glyceraldehyde via aldolase B.

The liver can extract 40–70% of dietary fructose in
both rats and humans. The high efficiency of
fructose extraction by the liver is due to the fact that the
liver is the main source of GLUT-5. Anatomically,
the liver is the first organ to receive absorbed nutrients
via the portal vein; in that way, it contributes to fructose
extraction. In contrast, the liver accounts for a smaller
percentage of glucose extraction for glycogen restoration

Above are two excerpts from Chapter 19 - Fructose-Induced Hypertriglyceridemia: A Review. This source also (albeit vaguely) states that the resulting triose phosphates (glyceraldehyde and dihydroxyacetone phosphate) can and will enter pathways like glyconeogenesis, gluconeogenesis etc.

Up until this point in fructose metabolism, there have been no rate-limiting steps and, as a result, there is an increased amount of substrate leading to metabolic pathways from triose phosphate (i.e. glycolysis, glycogenesis, glyconeogenesis, lipogenesis, and fatty acid esterification).

Another source for my assertion that fructose is mainly metabolized to fructose-1-phosphate (Elsevier's Integrated Biochemistry):

Unique Characteristics—Aldolase B Specificity
Fructokinase, like glucokinase, is found primarily in the liver. Unlike hexokinase and glucokinase, it phosphorylates the sugar at the C-1 position. Aldolase B, which is specific to the liver, works on both F1,6-BP and F1P. In extrahepatic tissues such as muscle or adipose tissue, fructose is phosphorylated to F6P by hexokinase.

Also, a possible lead, from Fructose: Absorption and Metabolism. Encyclopedia of Human Nutrition:

The allosteric inhibition of PFK effectively reduces the rate of glycolysis and decreases hepatic glucose uptake overall. In contrast, the entry of fructose carbons through the pathway proceeds without this limitation.

Using different enzymes (and therefore a different pathway) allows regulation of glycolysis in the liver without unnecessarily affecting fructolysis.

I have edited your question to make it more readable. You need to learn to keep to the point. Written communication requires you to work to decrease the number of words to those that are necessary and then make sure you use the right words. Irrelevant asides inhibit comprehension and the reader will become confused or give up. This is meant as constructive criticism. I shall try to answer your question in due course. Are you sure you meant to write "Fructose is first converted to glucose phosphate before glycolysis"? Do you mean glycogenesis? And which glucose phosphate? Please edit.

And while you are editing your question please give the sources of your assertions, particularly that fructose is not phosphorylated to F 6-P (and do you mean not or only a small proportion is?) and that fructose is is only metabolized in the liver. My text discusses the metabolism of fructose in adipose tissue. Let's try to construct a good question to justify a good answer.

@David Thanks for your helpful edit! Granted, that question was written in a panic and I didn't really proofread it, so it just read like a continuous stream of thought. I have tried my best to add relevant sources; most of my assertions are usually taken for granted, so I didn't think of doing it initially. Glad I did, though! Helped to clear some of the confusion behind this monster of a topic. Also, sorry if the sources aren't up to par, I really can't find anything better.

Thanks for updating your question.  I'll try to find time to research an answer over the weekend, although if someone gets in before me, all well and good.

"Also, why is fructose mainly metabolized in the liver while glucose generally is not?" There are newer evidence suggesting that most of ingested fructose is converted into glucose by intestine cells. If ingested in small amounts it probably never reaches the liver in fructose form. https://www.cell.com/cell-metabolism/fulltext/S1550-4131(17)30729-5

@paymanz The paper you cite seems solid, but if correct it is difficult to see why the liver expresses the enzymes for fructose metabolism. Something doesn't seem quite right. (And the poster's statement that glucose is mainly not metabolized in the liver is not quite right either, or at least misleading, because the liver is the main controller of glucose distribution.) The other thing I don't like about the paper is that is concerned with what happens in fructose excess — i.e.  when there is excess intake of sucrose. That is unlikely to be what the system evloved to cope with.

I have removed the second question about the preference for glucose or fructose by the liver as it is quite separate and should be posed separately. I have also separated your edit from the actual question. It is important people can see what your actual question is — what is the rationale for fructose to be metabolized via F 1-P. Make it clear, but keep it short. I have been busy doing other things (the sun disappeared long ago) but finally have written a long answer, which does not answer the question, but discusses possibilities and ways of approaching such questions.

Summary

The mechanistic reason why fructose is converted to fructose
1-phosphate by fructokinase rather than fructose 6-phosphate by
hexokinase is explained in terms of the Km values of fructose and
glucose for the latter enzyme.
A possible general rationale for the two distinct pathways of
metabolism is to allow them to operate and be regulated independently
of one another. Although plausible, I am unaware of further data
support this idea.
The manner in which the fructokinase pathway evolved is a matter for
conjecture. I discuss what types of approaches to this question may
be valid, and the types of arguments that I consider invalid.

“Why?” Questions — A Note of Caution
Before addressing this question I think it important to consider what is meant by a “Why?” question in biology. This can be a trap for the unwary if one is not clear whether a question is answerable objectively or only speculatively. There are two main types of “Why?”questions:

Mechanistic “Why?” questions. For this SE Question this would seem to be: “What is the mechanistic explanation of the fact that
fructose is converted to fructose 1-phosphate, rather than to
fructose 6-phosphate, in liver?”
Rationalization “Why?” questions. In this case it would seem to be
“How can one rationalize the fact that a separate pathway for
fructose metabolism exists?”

Mechanistic questions can be answered objectively if there are sufficient experimental observations. Rationalization questions cannot.
Rationalization is helpful to try to make sense of observations — to provide a framework for further experimental work. It is useful in teaching and learning, which is why one encounters it frequently in text books. But just because it is in text books it should not be regard as on a par with the facts described therein. It is just an opinion, an interpretation, which should be regarded critically. There is a danger in accepting an inadequate explanation, just because it is the only one that has been proposed for something that is difficult to understand but we think that must have an explanation.
Rationalization “Why?” questions are often confused with questions about how something Evolved. These should be clearly distinguished. Rationalization explanations refer to the functional utility of a system, not its evolutionary history. If the only explanation is in terms of evolution, then there may be a plausable evolutionary explanation but no rationale.
An Answer to the Mechanistic Question
Fructose is not converted to fructose 6-phosphate in the liver because it has a much higher Km for hexokinase than glucose does. Furthermore, glucose is present normally at a higher concentration and will therefore act as a competitive inhibitor. Instead, as the poster writes, there is a specific fructokinase, which converts it to fructose 1-phosphate and a further enzyme converting to the fructose 1-phosphate to glyceraldehyde and dihydroxyacetone phosphate. The glyceraldehyde is phosphorylated to glyceraldehyde 3-phosphate.

Trying to Answer the Rationalization Question
“How can one rationalize the fact that a separate pathway for fructose metabolism exists?” The explanation given in the Encyclopedia of Human Nutrition — that it allows separate regulation of glucose and fructose utilization — seems possible, but fails to explain the circumstances in which it would be advantageous for fructose to be converted to pyruvate, but glucose to, say, glycogen. In the absence of this I would say that there is no convincing explanation, and that one should carefully consider a number of different possibilities:

It is chemically difficult to create a enzyme specific for fructose
to catalyse the formation of fructose 6-phosphate.  This seems
unlikely — we are not dealing with two molecules as similar as serine
and threonine.
Fructose 1-phosphate has functions (metabolic fates or regulatory
roles) other than energy generation in the latter stages of
glycolysis. The Kegg pathway map doesn’t suggest anything in the
former respect, but the entry in the Encyclopedia of Human Nutrition
states: “As fructose-1-phosphate is formed, it feeds forward and enhances the activation of pyruvate kinase thereby facilitating the passage of fructose carbon to pyruvate and lactate.” I do not have access to the book, so cannot say whether this argument is developed further. However as pyruvate kinase is also activated by fructose-1,6-bisphosphate (generated from fructose 6-phosphate) there would seem to be no regulatory difference between fructose and glucose metabolism in this respect.
Fructose 1-phosphate lacks some regulatory role of fructose
6-phosphate (or fructose-1,6-bisphosphate) and hence results in
different flux of fructose and glucose through glycolysis. This is
the converse of the previous possibility. It is true that
phosphofructokinase is activated by fructose 2,6-bisphosphate, which
is formed from fructose 6-phosphate, and so there is a feed-forward
effect when the concentration of fructose 6-phosphate is high.
However the fact that fructose 1-phosphate does not have this effect
would not seem to have any significance as it does not use
phosphofructokinase. Another possibility is proposed in the
Encyclopedia of Human Nutrition: “Since fructose enters the glycolytic pathway [later than the phosphofructokinase reaction] it does not exert an inhibitory effect on the gluconeogenic rate-limiting enzyme, fructose-1,6-bisphosphatase” As the only
relevant molecule that regulates fructose-1,6-bisphosphatase is
fructose 2,6-bisphosphate — inhibiting it — the argument would seem
to be that the entry of fructose into glycolysis through fructose
1-phosphate allows more glucose production for other tissues. Why
this would be a “good thing”, however, is not clear to me.
Unphosphorylated glyceraldehyde has other roles in metabolism, so its
production independently of glyceraldehyde 3-phosphate is more
energy-efficient. Unfortunately the other metabolic fates of
glyceraldehyde are specialized and minor, and do not seem to support
this possibility.

In conclusion, I personally cannot see a rationale for the separate pathway of fructose metabolism to pyruvate, although I believe that there must be one.
The Evolutionary Question
Let us use the question to consider arguments in this area. The approaches that I suggest may — in principle — be valid are those relating to actual mechanism. One can consider the number of evolutionary events that need to occur for a new pathway to evolve — the more steps, the more difficult. (I have used a similar argument in another SE answer). In this question the implicit argument is:

“The evolution of the pathway from fructose to glyceraldehyde
phosphate via fructose 1-phosphate requires three steps, whereas that
for a highly specific enzyme that converted fructose to fructose
6-phosphate would require only one.”

If one accepts this argument, it would suggest that there is some rationale for the fructose 1-phosphate pathway that has escaped us. Although this also seems likely for other reasons, one needs to ask whether the argument is correct. Did three separate enzymes really evolve to accomplish this, or were perhaps some of the enzymes already present and serving other purposes?
Two examples of common type of argument that I think are invalid are in the original question.

“As there are several disorders that arise from the deficiency of
enzymes used in fructolysis, wouldn’t there be a selection pressure
against two separate metabolic pathways?”

Selection pressure against causes of a human disease require them to have a severe effect on the survival of the species, to cause death before the individual is of a reproductive age, and to be relevant to early humans. Minor enzyme deficiency disorders of fructose metabolism, or even disorders arising from modern over-consumption of sucrose would exert absolutely no selective pressure. As it turns out fructokinase (EC 2.7.1.3) is widely distributed in nature — If one looks up fructose metabolism in fruit flies on KEGG one can follow a trail to a long list of species in which the enzyme is present. The point that I think this demonstrates is that for biochemical evolution, one needs to think when and where the pathway might have evolved.
The second example of argument that I think are invalid is

“Wouldn’t it be more economical to use a single reaction, so
everything would be easier to regulate?”

I refer to this type of argument as “playing God” or “second guessing Nature” as to me it presumes that one is in a position of such knowledge and wisdom that one is able to propose the optimal design for life.
Economical in what sense? Is our concept of economy the over-riding feature driving mammalian evolution? Multiple reactions and isoenzymes abound in the metabolism of animals. Apparently ‘wasteful’ energy- or material-consuming reactions like splicing are everywhere. And the regulation of intermediate metabolism is mind-boggling in its complexity. Regulation clearly evolved after the pathways, and “ease” of doing this does not seem to have been a driving force in evolution.
The lesson I draw from this is that even the most knowledgeable molecular scientist is in a poor position to say what is economical or efficient, and to predict the outcome from the cost/benefit tradeoff Nature will make or has made to do things “better”. And it is difficult to say what is “better”.


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What is this snake in South Florida, USA
I observed this snake for about 10 minutes. It was slithering back and forth in about 50x20 yard (50x20 meter) area. Just kept going back and forth (then I left). There was a similar snake at the same time in roughly the same 50x20 area, but they didn't seem to be paying attention to each other.
This is in South Florida, near Naples, Florida, USA.
I took several pictures, but I think this one is the clearest.

Google helped me find this site. Using this tool, it might be a North American Racer, but I'm not positive.  It'd help if you had pics of its underbelly color or scale texture

@Punintended - I think I see a white throat. I agree it's a racer. Your guess is probably correct.

Thank you. Any idea what it was doing, running around back and forth?

Laps?  IDK, it is a Racer


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How was gene knock out done in pre CRISPR era?
I am trying to understand how CRISPR has made the gene knockout or gene editing process simpler to make transgenic animals. Here is an old (pre CRISPR) flowchart from Manis, 2007 that shows how knockouts can be made.

I assume much of this process remains the same even with CRISPR. But I want to understand what part of this flowchart has become easier with CRISPR? Is it that we do not need to wait for a random recombination event to occur? Is it that the yield has increased because we directly cut at the site and ask for HDR to happen rather than just sit and wait for it to happen?

Before CRISPR, homologous recombination at the target site (first step in left chart) relied on such events happening spontaneously. With CRISPR, the ability to generate double-strand breaks (DSBs) at the target site dramatically increases the frequency of homologous recombination events, since the DSB activates the cell´s own DNA repair mechanisms (of which homologous recombination is one) and directs them to the target site.

The wiki page for gene knockout lists several non-CRISPR methods for gene knockouts including zinc-fingers.


text:
Does estrogen have a more potent neural pruning effect in adolescence than testosterone?
I have read a study here which finds that female rats with their oestrogen inhibited had more neurones in a region of the visual cortex than intact female rats. To me, this suggests that estrogen may have a more potent neural pruning effect than testosterone, and that this may explain why female brains are on average slightly smaller than male ones. However, this study is A) not on humans and B) not on the whole brain. Further, the difference between average brain weight extends into childhood when sex hormones are low (but not non-existent. So, I wanted to know whether there was any consensus on the difference between testosterone-controlled neural pruning and estrogen-controlled neural pruning, and whether my conjecture is reflected by any evidence.


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Is CRISPR being utilized when scientists use the CRISPR/Cas9 system to edit genes?
"CRISPR" and "Cas9" are different things. When a virus attacks a bacteria, the bacteria stores the viral code of the virus in CRISPR. And when the virus attacks again the Cas9 protein uses the RNA in the CRISPR to find the viral DNA and then destroy it.
So, what is the use of CRISPR when scientists use the CRISPR/Cas9 system to edit genes, as we have already given the Cas9 protein a guide RNA?
Sorry if this is a stupid question, I am new to genetic engineering and couldn't find the answer on google.

I might be wrong here. But, when a virus attacks a bacteria, the bacteria stores the viral code of the virus in SPACERS and not CRISPR. 'Spacers' refer to the segments of DNA between the CRISPR.

Figure 1. Process of bacterial immunity mediated by CRISPR/Cas9. Scissors are Cas9 enzyme, black diamonds are CRISPR elements in DNA.
As suggested in the comment, there are some subtle differences here. Cas9 knows where to cut based on the spacer (the colored squares). That serves as a guide to the enzyme through sequence complementarity of the transcribed spacer RNA in the crisprRNA (crRNA, shown as the squiggled black line with a green piece).
The crRNA itself is composed of the spacer and also a transcribed CRISPR repeat (black diamonds), which form the structural hairpin of the RNA molecule (the squiggly black piece) that allows Cas9 to recognize it as a crRNA. Otherwise the spacer would just be a random little piece of RNA floating around the cell; with a full mature crRNA Cas9 knows how to bind to both the crRNA and the spacer-defined target to do its cutting.
To directly answer your question then, the crRNA is the guide RNA. You have a CRISPR (or CRISPR-like) sequence already in there. It doesn't exist in the array named as CRISPR in bacteria, but the functional component allowing the enzyme to bind and then recognize the target exists in there.
It's a little more complex than that in the actual organisms, if you have more questions I recommend reading more on wikipedia.


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Can I use TBE to elute a plasmid shipped on filter paper?
I'm receiving a plasmid shipped to me dried on sterile filter paper, as described in this question. This protocol and many others like it call for eluting the DNA from the paper using TE buffer.
My question is can I also use TBE to elute, as I already have a bunch on-hand? And in general, what concentration should the buffer be as I never see that mentioned in any of the protocols (including the AddGene version).

In my experience it does not matter if you use water, TBE or TE buffer. Even with a little EDTA in it, it will not mess up enzymatic reactions as the concentration is way too low. TBE/TE buffer usually contains 1mM of EDTA which can chelate 1mM of bivalent cations.
Since you not use the DNA undiluted (which also binds a lot of magnesium needed for most enzymes btw.) this really doesn't affect you in reality (been there, done that multiple times).
Additionally, I would recommend not using this DNA directly but transform it into bacteria first and then do a proper miniprep so you have enough material to work with (maybe even do a few restriction cuts and run it on a gel, to ensure the right identity) and a stock you can go back to if something goes wrong.

This is not exactly an answer to your question, i.e., how borate ions affect storage of your plasmid DNA.
But I would recommend you to use neither TBE nor TE, as they contain EDTA that might interfere with downstream enzymatic reactions. Use water (ddH2O) instead. As long as you store your plasmid DNA at -20°C it will be perfectly stable for many years. Alternatively, use a simple Tris buffer.
Addgene has a good article on this.

It really depends on the downstream applications, but the concentration of EDTA present in 1X TE (1 mM) is generally not enough to interfere with enzymatic reactions like restriction digestion, since the buffers used in those reactions supply Mg2+ at a final concentration of 10 mM or greater. EDTA chelates Mg2+ at a 1:1 stoichiometric ratio and prevents the activity of contaminating nucleases by sopping up the trace amounts of metal ions that those nucleases need as cofactors, greatly increasing the stability of DNA in aqueous solution.

Yes, you're right, the final EDTA concentration in an enzymatic reactions ends up being incredibly low. Also, as @Chris points out, you would most likely want to transform the eluted plasmid in bacteria and prepare new plasmid before any downstream enzymatic reactions.


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Why do nerve impulses utilize potassium and sodium instead of other Group 1 metals?
Rubidium and potassium are very similar, yet the body utilizes sodium and potassium for nerve impulses. Why is this the case? Why not any other element? Likewise, why not Lithium? I've read a research (https://www.ahajournals.org/doi/pdf/10.1161/01.RES.24.2.157) that says that rubidium has similar results as potassium in nerve impulse transmissions, the only difference being slight differences in intensity of muscle contraction (K leading to slightly stronger contractions). Additionally, it seems Rubidium, Lithium, Potassium, and Sodium have very similar Standard Electrode Potentials in Aqueous Solution at 25°C. Furthermore, why wouldn't calcium be used for nerve impulses? Does that extra electron make a difference?
Background: I am currently preparing a presentation for a chemistry class at my university. The presentation deals with periodicity. Basically, I am required to select three elements and explain how their chemical and physical properties differ according to their place in the periodic table. Thus, since there are differences between Group 1 elements, I believe there should be a reason as to why we use potassium and sodium for nerve impulses instead of other elements. In other words, I want to be able to explain why the body uses potassium and sodium instead of other elements by basing myself off the periodic table (i.e. atomic radii, electron configuration, etc).

Look to the stars to see your fate.  No, seriously!  Rubidium costs about 1/3 as much as gold because it is a heavy, rare element.  Lithium is cheaper, but it is still a comparatively rare element.  What the two have in common?  The CNO cycle doesn't make them.  (I'll leave you to guess three elements of life it does make)  You could go into nucleosynthesis much more deeply than I understand it, but rubidium is apparently r process or s process, while lithium is apparently produced in small amounts by proton bombardment.
The problem for living things is that they can't make elements.  A biochemistry that depends on an ion will be restricted according to its occurrence.  Related taxa that lack this limitation should thrive and evolve over a wider area, eventually supplanting their competitors.

It does make sense if we look at abundance. However, why not use Calcium. That element is quite abundant. I think what I am trying to ask is if there is some sort of chemical or physical property that both K and Na have that makes them ideal for nerve impulses.

@BrianBlumberg Calcium is quite important for neurons as well.


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Hodgkin-Huxley Model and Propagation of Action Potential
I'm studying Hodgkin-Huxley model of action potential, and I have some confusion.
In the well-stated HH model, we have time constants for each ion currents, described as the reciprocal of the sum of forward rate and backward rate.
In the caple theory, there is another time constant that is defined as the multiple of cell resistance and cell capacitance.
Is there any relationship between the two time constants? Do we have to think the two processes, which means the 'generation' of action potential and the 'propagation' of it separately?
Thanks.


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Why is only the donor's antigen seen during a blood transfusion?
I am a high school student and I am a little confused that why only donor's antigen matters during blood transfusion? for e.g if the donor's blood is O- so it means that it will antibodies against all antigens so if he donated blood to say some A+ blood group then those antibodies will attack on that antigen and agglutination will occur, isn't it? At first I thought may be the antibodies do not work outside our body then later I heard of passive immunity so this thought is not correct then what's the correct reason?

The donor only donates a limited amount of antibodies, which will bind to a small amount of the receiver's red blood cells. With "bad" matching, the receiver has an unlimited (and increasing) amount of antibodies to bind to the donated blood cells. In practice, matching is always done to exact type.

Blood transfusions are done with erythrocyte concentrate and not whole blood. The antibodies are dissolved in the blood plasma. Grafting parts of the donor's immune system by transfusing white blood cells (the leukocytes) would cause even more problems than just agglutination in most cases. That's why care is taken to separate the red blood cells.

This looks like it might be a good answer, but answers are much more likely to receive a favorable response if you include supporting references (primary literature is best). Without that support, your answer is indistinguishable from opinion and very difficult for a non-expert to verify. This is a good example of how to format references. ——— You may also want to take the [tour] and then consult the [help] pages for additional advice on [Answer] effectively on this site. Thank you!

You ask me to support my answer to a general question about blood transfusions with primary literature sources? Why is a link to tertiary literature like wikipedia not sufficient to differentiate my answer from an opinion? The cited article cites several secondary sources to support its claims. Primary literature is close to original research, difficult for non experts on the field to understand and inappropriate to form an opinion unless you are an expert on the field.


text:
Do jellyfish have extra energy reserves for emergencies (a "fight or flight" response)?
My friend is writing a story about jellyfish, and we couldn't find out if jellyfish have the equivalent of a "fight or flight response" or an adrenaline rush. In other words, do they have reserves of energy which lets them do things they wouldn't normally be able to (such as surpass harder obstacles, or move faster even when exhausted) which only get released during emergencies?
I know that jellyfish have a distributed nervous system and no brain, but searching the web for "adrenaline rush" and "fight or flight response" only returned results about how adrenaline/epinephrene is a cure for jellyfish stings rather than speaking about equivalent phenomena for jellyfish themselves.

Side note: This comprehensive article in Current Biology mentions something called "escape swimming":

One of the most extensive studies of the neuronal mechanisms of jellyfish behavior has been done on the control of swimming in the hydromedusa Aglantha digitale. Atypically for hydromedusae, Aglantha has two different swimming modes: slow swimming and escape swimming. Slow swimming is their normal mode, and is mediated by relatively regular and weak propulsion of the bell governed by pacemaker neurons in the nerve rings. Escape swimming produces a much stronger contraction of the bell, and is triggered when one of the giant neurons in the nerve rings (ring giant) is excited by mechanical stimulation of the tentacles

This is more related to neuronal impulses than energy reserves, but perhaps escape swimming bears some relation to energy reserves as well (if that's something that exists for jellyfish)?

This paper, Passive energy recapture in jellyfish contributes to propulsive advantage over other metazoans (pdf is freely available) might be of interest. It includes the following "Medusae can exhibit such low respiration rates due to the large proportion of metabolically inactive tissue during swimming. Jellyfish have low body carbon relative to other swimmers, which results in ≤1% of the body mass represented by muscle. Fish, in comparison, have a body mass that is ≥50% muscle" and much more.

Interesting! I'm beginning to suspect there's no concept of an energy reserve for them, if their energy use is already so low anyway (not to mention the passive energy recapture described later in the link).

Search for glycogen and jellyfish (or whatever the proper word for the beasties is). Idly playing I found a paper that implied it was present. I would find it hard to believe they do not build up energy reserves — lack of information does not mean it doesn’t exist. What stimulates breakdown is a different question.


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Can you please identify this mosquito-like insect?
I've seen these insects before (here in Cambridge, UK) and thought that they were probably mosquitoes, but they don't make the annoying noise that mosquitoes do (they fly similarly, but silently):

I also noticed that they are perhaps slightly larger than mosquitoes (maybe 12mm long) and don't have the long mouth which mosquitoes use to sting you.
Sorry for the poor photos, I don't have a camera with a macro lens anymore, and it's night-time. It's casting a strong shadow as you can see in the second photo.

It is most certainly a fly from Chironomidae, which belongs to the same suborder (Nematocera) as Mosquitoes (Culicidae). They have an overall resemblance to mosquitoes, but lack the large sucking mouthparts, and often have the large feathery antenna that are seen in your pictures. Some species are found in large swarms in early spring (but also later in the summer). Larvae can be found in most freshwater, and are called bloodworms due to red colour (high in hemoglobin, adapted to live in oxygen-poor sediment environments)
I doubt that the exact species can be determined from these pictures though.

Agreed as to family, and also to the doubt that further identification is possible: these midges are among the "some disassembly required" insects; the book "Chironomidae of the Holarctic region. — Keys and diagnoses. Vol. 3. Male imagines.(Diptera)" (Entomologica Scandinavica Supplement 34) summarizes a procedure that ends with FIVE cover slips on one slide, each holding part of the specimen!  (The number goes up to seven if you have the last larval and pupal skins of the same specimen.)


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Is this some form of cabbage?
I would appreciate if someone could identify this plant. It's tall, but not very difficult to pull from the ground, and it has yellow flowers in large groups. I was told it's not mustard. Is it wild cabbage, and if so, what variety?
Location: western Illinois, in a garden.
Season: it's late April, and their roots are now rotting.
Height: I think they were around 3 feet.

More pictures:

Welcome to Biology.SE! Please [edit] in size information (e.g. how tall) and if possible add closeup pictures of flowers from both the front, top, and side. It would be great if you could also include pictures of dissected flowers — i.e. cut up using a razor blade and spread out on a dark background. Without being able to see details of the flower structure I wouldn't try to narrow this down to a family let alone a species! However, it does look like it could be in the mustard family ...

@tyersome Hi, thank you! I will update it soon

The Brassicaceae family (of which cabbage and mustard are members) has a characteristic pattern of flowers - each flower has four equal sized petals, arranged in a cross-shape hence their other name - crucifers.

[h/t wikimedia commons]

It's not easy to see from your photos whether this is true, but I'm going to say, yes, it does look like a member of the Brassicaceae family. The cross-shape of the petals would confirm this.
I don't think these plants are native to Illinois, and it also does look somewhat like a crop plant, rather than a weed, so maybe it is an escape from a farm/garden. It could be canola, possibly.
Wild cabbages are native to the Mediterranean and Atlantic coasts of Europe , so it is probably not a wild cabbage, unless someone planted it in Illinois.

Thank you! This is helpful. The flowers are definitely cross shaped. I'm wondering what to call this plant. Is it canola? And yes I found it in a garden, in an urban area.

@JonathanMoore is correct, this is indeed a Brassica species. The brassica family (Brassicaceae) is a quite diverse family with something like 370 genera and 4000 species. They are found world-wide (apart from Antarctica, although Tryggve Gran tried mostly unsuccessfully to grow Sea Kale during the Terra Nova Expedition to the South Pole). You likely walk past several different types of Brassicaceae every day without knowing that they are there as they are common weeds of untended areas and will take advantage of small cracks in footpaths/pavement to grow.
There are a number of species that are common garden weeds throughout the world. They include many varieties of the Brassica rapa species (known for bok choi, Napa cabbage, choi sum and turnips amongst others, and is known for the oil "canola/colza").
In particular there is one variety called field mustard (Brassica rapa var. rapa, AKA common mustard, wild mustard, wild rutabaga, rape mustard) that is very commonly spread among gardens by its abundant seeding.
It has the long narrow leaves and the clusters of bright yellow flowers characteristic of the Brassica rapa group. However, the Brassica species commonly cross-pollinate and produce mixed varieties, so it is quite difficult to pin down exactly which one you have.


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why are dizygotic twins genetically dissimilar
I am a high school student and I am a little confused in a topic related to dizygotic twins, I get to know that dizygotic twins are genetically dissimilar because they are formed as a result of two different fertilizations but my question is that we know sperms are formed by meiosis in germ cells and each germ cell produces 4 sperms which are genetically different from each other but there is not only a single germ cell ,they are in millions so every time meiosis occurs 4 sperms are produced from each in millions so 1/4th of them should share common genetic material? so dizygotic twins can be genetically similar ,isn't it?

When sperm cells are formed via meiosis, all resulting mature sperm cells are unique from each other due to meiotic recombination; their genomes are shuffled in such a way that they will never be identical, even between daughter cells of the same germ cell. The deck of cards is always shuffled uniquely, so even if the same daughter pair of sperm meet with a pair of same-daughter eggs, it will still produce a unique individual (zygote). See here.

Dizygotic twins are formed as a result of fertilization of 2 different eggs by 2 different sperms.
For the 2 zygotes to be genetically identical it is necessary that both eggs and sperm have exactly same genetic material.
You cannot say that 1/4 th of sperms will share same exact same genetic material..during meiosis there is recombination..now there is no defined way that only a certain gene will recombine  with the homologous pair..these recombinations are quite random..so each time a new recombinant is formed. Further variation comes during Anaphase as the sister chromatids seperate hence generating even more variant sperm.
Even if 2 in million sperms are same..it is not certain that these 2 will fertilize eggs..it can be any other sperm
Moreover for dizygotic twins to be genetically identical the 2 eggs should also be genetically identical..but again the above reasons show that this is quite difficult..(here the eggs won't be in millions.. instead 2 eggs will be released during ovulation but recombinations happen still)
Now probability of  fertilization of these 2 similar eggs by 2 identical sperms out of millions is almost nil

It would be best to include citations.  Also, while you talk about meiotic recombination you completely neglected to mention the more fundamental concept of independent assortment, which in and of itself yields an identicalness probability of roughly 1 out 70 trillion on humans.


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Why do I see purple stripes when moving a small source of light (flashlight) quickly in a dark room?
I was playing with my phone's flashlight (white) in a dark room, Just moving it around quickly when I noticed that I could see thin stripes of purple in the same shape as my hand moved, they didn't disappear instantly rather I could see them like a net of thin purple strips, but vanished when I looked at them for more than 2 seconds. I don't understand why it happened and was curious.

This phenomenon is called afterimage and happens because of adaptations of the photoreceptors in the retina of your eye to the stimulation by light and adaptations by your neurons in the visual processing in your brain.


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Can oxytocin travel from one cell to another via gap junctions?
Oxytocin is a 9-residue secreted peptide. As a hormone, can it travel through gap junctions, assuming that it is stored in pre-synaptic neuronal vesicles?

Synaptic vesicles are on the order of tens of nanometers (for example Zhang et al give a mean diameter around 40 nm).
Gap junctions are much smaller, on the order of 1-2 nm. Maeda et al measure one at 1.4 nm.
Peptides the size of oxytocin present in the cytosol could theoretically travel through gap junctions. Vesicle-packaged peptides or molecules of any size cannot.

Maeda, S., Nakagawa, S., Suga, M., Yamashita, E., Oshima, A., Fujiyoshi, Y., & Tsukihara, T. (2009). Structure of the connexin 26 gap junction channel at 3.5 Å resolution. Nature, 458(7238), 597-602.
Zhang, B., Koh, Y. H., Beckstead, R. B., Budnik, V., Ganetzky, B., & Bellen, H. J. (1998). Synaptic vesicle size and number are regulated by a clathrin adaptor protein required for endocytosis. neuron, 21(6), 1465-1475.


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Hydrogen Ions — Common, right?
The Wikipedia entry for Ion states "A positively charged hydrogen ion (or proton) can readily combine with other particles and therefore is only seen isolated when it is in a gaseous state or a nearly particle-free space."  Cells pumping ions across membranes is very common so can someone help me understand what context might be implied by the quote?

It's not clear what you mean by "what context might be implied by the quote". What specifically are you asking about?

Welcome to Biology.SE! This appears to be a chemistry question and is almost certainly answered on [Chemistry.SE]. The short answer is that aqueous H+ is actually H3O+. Please take the [tour] and then go through the [help] pages starting with [Ask] questions effectively on this site. Note in particular the section on "homework" questions. Thanks!

I'm still not entirely sure what specifically you're asking about, but I have a guess. It is true that positively-charged hydrogen ions, or bare protons, are typically only observed in gaseous/plasma states and hard vacuums, and it is also true that cells routinely pump positively-charged hydrogen ions across membranes. This is not a paradox because in aqueous solutions, hydrogen ions exist as $H_3O^+$, also known as hydronium or hydroxonium.

Image from Wikimedia Commons

You are on the right track with your thinking about the paradox of an actual proton being pumped across the membrane, and it's just a problem of how the chemistry is communicated. The protons actually move along what is called the proton channel, which essentially is a row of protonated amino acids like glutamate (glutamic acid) or histidine.
If we think about complex 1 in mitochondria (below), when a proton in the matrix is "pumped" across, it actually "pushes" protons down the proton channel into the matrix (See the light blue line in the figure below). Think of a series of train cars on a track getting pushed.
Finding these proton channels and figuring out how they work is actually a very competitive field. Since they are buried in the membrane, they are challenging to work with, and we don't know much about them.

Even as someone who works in the field, I have to remind myself that all chemistry works this way. If it is water, protons, or electrons, talking about a single molecule is the wrong way of thinking about it.
Citation for Figure https://www.nature.com/articles/s41467-020-17957-0

"talking about a single molecule is the wrong way of thinking about it" super helpful


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

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

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

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

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

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

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

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

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

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

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

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

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

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


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How do you determine "in which direction" DNA is shared between groups of people
In popular DNA ancestry tests you can read lines like "you have 2% neanderthal dna" or "you have 20% italian". How can you distinguish between a person having 20% italian vs italians having 20% of your dna.
Like if we bred with neanderthals, that means neanderthals would have some of our DNA, but that wouldn't mean that we would have some their neanderthal DNA. Is this reasoning true? Is it possible to distinguish and does this apply to modern groups of people aswell?

The two cases are slightly different.
'Ancestry proportions', such as those given by 23andme, are given in the context of a reference panel. This means that they aggregate genetic data from individuals into particular countries, say Spain, Italy and France. They would then look at the genome of the individual they are testing, and find how much of the genome most closely matches individuals from any of the 3 reference populations. So an individual from the U.K. may share 70% of their genome most closely to the French reference individuals, 20% most closely to the Spanish and 10% most closely to the Italian. These proportions will change if we use different reference panels. In this case, the proportions only make sense in the context of which reference populations have been used. This information is available on here.
Humans have around 2% Neanderthal DNA because (we think) a small group of less than 10 Neanderthals mixed with the ancestors of all extant modern non-Africans. This Neanderthal ancestry was then propogated throughout all modern non-Africans today. The first human - Neanderthal hybrids would of course have been ~50% human and ~50% Neanderthal. However, because the effective population size of humans was much larger, the Neanderthal ancestry became diluted over time. If some early Neanderthal hybrids had then moved back into a population of only Neanderthals, they would have carried with them the human ancestry and we would say that Neanderthals contain x amount of human ancestry. However, as far as we know, this didn't happen and Neanderthals relatively quickly died out.


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Can a constitutively active kinase be highly regulated?
I am studying the protein kinase GSK3 and I am learning about the regulation of its activity. Many journal papers that I have read have stated that GSK3 is unique because it is a constitutively active kinase, meaning that it is always active and is not activated in response to a specific stimulus/condition. I have read that phosphorylation of GSK3 at specific tyrosine residues only enhances its activity, but the GSK3 itself is always active.
However, many of these papers also talk about the various mechanisms through which the activity of GSK3 is regulated (e.g. through phosphorylation at specific amino acid residues, subcellular localisation, protein complex formation). One paper states the following:

The many functions regulated by GSK3 (through its phosphorylation of
numerous substrates) suggests that the activity of GSK3 must be highly
regulated. Four key mechanisms have been identified that contribute to
regulating the actions of GSK3 in a substrate-specific manner. These include regulation by phosphorylation of GSK3 itself, the subcellular localization of GSK3, the formation of protein complexes containing GSK3, and the phosphorylation state of GSK3 substrates.

I am wondering how is it possible for a kinase to be constitutively active and be highly regulated at the same time? If it is constitutively active, doesn't this imply that it is always active? Any insights are appreciated.

Find a paper on GSK3 that explains precisely what is meant by describing it as “constitutive”. This appears to be yet another case of imprecise usage of English words for which there is no official definition in biology (because biology is not physics, as I have said previously). Only those who use the expression can tell you what they mean by it.

I think you have answered your own question, but yes, the nomenclature is confusing. When they say it is a constitutively active kinase, you are right, it plainly means the enzyme can always phosphorylate other molecules/proteins.
The regulation part is what you have in the review paper you cited. If the kinase is always on but localized in a compartment where there is nothing to phosphorylate, it could be considered "regulated". The same logic applies to the other regulation methods listed.

Welcome. I think you answered  the question, but it would be good to back up your claims by adding links to credible sources to allow other users to background read on your material.


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The effect of low pH on HIV virus
I've read a couple of articles that state that HIV is an enveloped Retrovirus that is so sensitive to the acidity of the environment and it cannot survive or will be inactivated at pH below 7. What exactly happens to the virus when exposed to an acidic environment. Does it denature the GP120 AND GP41 proteins on the virus envelope and make them ineffective? If not, how do hydrogen ions in the acid react with the virus?
Thanks for your attention.


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Is there an 'opposite' neurotransmitter to dopamine?
Dopamine is a neurotransmitter  (i.e. chemical) in the brain that gives us great feeling. From here:

Dopamine plays a role in how we feel pleasure. It's a big part of our unique human ability to think and plan. It helps us strive, focus, and find things interesting.

Is there any chemical(s) released in the brain that have an opposite effect to dopamine, that is, some chemical that makes us feel bad?

There's MOA which break down dopamine and therefore has sort of the opposite effect by reducing the dopamine-levels, sometimes even under the normal level - which basically induces the opposite of high levels of dopamine

The release of dopamine has a positive effect on the reward center in the nucleus accumbens. The neuron that releases the dopamine can be inhibited by other neurons, so there gets less dopamine released.
The response elicited by a neurotransmitter, either excitatory or inhibitory, is determined by its receptor on the postsynaptic cell. ~https://www.ncbi.nlm.nih.gov/books/NBK21607/def-item/A7678/


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Acquiring Covid-19 vaccination through kissing with viral vector vaccinated person
The mechanism of COVID-19 viral vector based vaccines (AstraZeneca - Vaxzevria, Johnsen, Sputnik V - Gam-COVID-Vac, Johnson & Johnson - Janssen, etc. ) is delivering the genetic information of the corona virus through adenoviruses.
Would it therefore be possible to get "infected" by droplets (f.e kissing) with the manipulated adenovirus from a viral vector vaccinated person and consequently acquire the same vaccination?

No, this is not possible, as the vectors used for the vaccination cannot replicate anymore. Some of the genes necessary for this step have been removed from the viral genome to prevent the uncontrolled spread and replaced by the spike protein which is used as the antigen for the vaccination.
To replicate the virus in the production process, a special cell line with a plasmid carrying the genes necessary for the viral replication has to be used, afterwards the virus is purified and outside of these special cells not able to replicate.
For an overview about the adenovirus type 26 based vaccines, see here:

Vaccines based on replication incompetent Ad26 viral vectors:
Standardized template with key considerations for a risk/benefit
assessment

I'd add that there are vaccines for other viruses that are made from attenuated viruses, but this type of vaccine is not used in SARS-CoV-2.


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How does the original ionic distribution restore after synaptic transmission
During synaptic transmission the calcium ions around the presynaptic membrane diffuse in due to the influx of Na+ ions and the resulting depolarization. This happens because the calcium channels are voltage regulated ones. At the same time on the other side of the membrane there is efflux of K+ ions in order to repolarize the membrane. My question is how does the original ionic distribution restore which is more K+ on the inside and more Ca2+ on the outside? What kind of pump does this job and what is the exact mechanism? As contrast to the nerve membrane where the Na+/K+ pump does this. I don't find a pump like K+/Ca2+ pump to do this.

Most of the depolarization in the presynaptic terminal is still sodium-based, it's just that there are also calcium channels there. Very little calcium actually moves, as these channels are closely coupled to the synaptic release machinery (see for example Stanley 1993 Single calcium channels and acetylcholine release at a presynaptic nerve terminal).
The calcium concentration gradient has to be established everywhere in cells that have this gradient (all animal cells, as far as I know), not just at a synapse, since calcium is typically a powerful "second-messenger" signal.
The two common mechanisms for transport are by using the gradient of sodium via calcium antiporters (this mechanism: using sodium or proton gradients to move other ions/molecules, is quite ubiquitous in biology), and via a calcium ATPase. Calcium transport involves both the external space and intracellular calcium stores such as within the endoplasmic/sarcoplasmic reticulum.
In the short term, calcium concentrations are also dealt with via chelation by calcium-binding proteins.

What about K ions . Is their level is maintained by simple diffusion of K ions or some special type of transporters or ATPase come into action. Anyways thanks the links were of great help

@Ubaid You've already mentioned the Na/K ATPase - that's the primary way that K concentrations are maintained.


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SARS-CoV - relative size of the spike protein
I was given the task of determining the percentage of the S-protein of the SARS-CoV relative to the total of its proteins from the attached image. However, I have been given no explanation of the image, and with a physics background, I simply do not understand it. Can someone please explain to me how it would be possible to solve the task from the given image (i.e., explain the image).

I'm not going to give you the final answer, because this is still a class assignment, after all, but I'll give you some tips. What you are looking at is a Western blot of whole-cell extracts from a cell line called Vero, either on its own (vertical ane 9, from numbering across the bottom) or infected with various viruses carrying specific genes, as indicated. Lanes 1-7 are from Vero cells infected with the BHPIV3 viral vector (a live-attenuated virus that can carry genes from another organism). Lane 1 is just the viral vector itself, with its own proteins. Lanes 2-7 are from cells infected with the viral vector carry certain genes from the SARS coronavirus. Lane 8 is from cells infected with SARS-CoV itself (so it carries all the previous genes). The numbers along the far right side are molecular weights, in kilodaltons.
A Western blot is performed in three parts - 1) separating the protein samples (whole-cell extracts) by molecular weight (size) in an SDS-PAGE gel by using an electric field, 2) transferring the separated proteins to a membrane, also using an electric field, and 3) using some sort of probe (usually a specific antibody) to determine what is present and in what amount. In this case, two antibodies were used. The lower, narrow image shows the samples probed with an antibody that recognizes the HPIV3 F protein, which is present in all the BHPIV3-infected lanes, in relatively equal amounts. This can be determined because the size/intensity of the different bands in each vertical lane is directly proportional to the amount of that protein present in the original sample.
The upper part of the image shows the extracts probed with an antibody that evidently recognizes the SARS S, M, and N proteins, but apparently not the E protein (as Lane 6, with the SARS-E virus, is blank). Using this information, you can now determine which bands correspond to which protein.
Keeping in mind that Lane 8 contains all the proteins from the SARS-CoV virus, while the previous lanes just contain certain ones as labeled along the top, you should now be able to use ImageJ to answer the question. I will give you one hint - there is much more information present than you need to answer the question. You actually only need 4 (well, maybe 5) of the lanes. I'll leave it to you to figure out which ones.

Thank you for your very elaborate answer; it helped a lot. One question. You say that lane 8 contains all the proteins from the SARS-CoV virus, but that I need 4-5 of the lanes to answer the question. But if lane 8 contains all the proteins, could I not get an estimate of the relative amount of the spike protein from this lane alone?

@Physics101 You need the other lanes to tell you which band the S protein is, and to tell you which (if any) bands are background artifacts. The E lane is also important, as it affects how you report your results.

Okay, thank you very much.