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What is this insect flying in my Los Angeles bathroom?
We live in the Los Angeles area. This insect has been very common in our bathrooms recently:

They're about 1/4" long, and can often be found resting on our towels. In the months leading up to December, we've been seeing them more and more.

Do they cause any harm?
Could they be responsible for the holes I've
been finding in my shirts?
Even if they're just a nuisance, how can
we get rid of them?

Looks like the common clothes moth (Tineola bisselliella). And, yes, the larvae (caterpillars) are likely the source of the holes in your shirts. You can purchase traps online or from hardware stores, or you can go the pesticide route if necessary (e.g., Delta Dust is available from online retailers).
See this site for further info, or search the web for more info on this species. https://en.wikipedia.org/wiki/Tineola_bisselliella

I thought about moths, but I read that the larva only attack clothes in airtight storage. My shirts are in a closet where I rarely close the door, and I wear them frequently. Was I wrong?


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Why is the partial pressure of oxygen in blood same as that in alveoli
The partial pressure of oxygen in alveoli is about 104 mmHg, after gas exchange it becomes 40mmHg. I understand that during gas exchange, the pressure gradient drives oxygen into the blood and Co2 out. My issue is that: since the partial pressure of oxygen in the alveolus is 104 mmHg and that of blood in the pulmonary capillary is 40mmHg, why would the partial pressure of oxygen in the blood after gas exchange also equal 104 mmHg and not 72mmHg since as oxygen leaves the alveolus the partial pressure drops and and increases by the same amount in the pulmonary capillary. At equilibrium shouldn't they both be at 72mmHg?  Mathematically speaking:
104-X(Alveolar PO2)=40+X(blood PO2)

There are three unfounded assumptions in your equation that I can see.

You're treating partial pressure as a concentration. Partial pressures are not concentrations, though they're convenient representations of concentration for gases because the behaviors of gases, especially with respect to diffusion between gases and liquids, behave according to partial pressure via Henry's law. For oxygen in blood, partial pressures are even more distinct from the "amount of oxygen per volume", because most of the oxygen carried in blood is bound to hemoglobin rather than floating freely/dissolved in the liquid.

You're assuming there is a finite amount of oxygen present in the alveoli, as if 104 mmHg of oxygen is present in the alveoli, and then blood comes and takes some of it away. That isn't the case; blood is constantly coming in through the capillaries, and there is constant diffusion and bulk flow of gases throughout the lungs (resupplied with external inspired air).

Following (1) and (2), it seems you're assuming the blood and gas are the same volume. This need not be the case.

Instead, to understand why the partial pressure of oxygen in blood leaving the lungs is the same as the partial pressure of oxygen in the alveoli themselves, it's important to realize that the surface area of the alveoli is absolutely massive, and that gases diffuse quite freely across distances the sizes of capillaries. They're the same for the same reason that if you put some water soluble dye in a glass of water and shake it up vigorously for a few seconds, you're going to find the dye evenly distributed. If it weren't evenly distributed to start, it's going to be very close when you're done. Same with blood through the lungs. If you put a little more oxygen into the alveoli, then a little more would flow into the blood; both concentrations would be higher, but they'd still be the same.
So, that tells you why the number is the same, but why is this number about 104 mmHg? Well, that exact number is going to vary by specific conditions, but you can be certain that the number will be an equilibrium somewhere between the atmospheric concentration of oxygen and the oxygen of blood entering the lungs. That averaging has already happened and is happening constantly all the time.

@ Bryan Krause; if the pressure in the alveolus is constant, then why is it that after the diffusion of O2 into the capillaries( in external respiration) the PO2 of Alveolar air reduces to 40 mmHg. Also, in internal respiration, the PO2 of blood reduces to 40 after Oxygen diffuses into the tissues, if pressure was constant there should be no reduction. BTW, I would appreciate if you could give me another analogy, the "dye" one was difficult to imagine.

I read somewhere that the difference between the vol of air in the alveoli and the vol of blood in the capillaries also plays a role in why the partial pressures are the same. And you also said it in your explanation, so I was wondering how they could be related

@Taofeek "the PO2 of Alveolar air reduces to 40 mmHg" - it doesn't. If you stopped breathing for a long time perhaps it eventually would, but not for normal breathing. "the PO2 of blood reduces to 40 after Oxygen diffuses into the tissues, if pressure was constant there should be no reduction" - I never said pressure was constant everywhere. There is low oxygen in tissues due to cellular respiration. Blood leaving the tissues has lower oxygen than blood entering the tissues, but blood leaving the tissues has about the same pressure of oxygen as the tissues themselves.

Another factor to consider is that oxygen is not (primarily) dissolved in the blood, it's chemically bound to hemoglobin.  So partial pressure may not be all that relevant.

@jamesqf Added that as an additional point under (1). It still remains that you can't treat partial pressures as concentrations for any solution, but it's particularly true for blood and oxygen (or CO2) as these are primarily carried by hemoglobin, so even if you used the partition coefficients for water or plasma you'd come up with some very wrong numbers.

source: Stack Exchange

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

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What does equilibrium curve signify?
While learning about gas exchange, I came across the haldane effect. Then i came across the CO2 -dissociation curve. Apparently the curves are "equilibrium curves". Does it mean that the curves were plotted when the system of blood was in equilibrium? Otherwise what does it signify?

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


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What is static compliance?
If static compliance is change in volume with respect to change in transpulmonary pressure, when there is no gas flow. My question is; if there is no gas flow, how would volume Change?

First of all, the definition that you have stated, is absolutely true in all sense.
Static compliance, theoretically, is indeed the change in volume with respect to change in transpulmonary pressure, when there is no gas flow. Here gas flow means air should remain static at the time of measurement. Hence it is literally about taking snapshots at varying volumes and noting the transpulmonary pressure.
Here is a diagram (source: https://derangedphysiology.com/main/cicm-primary-exam/required-reading/respiratory-system/Chapter%20031/static-dynamic-and-specific-compliance) i.e. identical to the original diagram from -

Rahn, H., Otis, A.B., & Fenn, W.O. (1946). The pressure-volume diagram
of the thorax and lung. Federation proceedings, 5 1 Pt 2, 82 .

For the above study, they acquired normal men, occluded their nostrils with cork stoppers, and measured their airway pressures at different fractions of their vital capacity (the subjects exhaled fully and then inspired a known volume of gas from the spirometer before performing a breath hold). With these manoeuvres, the above relationship was demonstrated.


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Ways creatures evolove
I can't find the right answers to my questions online .
are there other ways creatures evolove apart form nsatural selection?
Thank you

Artificial selection, to name one

Yes, there are a number of processes that affect evolution of populations.
The classification of these processes can be open to some philosophical discussion. For example, most authors, don't really consider natural and artificial selection as being different. Also, most authors tend to consider sexual selection as being a subset of natural selection. At the end of the day, the details classification does not really matter to science as long as we have clearly defined (mathematical) models of these processes. I will just list concepts below ignoring potential issue of classification:

Natural selection
Artificial selection
Sexual selection
Genetic drift (incl. population bottleneck and other demographic elements)
Gene flow, interbreeding and hybridization
Linked selection (genetic hitchhiking, background selection)

For more information about what evolution is and what are the processes that affect evolution of populations, you might want to have a look at a short very introductory course to evolutionary biology such as for example evo101 by UC Berkeley.


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prokaryotes and Evolution
I have a question that I did not find an answer to online and maybe anyone here could help.
Why are there still prokaryotes today? Why didn't they all evolove?

You are very deeply misunderstanding evolution. Prokaryotes are still evolving and will continue to evolve. Prokaryotes on the whole are extremely successful organisms (i.e. are very far from extinction), so the whole lineage did not need to abandon 'prokaryote-ness'. I am honestly and wholeheartedly afraid a more technical answer will be beyond your understanding. A simple google search will provide you with a million varied, concise responses. Conclusion: evolution is not teleological, i.e. evolution has no end goal in mind.

They did evolve, and they keep evolving every single day, like all other organisms.
Let's take an example. Prokaryotes acquire antibiotic tolerance in hospitals, and have evolved resistance to pretty much every antibiotic available, within a few years of their discovery.
More fundamentally, what is evolution (in a classic Darwinian definition)? Evolution is 1) the random apparition of new traits and 2) the selection of some of these traits because they provide some kind of advantage - antibiotic resistance is a perfect example.
Prokaryotes mutate much, much more than larger organisms like us, so they constantly try new biological strategies, and because their generation time is short, selection occurs much faster. So prokaryotes actually evolve faster than most eukaryotes!
I think you are confusing "evolving" with "becoming more complex", and then "becoming more complex" with "being larger and multicellular". Both of these are incorrect.
Prokaryotes live everywhere on the planet, even in places where animals and plants struggle to survive. They can live in water, in air, in the cold or in extreme heat, in acid, in pure brine... When you think about it, micro-organisms really rock! They can adapt to conditions much harsher than what we can tolerate. This ability to adapt is pretty much the definition of successful evolution.
I'll conclude with a bad analogy: what do you think is the most "advanced": an iPhone, or a big gaming desktop computer? They're both recent, they can do lots of things (some identical, some different) but one if not per se better than the other, they simply have different ways of being awesome, in different contexts.


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Simple interpretation of effective population size?
I'm looking for alternate ways to explain effective populations size, in more conceptual terms. These need not be perfectly accurate "definitions" but should at least be generally accurate in non-edge cases.
For example, if I have a population with a supposed effective population size of 1000, what (if anything) can I conclude about the amount of genetic diversity present within a single individual sampled at random from the real (census) population?
Like, would it be overly simplistic to say that the sampled individual could be expected to contain ~1/1000 of the population's standing variation? Or to say that a given (observed) nucleotide state has a 0.001 probability of being   fixed?
Again, I'm looking for anything that is not the standard way to explaining Ne
to somehow get a student's head partly into the game without being wholly misleading. Thank you

Like, would it be overly simplistic to say that the sampled individual could be expected to contain ~1/1000 of the population's standing variation?

It is a little unclear what you mean by "variation" here. If you mean "genetic diversity" aka "expected heterozygosity", then it would not just be simplistic, it would be wrong to say that!

Or to say that a given (observed) nucleotide state has a 0.001 probability of being fixed?

Ah that one is pretty good. If the effective population size $N_e = 1000$, then the probability of fixation a a new neutral mutation is $1/2N_e$ (assuming diploidy). The probability you indicate would be correct in a haploid population if you are talking about a new neutral mutation.
Another simple statistic you might want to consider is that, in absence of mutations, the genetic diversity would decrease by a factor $\frac{2N_e - 1}{2N_e}$ at every generation (assuming diploidy again).
You can derive a whole bunch of statistics of interests. For example, the expected genetic diversity in the total population at a locus at which the mutation rate is $\mu$ is $\frac{4N_e\mu + 1 }{4N_e\mu}$. You can derive many other statistics you might be interested in such as the expected number of segregating sites in a sample of size $k$ or the expected coalescent times for examples.
For more information just have a look at an intro course to population genetics. You'll find book recommendation in this post.


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How is the electrical potential difference distributed between two stimulating electrodes?
Suppose I set the voltage value of an isolated stimulator with a floating ground. I place one electrode above the spinal cord (positive) and the other placed subcutaneously far away from the spinal cord (negative). The circuitry within the stimulator will operate in such a way that the electrical potential difference between these two electrodes is the value I specify.
The stimulator can fix the electrical potential difference between the two electrodes in multiple ways:

Hold the positive electrode's potential constant while changing the negative electrode's potential.
Hold the negative electrode's potential constant while changing the positive electrode's potential.
Adjusting both electrode potentials using a rule.

Although each of these ways can fix the voltage between the electrodes, they do not have equal effects on the biological environment that the electrodes are placed in. Going back to my example, if the stimulator obeys 1, I would expect a larger effect to be induced local to the spinal cord, in contrast to 2, which would would have a greater effect in the subcutaneous area. This is because there is an initial heterogenous charge distribution.
How should I assume my stimulator is fixing the potential difference between my electrodes?

The situation is quite reminiscent of a Voltage clamp experiment (Fig. 1), where one amplifier (amplifier 1 in Fig. 1) records the potential difference (V1 - V2 in Fig. 1) between two electrodes and the other opamp (2) is used to inject current (I2 in Fig. 1) to 'clamp' the system at a particular voltage using a computerized feedback system. The potential difference is thus kept constant. As OP already mentions in the question, in Fig. 1 the charge density is locally much higher at I2, because current is injected there that dissipates across the cell (or tissue in your case) the farther it gets from its source.
Having said all that and to get to the question proper...

How should I assume my stimulator is fixing the potential difference between my electrodes

...I can only say the assumption is the mother of   all fu&% ups   many experimental failures. Instead, I advise you to either consult the device manual, or contact the distributer or manufacturer of the device to make sure what the machine is actually doing to clamp the voltage at a certain level.

Fig. 1. Voltage clamp setup. source: wikipedia

None of the three scenarios you describe are really different from another. Whatever process is used inside the amplifier, a voltage describes a potential difference between two points. It does not relate that to any other universal reference. If you have a ground connection, you could describe a different potential relative to ground, but that's not relevant here since you have no separate ground that gives an alternative electrical path to either of the contacts.
When you have a voltage between two points that are connected with less than infinite resistance, as you have in the biological environment you are stimulating in, you will get a current. That current will be exactly the same at each electrode. All that matters to determine how much current will flow is the voltage and the resistance/impedance between the contacts. You could get some differences in the stimulation duration/intensity around the two contacts if either acts like it has substantial capacitance, and the current density through the electrolyte solution surrounding each electrode can vary by the surface area of the electrode, but those are properties of the electrode, not how the voltages might compare to some unconnected ground reference.


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Is an attraction to studying the philosophy of biology a good reason to pursue grad studies in the field?
I have always leaned more towards questions surrounding psychology, sociology, and philosophy but fate has me graduating with a BSc in Biology this year. Would it be smart to pursue it further more for the aesthetic beauty I find in its ability to shed light on questions beyond itself than for the science purely in itself?

Welcome to Biology SE! Your question is off-topic here, as it does not relate to how biology works or laboratory techniques in biology. Maybe Academia SE would be a better fit? In addition, a word of caution: many good questions generate some degree of opinion based on expert experience, but answers to this question will tend to be almost entirely based on opinions, rather than facts, references, or specific expertise.

I'm voting to close this question as off-topic because is not about biology in terms of SE Biology but about career choice.

In my opinion, yes and bioethics is a very interesting domain.
 First, there is a growing interest in ethics (which is a branch of philosophy) in the fast-growing field of synthetic biology ("next-generation" genetic engineering, the design of new organisms, genetic manipulations in humans etc.). In many publications (check out "synthetic biology" and "ethics" on google) and conferences, people are saying how far behind is bioethics, compared to synthetic biology. There are many burning questions such as: If we create new organisms, should we release them to the environment? Should we edit the human genome? To what extent? (Just curing illness, or maybe also to improve traits?) Should this ability be democratized?
Should a person's genetic information be used when looking for a job? Insurance? And so many more questions, not to mention the bioethics of the state healthcare (compulsory vaccinations etc.)
There are a lot of scientists that know nothing about philosophy and a lot of philosophy experts that know nothing about science. There are not enough people who know both and can help with these question.


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Molecular psychology/psychiatry literature/articles
I am new biology student which is on molecular biology subject on university. I would like to know something about genetic related to neurobiology, and certainly molecular psychiatry/psychology, perhaps evolution psychology. But i dont know where to start.
Can anybody give me type to literature/articles for beginners?

For the neurobiology I'd recommend to read: Mapping the Mind and The Quest for Conscioussness , but these are kind of long books.
For shorter articles as (merely) an introduction, I'd recommend:
Manoli, D. S., Meissner, G. W., & Baker, B. S. (2006). Blueprints for behavior: genetic specification of neural circuitry for innate behaviors. Trends in Neurosciences, 29(8), 444–451. https://doi.org/10.1016/j.tins.2006.06.006
Good philosphical and historical viewpoint can also be found here:
Marler, P. (2004). Innateness and the instinct to learn. Anais Da Academia Brasileira de Ciencias, 76(2), 189–200. https://doi.org/10.1590/S0001-37652004000200002
For something more practical: The Little Black Book of Neuropsychology.
Looking forward to suggestions by others :)


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How many nucleotides in the DNA molecule?
Suppose I cut a human DNA molecule that was 6800Å long into 5 equal sized pieces using molecular scissors, how can I find out number of nucleotides in each of the cut pieces? Please give a bit detailed solution. I'm kinda new to these kind of questions.

This is a homework question. Such questions are considered on-topic only if a significant effort has been made by the asker towards finding out the answer. Moreover, if we do your homework for you then what will you learn?

What kind of efforts do you expect? Moreover, I am in my 10th grade and have very little knowledge on this topic. (And this is not a HOMEWORK question. I found these sort of questions in bunch of question papers).That was why I mentioned that I was new to these questions and I needed a bit of explanation
.SideNote: This is not even in my School Textbooks and I am asking this out of my own interest. I failed to find a concrete answer to this question online (if there exists one, please post it.)

At least in Math, I can tell people what formulae or theorems I`ve used. What do you exactly mean by efforts here? (Please tell, I am new.)

@WYSIWYG is a moderator on this SE Group (you can tell by the diamond). He is explaining to you as a new user how the site works. The answer to your question "What kind of efforts do you expect?" is given in the Help on asking questions which we expect you to make the effort to read. The fact that you are still at school is really irrelevant. If you read the tour you will see that "Biology Stack Exchange is a question and answer site for biology researchers, academics, and students". If you don't fit, don't post.

Angstroms are a measure of distance. 1 angstrom is a tenth of a nanometer, i.e. 10 nanometers make 1 angstrom.
Your DNA molecule: 6800 A
Cut into 5 equal pieces: 6800/5 = 1360
Each cut DNA piece is 1360 A long.
A DNA helix has the following properties: 10 base pairs extend 34 A.
1360/34 = 40 = how many '10 base pairs' of length you have in each cut DNA piece.
If a cut piece has forty 10 base pairs of length, the full length has 40 * 10 bp.
40 * 10 = 400 bp.
Each cut piece is 400 bp long. The original DNA piece, uncut, is five times the size of its cut. In other words, the original DNA piece is (400 * 5) 2000 bp long.


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Lobed Nuclei still count as One nucleus?
Do the Lobed Nuclei of immune cells (such as Megakaryocytes) still count as one nucleus?

Yes. Lobation is when a nucleus deforms, but it is still a single compartment. How the nucleus deforms can be helpful in roughly determining the cell type by visual inspection.


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Typical DNA replication times
Just out of curiosity (I am completely strange to biology), as I have been unable to find this info on the internet:
How long does the whole DNA replication process take? (say, the replication of a whole chromosome)
Approximately, how long does the DNA spend in a single helix structure during replication?
I am curious about the time scales of these processes, from the moment the polymerase starts cutting the double helix till the moment there are two double helices perfectly formed (one of them a copy of the other). How long can this take? miliseconds? seconds?

A mammalian cell takes about 8 hours to replicate all of its DNA in its S phase; a yeast cell would take about 40 minutes.
Some other information that you seem to not have quite the right information about:

The DNA polymerase does not unwind/split the DNA—that is the job of DNA helicase. The DNA polymerase cannot bind to the single-stranded DNA until the helicase unwinds the double-stranded DNA ("melts"), or the dsDNA is artificially melted in a test tube via high temperature.

The dsDNA is not fully separated before it is copied. There are tens of thousands of sites—origins of replication—across the genome that unwind and begin replicating every time the cell replicates its genome.

"...DNA replication in most eukaryotic cells occurs only during a specific part of the cell-division cycle, called the DNA synthesis phase or S phase. In a mammalian cell, the S phase typically lasts for about 8 hours; in simpler eukaryotic cells such as yeasts, the S phase can be as short as 40 minutes."
"An average-size human chromosome contains a single linear DNA molecule of about 150 million nucleotide pairs. It would take (0.02 seconds/nucleotide) x (150e6 nucleotides) = 3e6 seconds (about 35 days) to replicate such a DNA molecule from end to end with a single replication fork."
"...Approximately 30,000–50,000 origins of replication are used each time a human cell divides."

–Molecular Biology of the Cell, 6e, Alberts, et al.

Thanks for the answer and the extra info!

I think your view of DNA replication is a little off-target in relation to strand separation (which produces what you call “single helix structure”). The strands of the DNA are separated continually as replication occurs and then they are copied quite quickly by DNA polymerase. They are not separated completely and then copied. (And DNA polymerase doesn’t cut anything.)
But here are some typical times from on-line text books, where you can read more about the subject:
Bacterial cells
According to the text book The Molecular Biology of the Cell:

“It takes E. coli about 40 minutes to duplicate its genome of 4.6 × 106
  nucleotide pairs.”

And this has been discussed in an answer to a previous question.
Animal Cells
According to the text book, The Cell:

…human cells in culture, which divide approximately every 24 hours.

However, as explained out in the section cited, S phase — when DNA synthesis occurs — only takes about 8 hours. (Thanks to @rotaredom for pointing this out.)

Good answer, though I feel like your last quote doesn't address the question.  I know this isn't the most authoritative source, but this suggests that replication time is around an hour in humans.

@David if it's dividing every 24 hours, most of that time is not spent in the S phase.  The cell has to grow in order to sustain proliferation; hence a long amount of time must be spent in G1.  And it takes some time to get through G2 and M, of course.

Thanks @rotaredom. Have edited my answer, still keeping it to the minimum so that people will go to read the sources for themselves.


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What is the most frequently occurring health problem of rodents caused by the usage of pesticides on the agricultural fields in the United States?
For centuries the mankind has used pesticides to protect its crops but within the last century the pesticides have become more artificial and toxic. It is a well known fact that most of the pesticides can have fatal consequences, when one consumes them to much, as different studies have shown links between the pesticides and different diseases like cancer, ADHD and also different birth defects. People today are more aware about it and try to eat more organic food, but the pesticides are still in constant use and therefore it is still a threat to animals, who are in direct contact with the pesticides.


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How do scientists determine the nature of ions passing through a channel/carrier/pump?
The NCE (Sodium Calcium Exchanger) transports 3 Na+ inside the cell for 1 Ca2+ outside.
How did we figure this out, and other mechanisms of this sort?
If it were a protein, we could tag it with GFP. But they're ions.
Looking at potentials isnt very informative either I guess; both K+ and Na+ have the same charge.
What is done, experimentally?


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Contracting mouth muscles as reaction to taking in specific food items
When eating very specific food items, especially confectionery like (salty) liquorice, (it feels as if) the muscles of my mouth contract, right when it hits my tongue.
Does anyone know why this happens?
The process is similar to experiencing relatively high levels of sourness - suggesting it is a similar reaction - but, as far as I know, there is, apart from the glycyrrhizic acid in the liquorice plant, not a lot of acid in this type of confectionery. I imagine other possible causes could be sugar substitutes like steviol or Maltitol.


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Can someone help me interpret these charts on fluorescent polarization?
I have to present an article about binding designed proteins to fentanyl for my biochem class; I understand everything except how to interpret these charts on fluorescence at the very top of Figure 2a: https://elifesciences.org/articles/28909#fig2
It seems fentanyl was tagged with PE and the proteins (Fen49 and 2QZ3) were tagged with FITC. Fen49 binds with fentanyl and 2QZ3 doesn't but I don't know what about these charts tells me that. Is it the blue specks scattered all over 2QZ3's graph? I'm also confused about the bar graph next to it representing mean fluorescence - does it represent the binding affinities of these proteins/mutations to fentanyl?

These charts are flow cytometry graphs, something not explicitly stated in the figure description, but obvious to everyone who has seen similar graphs before (and I assume it's at least mentioned in the method section of the paper, I didn't read that though).
Each dot in a flow cytometry graph represents a single cell and, as you correctly identified, the PE & FITC flourescence corresponds to fentanyl and the respective proteins of interest. (The labelling was done somewhat indirectly and as is typical for flow cytometry with antibodies but that doesn't matter for the interpretation.). The dots are coloured according to their density: blue indicates only single dots and warmer colors show increased number of overlapping dots (with red being the highest).
It is also important to note that all the axes in these graphs have logarithmic scales, so the shifts you see in the graph represent shifts in orders of magnitude.
The combination of the logarithmic scale with per cell data points means, that you also see 'negative cells' on each axis: along the FITC axis (which represents expression of the protein) you can make out two groups of points. The lower one of these groups has cells that don't express the protein (meaning the florescence detected is just background from staining), while the higher groups contains cells that do express the protein (the staining for the protein is significantly above background).
If you now compare the two proteins you can see that high (protein expressing) group for Fen49 also has an increased signal for PE (which represents fentanyl), meaning that these cells bind fentanyl. In contrast with that for 2QZ3 the fentanyl signal is independent of whether the cells have a low signal or high signal for protein expression.
The bar graph on the right gives the average PE (fentanyl) levels for other additional protein variants. The figure description doesn't explicitly say whether this is the average of all cells or only the ones expressing the corresponding protein at above background levels.


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How DNA probe binds
I am studying about southern hybridization now and I've a doubt.After the DNA has been fragmented using restriction enzymes and obtained on nitrocellulose blot , it is still double stranded (the fragments) so how do single stranded probes bind to it ?

The double-stranded DNA fragments are fractionated by size during the agarose gel electrophoresis.  Prior to the so-called “blotting” step, the gel is briefly soaked in a solution of NaOH, which has a relatively high pH.  Under these conditions, double-stranded DNA will denature, or “melt” into two single strands.  This is the material that is “wicked” or “blotted” onto the nitrocellulose membrane in the presence of monovalent cations.
If the labeled probe DNA is also double-stranded then it is advisable to denture it as well prior to the hybridization step.  We used to use boiling hot water to denature the probes.


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Can mutation take place in G1 and G2 phases during the cell cycle?
We know that the DNA replicates during the S phase in Interphase. There it might undergo a number of mutations. We also know that the forward half strands are more susceptible to undergoing a mutation since they live most of their lives single-stranded. But can mutation take place anytime before or after the replication? It is weird that the strands "wait" to open up in the S phase and only then undergo a mutation.

Yes, it can. A mutation can potentially occur at any given moment in the cell cycle, not only in S phase, which is why revision mechanisms remain alert during the whole cycle. Such mechanisms not only make sure every important event in the cycle takes place adequately (e.g. DNA replication, chromosome segregation) but also repair any damage associated with DNA (e.g. AP sites, single strand breaks, double strand breaks, to name a few). Once DNA damage takes place, specialized sensors detect such events and activate several mechanisms. One of these will pause the progression of the cell in the cell cycle, and another will repair the DNA-associated damage, in case that it can actually be repaired [1].
[1] Karp, G. (2009). Molecular and Cellular Biology: Methods and Concepts. Wiley. New York.


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Depolarisation of post synaptic neuron
When the post synaptic neuron begins to depolarise as positive sodium ions move into it and it reaches threshold- does the inside of the neuron actually switch to being more positive than the outside?
I thought depolarisation meant that the inside became less negative but still remained more negative than the outside, hence having a voltage of -55mV. If the inside became more positive wouldn't the voltage be 55mV?

How does relatively positive and positive make a difference, since what propagates is the change in voltage difference, which will be positive in both cases?

When the neuron reaches threshold, this is the trigger that leads to sodium channels opening and this creates a positive feedback process causing the neuron to become less negative and more positive, triggering more sodium channels to open until it is inevitable an action potential will be reached. During an action potential, the neuron cell becomes more positive compared to the outside for a very short period(ie, 1 millisecond or less).
Yes, depolarisation does mean the inside becomes less negative in this context.
You would expect the inside of the neuron to be at +55mV (or perhaps more) during an action potential, as the depolarisation of the neuron grows closer to reaching the sodium equilibrium potential which is estimated to be around +58mV. However, during the phase leading up to an action potential, potassium channels also remain open. The diffusion of potassium ions can lead to the cell becoming more negative. In other words, it limits the voltage of an action potential to around +33mV instead of +55mV.
Sources:
(1)https://www.khanacademy.org/science/biology/human-biology/neuron-nervous-system/a/depolarization-hyperpolarization-and-action-potentials
(2)https://opentextbc.ca/anatomyandphysiology/chapter/12-4-the-action-potential/


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What chemical test can be used to tell apart meat and plant-based meat?
Long story short, I thought about this question and simple Google searches weren't enough. I know there must be some nutrient that can only be found in one of the meats but not the other, but I can't seem to search for it.
For this scenario, just assume that the 2 meats are exactly the same in terms of texture, color, consistency, taste, etc., to the point where only chemical tests can tell one apart from the other.

Testing for cellulose seems like an obvious choice; unfortunately, cellulose (sometimes loving referred to as "wood pulp" in a food setting) is a common additive to processed foods, including meat. Ex: Is there wood pulp in your burger or taco?

@theforestecologist good point, though for balance, I might mention that the article you linked makes it sound like a bad thing that there be cellulose in your food, which is not the case.

@rotaredom ha, right! Thanks for "balancing out" my link! Good follow-up :)

There are a lot of things you could test for.  The thing that come to mind off the top of my head is cholesterol.  This will be present in all animal meat, since all animals muscles contain cholesterol, whereas meat substitutes usually do not.
That said, there are other options as well (such as starch vs. glycogen levels, for example), and even molecules such as collagen differ between plants and animals, so a careful analysis (provided the proteins have not been too altered by the commercial production process) should be able to reveal thousands of differences, even in molecules found in both plants and animals.
Further reading

Marzetta CA, Rudel LL. 1986. A species comparison of low density lipoprotein heterogeneity in nonhuman primates fed atherogenic diets. Journal of Lipid Research.  27: pp. 753-762

Sorry for responding so late. Nevertheless, based on the research linked, it seems that significant effort would be required to make meat substitutes taste like actual meat.


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What differentiates neurons in different parts of the brain?
For example: what makes a neuron in the hippocampus of the brain different from a neuron in, say, the amygdala, or the frontal lobe, or anywhere else in the brain? Do neurons in different parts of the brain have different structures, or are they differentiated solely by location?
By "different structure", I mean things like receptors that other neurons don't have and things like that.

There are differences in receptor expression and morphology, but it would be beyond the scope of an answer in this site's format to enumerate. The major differentiating factor is most likely the source of their inputs.

They express different genes as pointed out by @vkehayas. Is your question about why there is a difference or how the difference came to be?

During development of the brain neurons undergo several steps of differentiation. They transition from neuronal progenitors to mature neurons, resulting in different types of neurons, characterized most prominently by their primary neurotransmitter. During the differentiation, different genes are expressed, which in research is used to label specific cell types (to e.g. observe their distribution in the brain). Since timing is important in development and neurons migrate to their side of action, later born neurons often display different features than earlier ones. The final differentiation is also dependent on the environment, meaning surrounding cells can influence the outcome.
Not just neurotransmitters, also other surface molecules, types of synapses formed, morphology and many other genetic differences influence neuron function and their diversity. Each brain area has many different neuronal cell types, some are similar between brain areas, while others might be very specific to one area. As an example, there is a microRNA, expressed in only 6 neurons of the nematode worm C. elegans, that is essential for their specific function to sense CO2 by repressing other genes (publication).
Taking the example of your question, here is a paper on the diversity of GABAergic neurons in the amygdala (there are several different types of neurons having the same neurotransmitter but expressing otherwise specific markers, which results in different specific functions in the circuits). The author compares them to GABAergic neurons in the cortex (including hippocampus), where a similar function might be taken over by a different cell type (expression profiles are distinct due to different lineages and environments and can be labeled by different markers).


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How do painkillers prevent shock?
I was reading about the Placebo effect and came across this little story:

The roots of the placebo problem can be traced to a lie told by an
  Army nurse during World War II as Allied forces stormed the beaches of
  southern Italy. The nurse was assisting an anesthetist named Henry
  Beecher, who was tending to US troops under heavy German bombardment.
  When the morphine supply ran low, the nurse assured a wounded soldier
  that he was getting a shot of potent painkiller, though her syringe
  contained only salt water. Amazingly, the bogus injection relieved the
  soldier's agony and prevented the onset of shock.

https://www.wired.com/2009/08/ff-placebo-effect/
I also read that Morphine specifically lessened the effects of shock:

Only when it is severe, or when a severely wounded or injured person must be moved quickly (as from a wrecked vehicle or aircraft) it is wise to give Morphine at once. It may not always relieve the pain entirely, but will certainly lessen shock.

https://web.archive.org/web/20140420133119/http://www.med-dept.com/morphine.php
So, how do painkillers prevent wounded soldiers from going into shock and dying? What physiological mechanisms are responsible? Is it something to do with blood pressure? Heart rate? Pain itself?

A little clarification: what exactly do you mean by 'shock'? In modern medical terminology, it means a state of generalised tissue hypoperfusion. In days of old, it was often used for what is now called an acute stress reaction (which is a psychological phenomenon rather than a physiological one). Which one do you mean here?

1) Pain can aggravate hypotension, so painkillers may help to prevent shock.
A severely wounded person with significant blood loss can develop hemorrhagic shock due to drop in blood volume and consequently drop of blood pressure and insufficient perfusion of vital organs.
It is known that pain can trigger vasovagal syncope, also known as neurocardiogenic syncope in which a person faints due to sudden drop of heart rate and arterial vasodilation resulting in drop of blood pressure and reduced brain blood perfusion.
Here is an example how carbamazepine, which prevented pain, also prevented the episodes of neurocardiogenic syncope (The Korean Journal of Pain):

A 65 year-old male patient diagnosed with glossopharyngeal neuralgia
  complained of severe paroxysmal pain in his right chin and ear
  followed by bradycardia, aystole and syncope. We report a case
  successfully treated with a permanent pacemaker and carbamazepine in a
  patient with GPN who had syncopal attacks preceded by paroxysms of
  pain.

In an injured person who is at risk to develop hemorrhagic shock, severe pain could cause neurocardiogenic syncope that could proceed into shock, so, it sounds logical that painkillers could help to prevent shock.
From the first quote in the question (the patient was convinced he was receiving a strong painkiller), we cannot conclude that the painkiller prevented shock, because this has not even started to develop.
2) Analgesics for a person in severe pain who has lost blood and is in danger of developing shock.
According to Pain Control in Trauma Patients (Trauma Reports, 2011, fentanyl can be appropriate painkiller in shock since it does not aggravate hypotension:

Fentanyl is the best known synthetic agent and is widely used in pain
  control. It is 50 to 100 times more potent than morphine and has the
  added benefit of not causing histamine release and peripheral
  vasodilation, as found with morphine administration. Based on this
  physiology, fentanyl should not impact blood pressure as much as other
  narcotics and, therefore, is preferential in the critically ill trauma
  population who may have tenuous cardiovascular status from hypovolemic
  shock.

Morphine can cause hypotension, so it may aggravate shock. According to prescribing information for morphine sulfate oral solution by FDA.gov, 2018:

In patients with circulatory shock, Morphine Sulfate Oral Solution may
  cause vasodilation that can further reduce cardiac output and blood
  pressure. Avoid the use of Morphine Sulfate Oral Solution in patients
  with circulatory shock.

In conclusion, painkillers may help to prevent shock by reducing pain.

This answer is factually incorrect. It makes an incorrect connection between vasovagal syncope and shock. The two are fundamentally different entities.


text:
How do organophosphates affect kidney function?
Many organophosphates, besides inhibiting acetylcholinesterase, can also permanently inhibit the enzyme neuropathy target esterase, leading to nerve damage. NTE also happens to be found in the kidneys, and is involved in osmolyte production. Have organophosphates been known to affect kidney function through the inhibition of NTE in the kidneys? If so, how?
Source:
Gallazzini, M., & Burg, M. B. (2009). What’s New About Osmotic Regulation of Glycerophosphocholine. Physiology, 24(4), 245–249. doi:10.1152/physiol.00009.2009

One article suggests that NTEs in kidneys are important for regulating NaCl concentrations, whereby if increasing concentrations of NaCl are sensed in inner medullary collecting duct cells transcription of the building blocks of NTEs are increased to decrease this NaCl. If NTEs are inhibited due to being irreversibly bonded with moieties of organophosphates at their active sites then this would mean that the kidneys would lose their mechanism for controlling how much salt is excreted from the body.
Gallazzini, M., Ferraris, J. D., Kunin, M., Morris, R. G., & Burg, M. B. (2006). Neuropathy target esterase catalyzes osmoprotective renal synthesis of glycerophosphocholine in response to high NaCl. Proceedings of the National Academy of Sciences, 103(41), 15260 LP – 15265. https://doi.org/10.1073/pnas.0607133103
This loss of chloride and sodium, I posit, would then have a knock-on effect on the concentration gradients maintained in the kidney as necessary for effective absorption and excretion of other ions. My guess is that hyponatraemia would be one of the direct results of the presence of organophosphates in the kidneys.


text:
To what extent does loss of neurons in the substantia nigra affect movement?
There is a substance known as MPTP that is capable of crossing the blood-brain barrier. Once it does so, it is metabolized into a toxin called MPP+, which then selectively destroys dopaminergic neurons in the substantia nigra pars compacta of the brain, causing parkinsonism. This effect of MPTP was discovered when drug users were poisoned with it in the 1980s.
How much of an effect does this destruction of neurons have on movement? Were these patients completely paralyzed as a result, or did they retain some ability to move voluntarily?

Great questions!  Here's some quick answers, but I'll give an additional little recommendation at the end if you're interested:
How much of an effect does this destruction of neurons have on movement?

Answer:  A large effect.  The key term here is "Parkinsonism," meaning that the symptoms resemble Parkinson's disease. This often involves motor symptoms like shuffling gait, tremors, rigidity, and bradykinesia (which means slow movement).  While they typically don't result in total paralysis, these symptoms can be debilitating and require treatment, such as L-dopa.

Were these patients completely paralyzed as a result, or did they retain some ability to move voluntarily?

Answer:  Generally, these patients were still able to move, but they greatly struggled with controlled movements.  As stated above, Parkinsonism/Parkinson's disease is marked by many motor symptoms, but these do not result in complete paralysis.  Rather, they make voluntary movements more difficult and slower.  According to a paper entitled "The MPTP Story (doi: 10.3233/JPD-179006)" it appears that at least one patient was nearly (if not totally) catatonic and exhibited very little voluntary movement.

If you'd like to know why this is the case in Parkinsonism and Parkinson's disease, I'd encourage you to look up the direct and indirect pathways of the basal ganglia online.  There's likely a good lecture with helpful visuals on how these pathways work to facilitate (direct) and inhibit (indirect) movement by their effects on the thalamus and motor cortex.  Alternatively, you can let me know you're interested via a reply and I'll do my best to explain those pathways on here.  Hope this helps!


text:
What are the methods of prophylaxis against exposure to radioactive isotopes?
Potassium iodide is used as prophylaxis to prevent illness when one is likely to be exposed to Iodine-131 and other radioactive isotopes of iodine. Are there any other prophylactic treatments for exposure to other radioactive isotopes, such as Cesium-137, Tritium, Strontium-90, etc? If so, how do they work?

What research have you done to find this out yourself?

@David I read the Wikipedia articles on Iodine-131 and Potassium Iodide. I also searched "Tritium Poisoning Treatment" on Google and got this result: https://io9.gizmodo.com/drinking-a-beer-can-save-you-from-radiation-poisoning-1648955835 , so apparently one method of prophylaxis against tritium poisoning is diuretics and increase fluid intake, but I'm wondering if there are others. The Wikipedia article on Cesium 137 claims that exposure can be treated with Prussian Blue. This: https://www.dhss.delaware.gov/dph/files/strontiumfaq.pdf claims that there are no direct treatments for Strontium-90

So I am wondering whether there are any measures one can take (Besides donning protective equipment) before being exposed to Strontium-90 and Cesium-137, rather than after.


text:
Are there any proteins not found in the brain that are affected by prions?
A prion is an abnormally folded protein that is capable of causing otherwise normal proteins to also misfold and become prions. They are responsible for causing diseases such as Kuru and Creutzfeldt–Jakob disease. These are both diseases of the brain. Are there any non-brain proteins that also have corresponding prions that can cause disease, or do prion diseases only affect the brain?

Yes, malformed prion proteins can affect tissues outside of the brain.
Via: https://www.merckmanuals.com/home/brain,-spinal-cord,-and-nerve-disorders/prion-diseases/overview-of-prion-diseases

Another familial prion disease has been recently discovered. It differs from other prion diseases because it causes diarrhea and affects nerves throughout the body years before symptoms of brain malfunction develop. It is described as prion disease associated with diarrhea and autonomic neuropathy.

Via: https://www.merckmanuals.com/home/brain,-spinal-cord,-and-nerve-disorders/prion-diseases/prion-disease-associated-with-diarrhea-and-autonomic-neuropathy

Symptoms begin when people are in their 30s. People have persistent watery diarrhea and bloating. They may lose weight. Because the nerves that control body processes are affected, people may not be able to pass urine (called urinary retention) or may lose control of their bladder (urinary incontinence). Their blood pressure may drop when they stand up, causing them to feel dizzy or light-headed (called orthostatic hypotension). People may lose sensation in their feet. Later, when people are in their 40s or 50s, mental function deteriorates, and seizures may occur.

Prion disease is caused when cellular prion protein (PrPc) is misfolded to form abnormal prion protein called scrapie prion protein (PrPSc). These newly formed abnormal prions can't be degraded by enzymes so they keep on accumulating and are responsible for stimulating other normal proteins to fold improperly and form protein aggregates.
Accumulation of these amyloids cause diseases and these misfolded prions can't be converted back to normal prion protein.
Via: https://ghr.nlm.nih.gov/condition/prion-disease#genes
These prion proteins (PrPc) are present throughout our body but in lesser proportion as compared to brain cells and  recent studies have shown the possibility of this protein aggregation the cause of diseases outside the brain,
Via: https://www.ncbi.nlm.nih.gov/pubmed/21481020
MAVS, RIP1, and RIP3 are other prion-like proteins which are found in other parts of the body. These are not responsible for causing any disease. These proteins aggregate into filamentous amyloid and lead to cell death to prevent the spreading of viral infection.
Via: https://www.nature.com/articles/s41418-018-0172-x

Although it may hadn't be described, I think that nothing chemical or physical would be an impediment to affect other organs, so, said this, in my opinion they could exist.
I found this one affecting outside the brain
 https://www.nejm.org/doi/full/10.1056/NEJMoa1214747 , I hope that this it's useful to you.
Héctor.


text:
What particular genetic mutations gave Europeans increased resistance to smallpox?
It's widely stated that a large chunk of the Native American population was wiped out by diseases (Notably smallpox) introduced by European colonists to which the natives did not have a resistance. My question is: Exactly what mutations in what genes did Europeans have (Which the natives lacked) that conferred greater resistance to smallpox compared to the native populations?

First, it is unlikely to be one specific mutation. Such strong selective pressures can lead to many forms of resistance.
Second, even for the mutations we suspect, smallpox is not a heavily studied disease, so definitives are rare.
That said, CCR5 Δ32, a mutation in the CCR5 chemokine receptor protein on immune cells, is believed to be related to smallpox, although the black plague is also a candidate. Today, the mutation is studied because it confers resistance to HIV. We know it was not originally a response to HIV because it showed up long before HIV made the jump to humans.
https://www.pnas.org/doi/10.1073/pnas.2435085100.
Now, of course, for the original contact, the European's normal adaptive immunity from contracting it earlier in life would also come into play,  since many Europeans contracted it or the related cowpox during their life.  While for the native Americans, it would be a completely new disease, so no one had any adaptive immunity, meaning it could spread like wildfire.

None, because that's not how immunity works in the case of smallpox.
Most Europeans caught smallpox in childhood (or a variant; discovering that cowpox protected against smallpox led directly to the first vaccine).
A large proportion of those children died (or were blinded). Wikipedia says the death rate was 30%. This was just one of the many reasons that you'd have a large family, because 8 out of 10 children dying before adulthood from now-preventable causes was pretty normal. It's not clear - and it still isn't - whether surviving infectious diseases is down to some "better" genes, better care because of some familiarity with the disease, or simply blind luck.
You therefore have a preselected group of Europeans who, by their survival past childhood, had developed immunity to smallpox.  Conversely you have a group of Native Americans who had no immunity and who had no experience caring for people with the disease.
Tribes which survived first contact then also had this immunity, of course. Children continued dying in childhood, but surviving adults were immune after infection.

If that's not how it works, what's going on with sickle cell disease and malaria?

that's not how it works in this case ...

@PasserBy Different things! :) Sickle cell doesn't make you immune to malaria, it just makes it harder for the bug to get into blood cells. Think of sickle cell as putting armour on the blood cells to keep intruders out (which also stops them doing their job properly; it's not a good thing to have!) versus immunity which is like an army of security guards learning how to take down intruders.

That adaptive immunity largely explains Europeans' better smallpox survival rate does not imply there is no such thing as mutations associated with European ancestry and smallpox resistance. Smallpox usually kills in childhood, meaning that any resistance-associated mutations would indeed face significant selection pressure. The question is slightly misguided in focusing on mutations as primarily responsible for differential survival rates, but this answer is slightly misguided in simply dismissing their potential existence: https://www.science.org/content/article/smallpox-s-medieval-legacy

Basically, the fact that European individuals had adaptive immunity and Native Americans didn't does not mean that the European population did not have a genetic advantage after centuries of selective pressure killing off the least smallpox-resistant members of the population at an early age.

@Graham - That mechanism is really strange. Are you sure that's how sickle cell trait is helpful against malaria? That's very different from most everything I've read. (One source: https://malariajournal.biomedcentral.com/articles/10.1186/1475-2875-12-317.) Please don't guess at answers, even in comments.

I only now realized your claim pertains specifically to immunity. Yes I'm aware that sickle cell disease is not immunity, but OP is asking about resistance towards smallpox, which is now addressed by other comments.

Well, selection for beneficial genetic traits under adverse pressure is exactly how evolution works, so genetic differences which confer better resistance in populations where a disease is endemic compared to populations in which it is not are basically unavoidable (barring very special circumstances). That does, of course, not preclude the mechanisms you describe; but to start the answer with "None" and not provide a single reference for the very unlikely claim that such a resistance due to genetic differences does not exist is not up to the standard I'd expect here.

To put it bluntly, your answer does not even properly address the question beyond your initial "None"; you explain acquired immunity and survivor bias, while the question asks about resistance from genetic differences.


text:
Post-Translational Modification in insulin production
When searching "How is insulin produced commercially" on Google, most results simply say something along the lines of "The insulin gene is inserted into a bacteria, which then express the gene and produce insulin". As far as I know, the peptide produced from the INS gene is subjected to several post-translational modifications to form the actual insulin, but I couldn't find much information on how these PTMs are carried out in the recombinant organisms.
Therefore, my question is: How are post-translational modifications carried out during commercial production of insulin? Do E.Coli and yeast cells just naturally have the machinery to carry out the necessary PTMs on the peptide translated from the INS mRNA, are other genes inserted into the recombinant organisms as well, or is the formed peptide just taken as-is and manually subject to chemical treatment to carry out the needed PTMs?

The wikipedia page on insulin has some information in the last para in the Structural analysis and synthesis section; you might want to follow up the references there.

No E.coli are not able to perform PTMs for insulin production.
But additional genes or special modified strains of E.coli may be used for increased efficiency.
The gene sequence of the proteins is optimized to match the codon use of the strain.
tRNAs can also be coexpressed so that they are not limiting synthesis.
Chaperones can prevent formation of inclusion bodies, which facilitates the workup.
There are two common methods for insulin production:
Expressing proinsulin or expressing A and B chain separately and joining them chemically.
In E.coli the proinsulin sequence (containing a ZZ tail sequence for later purification) is inserted in a plasmid.The expressed protein forms inclusion bodies (protein aggregates of overexpressed protein). Those are isolated, the protein is subjected to multiple chemical treatments and purifications:

Solubilization
Denaturation
Renaturation
Purification over affinity tag chromatography
Site specific cleavage of the C-peptide
Reverse phase chromatography
complexation  with zinc for formulation purposes

For detailed and additional information:
http://bmrat.org/index.php/BMRAT/article/view/692


text:
How to isolate a high proportion of available helminth ova from animal faeces/feces without damaging them?
I need to isolate large numbers (tens to hundreds of thousands) of cat (and later dog) hookworm ova from cat/dog faeces.
I have a centrifuge, and various sieves with pore sizes of 20, 63, 75, 106, 125, and 180 microns as well as the ability to create various flotation solutions to any specific gravity
The specific gravity of the ova is 1.21 and they are oblong, their size is 50 by 38 microns varying by ±5 microns.
I have tried sieving the cat faeces after emulsifying them using a liquidiser. I pass them through successively smaller pore size sieves but the concentrated ova still contains a very large admixture of unwanted faecal material.
Flotation following sieving by bracketing the ova in successive flotations of iron sulphate results in too much contamination and many ova are lost.
My technique is self-taught and clearly lacking.
I need to remove 98-99% of the unwanted faecal material without damaging the ova, which are not very resilient.
My access to equipment any more sophisticated than that listed is unlikely but if costing less than a thousand pounds possible.
I am new to this area, so I am sorry if I have omitted anything required or failed to follow form and protocol.
Thank you very much in advance.


text:
Interpretation of genetic results
Result of genetic testing indicated: c.341del, p.Thr114Lysfs*37.
The c.341del probably means:deletion at the cDNA 341 nucleotide.
Buy what does the second part:p.Thr114Lysfs*37 ?

I think this question could use additional context. Please update with some more detail. Also, we ask that all question aksers do some of their own research and report what they've already learned or tried. Please take the time to see what you can find on your own, and the community can try to help you if you get stuck.

You are right about the cDNA 341 nucleotide deletion.
It is an exon deletion, meaning that the deletion is part of a gene that encodes to a protein.
This corresponds to the second part - the protein level (annotated with p.).
The mutation that is caused on the protein level is a frameshift mutation (corresponds to the fs).
A frameshift mutation changes the reading frame of the protein.
You can find more information on frameshift mutations annotations on the HGVS nomenclature website.
In your case (p.Thr114Lysfs*37) the annotation indicates that the cDNA 341 nucleotide deletion led to a frameshift mutation of the protein with a Thr amino acid residue being replaced by a Lys amino acid residue. Furthermore, this also altered when the protein terminates: there is a new translation termination (stop) codon after 37 amino acid residues instead of terminating at the end of the protein where it normally does.

Great additional information. You are right about all of your questions, according to the ref.


text:
Why is the ingestion of salt and water beneficial to muscle cramp
According to Wikipedia, muscle cramps are caused by the inability of myosin fibers to break free from the actin filaments during contraction, resulting in a prolonged contraction.
A lack of ATP would obviously produce cramping, as myosin requires ATP to become free from actin.
However, I have heard that potassium and sodium are useful for treating cramps and that their deficiencies can lead to cramping.

Your title says salt and water; your last line says sodium and potassium; presumably you mean electrolytes and water in general. The only reason this level of vagueness can be answered is that there's not much evidence for any of it.

After answering this, I see the question is very similar to https://biology.stackexchange.com/questions/7847/what-is-the-cause-of-muscle-cramps by the way, which however I think has a very bad accepted answer.

Magnesium!!! it's the most common mineral defficiency in the world, 40% of humans are magnesium deficient! Water and Salt are abundant. Magnesium is also used in nerves, and it known to reduce cramps. in fact, in hospitals they inject pure magnesium solution into asthma attack patients because it has an immediate effect. it also helps with deep sleep.

Maybe it isn't.

The standard theory: muscle cramps are caused by loss of fluids and electrolytes, which alters fluid balance in the body and increases the excitability of nerves.
The "new" theory: muscles cramps result from "altered neuromuscular control," which can be triggered by a variety of factors, including genetic predisposition, damaged or fatigued muscles, starting too fast, and not tapering enough -- none of which have anything to do with hydration or electrolytes. [...]
A few years ago, researchers at North Dakota State University published a study showing that dehydrating subjects by 3% of their initial body weight didn't change their susceptibility to muscle cramps (as measured by threshold frequency). Now, in a new British Journal of Sports Medicine study, they've extended those results to a greater degree of dehydration: their 10 subjects reached an average dehydration of 4.7% (greater than 3% is "significant" dehydration, while greater than 5% is "serious") after almost four hours of exercise in very hot conditions. Crucially, they exercised only with their non-dominant limbs, while the cramp testing was performed on their dominant leg, so that muscle fatigue/damage could be eliminated as a triggering factor.
The result: no difference in cramp susceptibility or intensity, despite an extreme dehydration protocol that saw them lose about 4 g of sodium! The researchers conclude that their data supports the "altered neuromuscular control" theory.

Even the older research that did find it more plausible that electrolytes were a cause wasn't very adamant that's the [only] cause, e.g.:

Consumption of a carbohydrate-electrolyte beverage before and during exercise in a hot environment may delay the onset of EAMCs [Exercise-associated muscle cramps], thereby allowing participants to exercise longer. However, it appears that dehydration and electrolyte loss are not the sole causes of EAMCs, because 69% of the subjects experienced EAMCs when they were hydrated and supplemented with electrolytes.

There are a few [not very well controlled, IMO] experiments from the 1920s and 30s (three papers to be more precise) that did find a role for sodium depletion in some cases of mild cramping. The most controlled of these (published in 1936) involved sodium depletion for 10 days (daily sweating and virtually no intake), which  is hard to argue is that common in most cramp suffers. The original paper notes that the level of sodium depletion involved led to quite a few other symptoms:

Such deprivation led to aberrations of flavour, cramps, weakness,
  lassitude, and severe cardio-respiratory distress on exertion. The nitrogen balance became negative and the blood urea rose.

And despite the severe sodium depletion, the cramps were mild but generalized:

These muscular cramps were not of the very severe localized type which are
  said to affect stokers and miners (Moss, 1923-24), but were widespread,
  frequent, not very painful, and generally controllable. Any muscle in
  the body was liable to go into spasmodic contraction, especially if some
  little effort was demanded of it (Moss, 1923-24). “ Coughed a little
  over something, cramps round chest, mild.” * R.B.N. experienced
  occasional cramps in the muscles lining the floor of the mouth but the
  extremities were most affected, and it was possible sometimes by suitable
  movement of the toes to alternate the spasms for hours on end between
  the extensor and flexor muscles. Perhaps the most characteristic of all
  were the manual cramps. R.A.M. experienced “ constant mild cramps
  of the fingers and thumb when using forceps at the balance,” * and R.B.N.
  found that he “ cramped quickly when working, telephoning, or using
  pipettes.” *

So that's why I say these types of cramps probably have little relevance for those experienced by most people.
I'm not sure there any studies for potassium. The paper reviewing the sodium evidence notes:

Mechanisms in heat cramping remain murky. Sodium loss contracts extracellular fluid space and may alter ion channels to make neuromuscular junctions or muscle units hyperexcitable, thus evoking
  involuntary and sustained contractions, or heat cramping. And, not all camps buy salt loss for  cramps. Bananas, for example, remain popular in some football camps, to prevent heat cramping by ‘replacing potassium’. But here, bananas are yellow herrings because little potassium is lost in sweat. The same applies to calcium and magnesium. Sweat after all, is mainly water and salt (sodium chloride).

And do note that his latter paper is written by a Gatorade consultant.
One 2009 review in clear opposition to relevance of electrolytes-water for the usual exercise-related muscle cramps notes:

In summary, dehydration and electrolyte depletion are often considered together (and recently together with muscle fatigue) as the “triad” causing EAMC. The key components of this hypothesis (fig 1) are that electrolyte (mainly sodium) depletion through excessive sweat sodium loss together with dehydration causes EAMC. However, results from prospective cohort studies consistently show that athletes suffering from acute EAMC are not dehydrated, neither do they have disturbances in serum osmolality or serum electrolyte (notably sodium) concentrations. Furthermore, sweat sodium concentrations measured during exercise in 23 reported cases with a past history of EAMC are not higher than those reported in many other studies. Both electrolyte depletion and dehydration are systemic abnormalities, and therefore would result in systemic symptoms, as has been observed in other clinical conditions. However, in EAMC, the symptoms classically are local and are confined to the working muscle groups. Thus, the available evidence to date does not support the hypotheses that electrolyte depletion or dehydration cause EAMC — therefore an alternate hypothesis for the aetiology of EAMC has to be considered.

Suffice to say that this field is still quite contested... and plagued by conflicts of interest. Witness a 2019 paper finding that a magic electrolyte formula (contents not disclosed) from a pharma company absolutely does lower the risk of cramps after exercise compared to water. Study funded by aforementioned pharma company, of course. And the press reported this as "water after exercise increases risk of cramps" (by diluting the electrolytes in your body, of course), arguably due to the authors' summary.

And while most of the previous material was about exercise-related cramps, even for the nocturnal cramps more often experienced by the elderly, the role of electrolytes appears uncommon; according to a 2007 review:

Muscle cramps, notably nocturnal leg cramps, are common symptoms experienced by general medical patients, particularly the elderly. Their etiology is varied; most commonly, these cramps are idiopathic. With the notable (and relatively rare) exceptions of serious electrolyte imbalances including hypokalemia, hypomagnesemia and hypocalcemia, these cramps are typically benign in nature. [...]
The second recent study to challenge the notion that diuretics [which promote a loss of electrolytes through urine] are a common cause of muscle cramps was a cross‐sectional survey of 365 general medical patients. Although the prevalence of leg cramps in this cohort was 50%, no associations were found between these cramps and any medication except analgesics that were used to treat the cramps. [...]
Nevertheless, a review of the Physicians' Desk Reference database (available at www.pdr.net) suggests a consistent association between diuretics and muscle cramps. [...]
The mechanism of diuretic‐associated cramping (if such an entity truly exists) is likely related to hypokalemia, hypomagnesemia, or volume contraction (with or without metabolic alkalosis). Hypocalcemia is a possible cause during therapy with loop‐diuretics such as furosemide, but is unlikely with the hypocalciuric thiazide‐type diuretics. Interestingly, potassium‐sparing diuretics, such as amiloride, are also associated with cramping. Thus volume contraction appears to be the one mechanism that is common to all classes of diuretics.

A 2012 new large-scale investigation did point to some epidemiological associations between cramps and diuretics:

Cramp treatment was substantially more likely in the year following introduction of LABAs [long-acting β2-agonists], potassium-sparing diuretics, or thiazide-like diuretics, and 60.3% of quinine users (individuals experiencing cramp) received at least 1 of these medications during a 13-year period. In contrast, statin and loop diuretic associations were small. Physicians should be mindful that the use of these medications may worsen symptoms in patients experiencing nocturnal leg cramps.

And they also have some comments on putative mechanisms:

Physicians may be surprised that potassium-sparing diuretics have a stronger link to cramp treatment than loop diuretics. Yet, hyperkalemia facilitates neuronal excitation, and hypokalemia suppresses motor neuron activity. β2-Agonists are known to have a stimulatory effect on motoneurons, and β2-adrenergic receptors are found on peripheral nerves.


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What trajectory do action potentials take, from initial visual stimulus all the way to motor function?
Say we see a mosquito, and our brain tells us 'hey that's a mosquito, you should kill it.' Then we move our hands and slap/clap it.
The initial visual stimulus is translated to an action potential via the phototransduction cascade. Light hits retinal, bla bla, glutamate release is decreased, turns a few cells on and off, which eventually sends the action potential down the optic nerve through the lateral geniculate nucleus and to the 'final' target, the occipital cortex.
Then, something happens from this point in the occipital cortex, which eventually 'translates' to action potentials beginning in an upper motor neuron (UMN). This UMN located in the  motor cortex of the brain, propagating its message eventually reaching the muscle.
The question is, what happens in this intermediate phase, where visual input lands on the occipital cortex, and then eventually translates to an action potential being propagated at the UMN located in the motor cortex? Do neurons directly synapse from the occipital cortex to the motor cortex? Is there a particular neurotransmitter responsible for communication between neurons of the occipital lobe and motor cortex, or whatever lies in between (glutamate, acetylcholine, etc)?
And finally, the hardest question... light provides a simple stimulus which translates to an action potential, making it the 'origin' of the action potential in this case. But if we close our eyes, and imagine a mosquito, we'll still have activity in our occipital cortex, and willingly provoke the same motor response. What was the stimulus for this visualization, if light wasn't the firestarter? Does some other molecule isomerize cis-retinal to trans-retinal, or affect some other step down the photoreception cascade?


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Visibility of a spiders web from a distance
Given that the diameter of a spiders web is, for instance, far smaller than a thread of cotton. Why are spiders' webs so visible from a distance?
What property of spiders' webs makes them so obvious (in the right lighting!)?
I guess I'm asking, is their visibility something that could be leveraged to create highly reflective surfaces that outperform current standards?!

Are you referring to spider webs with dew on them? Otherwise I think I'd argue that spider webs are not particularly visible, and being not particularly visible is important to their function of capturing prey that would likely avoid the webs if they were easily seen.

Thanks for the answer. No I mean in dry conditions. However, interesting you should mention dew, there must be an evolutionarily advantage for why they are more visible when adorned with dew, and thus aren't hydrophobic?

Another Q&A to read when thinking about why certain traits do or do not exist in light of evolution: https://biology.stackexchange.com/questions/35532/why-do-some-bad-traits-evolve-and-good-ones-dont

Can you provide some evidence that spider's webs, when dry, are more visible from a distance than other substances of similar thickness?

I can't provide any evidence for that. However, having got older I see cobwebs before I see other "threads" of a greater thickness, so I assumed they're must be some property of web that makes this possible.

I think this is actually a physics question. I forget the name, but for every material (and yes, apparently every material) there is a range of angles where the material becomes reflective. This angle might be so close to 180 degrees and the range so small that you never notice it though.

Clearly you've never walked face first into a spider's web in the woods.


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Is Wikipedia a good source of taxonomy?
I have been quite interested in biology lately,and I would like to know whether it is a good choice to look up taxonomic information there.

totally depends. Depends on 1) if you want Linean vs phylogenetic taxonomy, 2) organism of interest, 3) taxonomic rank of interest, 3) area of the world, 4) how well-known/studied/interesting a taxonomic group is, 5) how complex or unclear the phylogenetics are, 6) how up-to-date or accurately stitched together the Wikipedia page is, 7) what sources (and their age + reception) are used to inform the Wikipedia page,  etc...

Perhaps equally important is: why do you care? If this is for any formal, professional, academic, or research-focused interest, then I'd say no. If you're simply curious how the world is all organized or learning about different groups of organisms then I'd say Wikipedia is more than adequate most of the time. Just go into it realizing it's not perfect or consistent, so sometimes you need to use outside (reputable) sources to help better inform what you're looking at.

Thank you! I am only a 15 year old student,so it is not for formal interest.:)


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How can I learn biology by myself?
I am only 15 years old,and my primary school education hasn't been that good,also I forgot a lot of things. I would like to start again,and I am asking for your advice. What are some of the good websites/books/methods that can help me?

I'd look into MOOCs on a site like edX. These courses are recorded by talented and engaging professors and are often available for free (at edX you only need to pay to get a certificate of completion, not to take the course)

There is a game on google where you type 2-3 unlikely words like " silver microbiology horn" and " indigo evolution chemical" and "photosynthesis cell jogging" see what information arises. Wikipedia is good for the main biology course: mitochondria, microbiology, photosynthesis, gametes, recessive, inheritance, all that kind of thing.Read what you are interested in, cell biology, zoology, biomimetics, nature magazine,  paleobiology...


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Tiny bug in Amman-Jordan

I saw this bug many times in my room this spring. Can any one help identifying it?!

This is likely a duplicate of Small mottled beetle identification; the species involved is a widely distributed pest.

Is it dangerous? How can I get rid of it?

Not so much dangerous as a nuisance; the question I've linked to has an answer that eventually links to web pages that discuss control measures.


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The truth behind human urine and marking territory?
So some years ago, I remember watching a survival show in which the host said that human males produce a type of chemical in the urine that animals such as wolves can acknowledge as a territory marker. The host also said that women do not produce it, and therefore cannot mark territory in the same way men can.
Would this be accurate? Would the results of this change at all if the individual was a fully transitioned transgender person?


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Can DNA be flattened?
DNA is always shaped like a double helix. But could you flatten the double helix (which is essentially just a twisted ladder) and would DNA still be able to duplicate and control cells?

The double helix is the thermodynamically favourable conformation. You can possibly flatten it but it would consume energy. In general, the DNA does get unwound during translation and replication. As a part of the site policy, we insist that users put in some research effort from their side before asking. Provide a reasonable background and rationale for your question.

What precisely do you mean by “could you”? Being too large to crawl into a cell, I certainly couldn’t. And what do you mean by “flatten”. In the literal English meaning of the word this would violate the laws of chemistry, and if you don’t appreciate this you shouldn’t be posting here. If you mean unwind the helix, keeping the strands parallel, say so. But please take the trouble to express and explain yourself clearly.

And DNA is not always shaped like a double helix, as you say. There bacteriophages with single-stranded DNA genomes.

Flattening the double helix, i.e. making it look like a ladder (like in the usual diagrams of DNA, shown in the first figure below), would not be possible because of bond angles.

Figure 1

Figure 2
The only way for everything to be flattened out completely (as in Figure 1), is for all the bonds to be planar. However, we know that this is not true, as the C1 (carbon 1) is sp3 hybridised, not sp2, which means that the bond from the sugar to the nitrogenous base is not planar. The bond with the phosphates is also not planar. Hence it would be impossible to flatten DNA out like paper.
Moreover, there are relatively strong London dispersion forces between the layers of bases in the 3D structure (helical form). You can see on Figure 2 that the bases lie parallel to each other in each "step" of the helix. This adds to the stability of the molecule.
To answer your second question about whether DNA would be functional if flattened out, the answer would be no. The helical shape of DNA means that there is a minor groove and major groove, which is a property of its 3D shape. This is where proteins bind, which will help the process of replication (duplication) and transcription ("controlling" cells).

Figure 3

would DNA still be able to duplicate and control cells

The structure of DNA in a cell is more complicated than a double helix and its structure determines its function. DNA gets bundled up into chromatin, made up of units of nucleosomes: DNA wrapped around histone proteins.
Specific histones are chemically modified to allow the DNA inside to be unpacked, to "open up" the DNA to transcriptional machinery to generate specific proteins. The segments of DNA that open up are dependent on the type of cell — heart, brain, kidney, etc.
While an input of energy might allow DNA to be stretched out flat, it would almost certainly prevent cell-type specific proteins from being made, which rely on the condensed, three-dimensional structure of chromatin to regulate gene expression.

This only applies to eukaryotes and is therefore irrelevant to the question, which is badly thought out and is best ignored.


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What is meant by 'fixing' of an antigen presenting cell?
Can someone please explain what does 'fixing' of an antigen presenting cell mean?

In which context did you find this term?

in the chapter of MHC and APC (Kuby).

You can also read about purpose and the procedure of hostological fixation: https://en.m.wikipedia.org/wiki/Fixation_(histology)

According to this paper, fixation of an antigen presenting cell refers to the exposure of antigen presenting cells to paraformaldehyde prior to immunostaining. This treatment is used to aggregate membrane proteins and strengthen the intercellular transient protein-protein interaction.
Resource
Barisas BG, Wade WF, Jovin TM, Arndt-Jovin D, Roess DA. Dynamics of molecules involved in antigen presentation: effects of fixation. Mol Immunol. 1999 Aug;36(11-12):701-8. doi: 10.1016/s0161-5890(99)00091-7. PMID: 10593509.


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What is the meaning of expansion of T cells?
In immunology, what does it mean by the term 'expansion' of T cells ex-vivo and activate it (generally with reference to cancer immunotherapy)?

In immunotherapy, the T cells need to hit a therapeutic dose. The dose is normally determined pre-clinically or in a phase I or I/II trial. A good example is the YESCARTA label dose information:

YESCARTA comprises a suspension of 2 × 10^6 CAR-positive viable T
  cells per kg of body weight, with a maximum of 2 × 10^8 CAR-positive
  viable T cells in approximately 68 mL (3).

YESCARTA commercial label
Lets run through a hypothetical situation based loosely on information obtained in this publication.
So say you have a cancer patient that weighs 70kg on the day they obtain a leukapheresis for their starting material. The manufacturing facility is going to say okay, we need to produced 2E6 viable CAR+ cells/kg for a 70kg patient in 68mL per the label indication. So your final product needs to have 140 million viable CAR+ cells.
The patient leukapheresis can go wildly different on a patient-specific basis due to factors such as current treatment or disease. Your separation method can result in loss. Cells die in their initial culture period pre-transduction, and they can die post-transduction. So case study in point from the paper I linked:
Their patient 029-03 ended up with 0.494E+09 cells in their leukapheresis. Transduction efficiencies aren't published for a lot of these, but lentiviruses are typically employed and efficiencies can range from 1-90% depending on numerous factors. The manufacturer needs a target efficiency of ~28% to hit 140E+06 total cells if they manage to isolate every single CD3+ cell, but if they're 85% viable for example, they still wont hit the target dose. So you need to expand the cells aka make them divide so you hit the target therapeutic dose.
You typically culture your cells in IL-2, a potent T cell stimulator, but activation can improve transduction and stimulate cell division aka expansion. You can use something like CD3/CD28 beads, for example. These provide the so-called signals 1 and 2 that stimulate T cells in a similar way antigen challenge would.
Let me know if anything is unclear.


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Do tarantulas and humans have the same mechanism for growing hair?
There's hair on my arms.
Tarantulas also have hair on their arms.
Is this the same type of hair?

Welcome to Bio.SE! What attempts to answer this question have you already taken? We ask that all question posters here attempt to search for an answer to their own question and explicitly indicate what research they've already done, what they learned, and what is still confusing or unknown to them. Our goal is not to simply be an answer site, but rather a site that promotes self-learning with some expert help along the way :). Please take a moment to edit your post with this additional detail, and it will likely be received more positively by our community. Thanks!

Arthropod hairs are called setae and are not homologous to human hairs. Each setae forms from a single cell called a trichogen. The hair follicles in mammals contain 20 different cell types and produce hairs made of keratin. Arthropod hairs are made of chitin rather than keratin.


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How to do a nucleic acid or genome and amino acid search
I have been looking to find a database where i can search for genome and amino acid search. Are there any open source databases available for the same.

Welcome to Bio.SE! What attempts to answer this question have you already taken? We ask that all question posters here attempt to search for an answer to their own question and explicitly indicate what research they've already done, what they learned, and what is still confusing or unknown to them. Our goal is not to simply be an answer site, but rather a site that promotes self-learning with some expert help along the way :). Please take a moment to edit your post with this additional detail, and it will likely be received more positively by our community. Thanks!

In my experience the most popular sequence database is https://www.ensembl.org/ (other databases are available, eg. NCBI).  If you have a sequence of either nucleotides or amino acids that you want to find matches for then the BLAST/BLAT search is probably what you want.

Really? Primary in what sense? Ever heard of NCBI?

I thought about that when writing.  I work in Europe, and I do not know anyone who uses NCBI rather than ensembl.  I shall alter my answer to indicate others are available.

I work in Europe too and have worked at EMBL. However I do not know anyone who uses ENSEMBL for database searching. Part of the reason is that the ENSEMBL interfaces have always been so much worse than those at NCBI because the latter had the money to make it a priority whereas I suspect EBI had neither the motivation nor the money. The worst on-line experience I have ever had was trying to submit RNAseq data to ENA.


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Mushroom Identification: Small conical light-brown mushroom
I found a small single mushroom growing on grass and I decided to try to identify it.
Characteristics:

Region: Brazil southeast coast, state of São Paulo, predominantly Atlantic forest
Gilled mushroom
Substract of growth: Grass
Dark coloured spores (I'd say yellow-brown. Picture Below)
Gills either free or adnexed (My mistake this time, the cap was conical and small, so I couldn't have a clear view of the end of the gills. Should have cut it)
Cap 1.6cm in diameter, conical shaped
Height of about 6cm
Very fragile, specially stipe. Dry texture
Cap color: Like a faded orange or very light brown. Stipe color: Light cream

I tried to follow some identification keys (mostly this one, but that one also seemed to go the same direction) and it pointed me towards the Conocybe genus, possibly Conocybe apala (item 45a on the key from the link, you can follow back to the beginning going to the item on the parenthesis).
However, from what I read it's very hard to identify Conocybe mushrooms to the species level, because some are only differentiated by some microscopic features. They are also sometimes confused with mushrooms of Bolbitius or Galerina genus. Most mushrooms pictures I found from Bolbitius and Galerina give the impression they are a little more "fleshy" (not sure that's the word), and mine had this dry-fragile texture, which most pictures of Conocybe apala seem to align with.
Below are some pictures:

Is it likely a Conocybe apala or are there any other possible candidates?


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What determines the influx of calcium ions in the voltage-gated ion channels?
Calcium channels play a crucial role in neuronal signaling by helping the synaptic vesicles to fuse through the synaptic active zone and release their neurotransmitters. My question is, at a given moment, what determines the influx of calcium ions in these channels? Where are the ions coming from and what is their source? Is the influx determined by the source by changing the ion flow, or the ion flow is constant and the influx of ions into the synapse is only regulated by opening/closing of the channels?

Short Answer
Extracellular calcium ions’ “source” are probably cells called astrocytes that connect to both neurons and blood vessels.
Calcium ions outside the pre-synaptic neuron are high in concentration, but since they are polar molecules they cannot passively diffuse in, where they are low in concentration, so they stay stuck outside the neuron.
Voltage-gated calcium ion channels are closed at rest. These channels will open when depolarization occurs, as the membrane reaches a high-enough voltage threshold. Calcium ions rush in when these channels open. These voltage-gated channels are the primary regulator of calcium ion pre-synaptic neuron influx.
Calcium ions, once inside the neuron, will be used to release neurotransmitters into synaptic cleft.
Long Answer

What determines the influx of calcium ions in these channels?

Whenever dealing with flux, it’s helpful to start with what determines the flux rate of anything:
Rate of flux ∝ gradient / resistance

The calcium ion (Ca2+) gradient is established by an extracellular concentration > intracellular concentration (at rest) across the neuron’s cellular membrane at the terminal end (pre-synaptic neuron). Le Chatelier’s Principle (equilibrium) indicates that potential energy will build from the unresolved Ca2+ gradient, which will drive flux from high to low when given the chance.
The Ca2+ resistance is established (mainly) by voltage-gated Ca2+ (VG-Ca2+) channels. These are also on the terminal end of the neuron (pre-synaptic), and resistance is determined specifically on if channels are open or closed (closed at rest), AND the number of VG-Ca2+ channels present on the membrane.
To create an influx, gradient has to become > than resistance. Once an action potential travels down the axon and depolarization occurs at our local site, the increase in membrane potential (voltage) opens the VG-Ca2+ channels, thus decreasing resistance. Influx of Ca2+ into the axon terminal occurs.

Where are the ions coming from and what is their source?

Neurons are the flashy & exciting (no pun intended) cells in the nervous system, but to answer this question we must acknowledge that glial cells exist.
Neuroglia, glia, or glial cells
are cells that DO NOT produce electrical impulses, but are cells within the nervous system.
One type of glial cells are called astrocytes, or astroglia, and a couple of their many functions includes distributing nutrients to nervous tissue, and maintenance of (neuronal) extracellular ion concentrations, including Ca2+. Astrocytes also have access to blood vessels, giving them access to nutrients (supposedly like calcium ions).
Research on the specifics is very up-and-coming, so it is difficult to find much on it. We know calcium is coming from blood (crossing the blood-brain barrier), glial networks (including astrocytes) distribute nutrients, and astrocytes specifically are tied to extracellular neuronal ion homeostasis.
If you are interested in researching this further, the connection (and network) of a neuron to its blood supply is called neurovascular coupling.

Image: a neurovascular coupling

Is the influx determined by the source by changing the ion flow, or the ion flow is constant and the influx of ions into the synapse is only regulated by opening/closing of the channels?

Ion flow from source is fairly constant (in a healthy individual), the biggest regulator of ion flux into the pre-synaptic neuron will be the actual VG-Ca2+ channels.
Ca2+ outside of the (pre-synaptic) neuron’s axon terminal will influx when depolarization reaches the axon terminal, as that decreases Ca2+ resistance across the membrane:

Action potential travels down axon
Depolarization occurs at axon terminal
Increase in membrane potential (voltage)
VG-Ca2+ channels open
Ca2+ flux down its electrochemical gradient (influx, pre-synaptic neuron)

Ca2+, once inside axon terminal, interacts with SNAP and SNARE proteins to shuttle vesicles containing neurotransmitters to the synaptic cleft (Ca2+ - regulated exocytosis).

Sources

Image
University of Texas: Astrocytes
Astrocytes-Endothelial Reactions at the Blood-Brain Barrier
Wikipedia: Astrocytes

I have edited your answer 1. to remove the internet slang heading — we use standard English here as it is understood by most users 2. marked up the superscripts for the calcium ion by using HTML markup Ca2+. giving your answer a more professional look. (There are also other ways of doing superscripts.)

So, let's use a neuron to neuron connection as an example.
Calcium is released into the neuron when voltage gated ion channels, specific to calcium, open. These channels can only open when there is a significant depolarisation in the axon terminal of the neuron.
Where do the calcium ions come from? The majority of them are outside of the cell by the plasma membrane and adjacent to the synaptic vesicles.
I'm not too sure what you mean when you ask what the calcium ion's "source" is. It is common for calcium ions to sit outside the cell, not just in neurons, to help maintain potential difference for example.
And yes, the influx of calcium in a neuron is determined by the opening of voltage gated calcium channels.
Sources: https://web.williams.edu/imput/synapse/pages/IIA1.htm , https://en.wikipedia.org/wiki/Calcium,  https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3249630/


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How long does it take the neurotransmitters to diffuse accross the synaptic cleft?
Neurotransmitters get from the pre-synaptic neuron to the receptors on the post-synaptic neuron by diffusion across the gap between these two (the synaptic cleft). My question is, how much time does it take the neurotransmitters to diffuse from the edge of the pre-synaptic neuron to the receptors on the other side?
I have seen different values online, ranging from 0.05 ms to 1 ms. Which one is true?

Would be helpful to cite some of the examples you see. I suspect they refer to different conditions and have different definitions.

@Bryan I just want to know the average value in a typical synapse, which should has a cleft nearly 20-40 nm wide.