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Why does UV radiation from the Sun cause skin cancer?
What is the specific mechanism makes non-ionizing UVA and UVB radiation carcinogenic? Can lower energy light, like visible light, be carcinogenic because of this mechanism, or is there some kind of threshold within spectrum at which electromagnetic radiation does not induce cancer in humans?

Ionizing radiation can be mutagenic, which can cause cancer. However, this only applies to high-energy electromagnetic radiation with photon energies exceeding about 5 eV, or about 248 nm. (The FCC defines this threshold even higher at 10 eV, or about 124 nm!) These photon energies correspond to UVC, which is blocked thoroughly by the atmosphere, meaning Sunlight does not appreciably contribute to the ionizing radiation we receive on Earth. Therefore, the mechanism with which solar UV radiation induces cancer must be different from higher energy electromagnetic radiation, right?

https://pubmed.ncbi.nlm.nih.gov/21436607/

Some more useful links: https://pubmed.ncbi.nlm.nih.gov/20883261/ ... https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2564815/

It's not an answer which is acceptable on this site, but the best explanation of the electromagnetic spectrum I've ever seen is ElectroBoom on YouTube. This is in relation to 5G but explains why radio is safe and why UV-C isn't: https://www.youtube.com/watch?v=i4pxw4tYeCU

Rather than 'breaks' caused by high energy radiation, UV radiation causes chemical modifications of the bases ('letters') that make up DNA. There are four bases in the DNA alphabet abbreviated to A,T,G or C belonging to two classes. A & G are guanines while T & C are pyrimidines.
When you have pyrimidine bases next to each other on a DNA strand, they can react to form photoproducts or pyrimidine dimers. These block transcription and replication and need to be repaired by nucleotide excision enzymes (only route in mammals) or photolyase enzymes (plants, many other organisms). TT dimers are the most frequent but dimers with a C cause more trouble as they can be imperfectly repaired causing a transition mutation. If they don't get repaired in time they can cause stalled replication which causes all kinds of trouble and can result in mutations that lead to cancer. You can find more on the wiki page.

There are very many photochemical reactions: Up to 50–100 mutagenic reactions on DNA per second might occur in a skin cell during exposure to sunlight, but are usually corrected within seconds by photolyase reactivation or nucleotide excision repair. (That's just DNA, excluding O2 and other cell constituents)
chemist ref and wiki ref
Molecules that absorb photons can adopt transient excited states whose chemical and physical properties differ greatly from the original compounds.
New chemical species arise, which can cleave, glue in different places, change structures, combine with other molecules. They can also transfer electrical charge, protons and hydrogen atoms, to other atoms.
The elevated states of compounds are stronger acids and reductants than the ground states.
Free radicals from UV have an indirect effect on DNA:

Superoxide is partitioned by the enzyme Superoxide dismutase into O2 and H2O2, eventually giving way to hydroxyl radicals OH.
Hydroxyl radicals can attack the deoxyribose backbone and bases, potentially causing a plethora of lesions that can be cytotoxic or mutagenic.
UV's can also detach iron atoms in the mitochondria, which can breach the mitochondria and cause havoc inside the cell.
Cyclobutane pyrimidine dimers are the most common DNA mutation cause by photons.

Two "T" bases forming thyamine dimer:

it can also be thiamine-cysteine.
UVB is a lot more reactive with DNA, and recent studies find that UVA travels deeper and can also cause CPD dimers.
Photochemistry in cells is a bit like throwing a spanner at a billiard table, reactions can occur with hundreds or thousands of organic compounds, one of those being DNA.
The following is the answer I posted prior to that:
Radiation/electromagnetic waves are an extended version of the visible light rainbow spectrum, which go from radio waves to X-rays and Gamma rays.

The lower energy waves (longer wavelengths) can raise electrons to higher energy levels in the atoms. The higher energy waves (shorter wavelengths) can knock electrons totally off of the atoms, leaving a positively charged atom (a positive ion) and an electron. Since electrons are often shared between two atoms of a molecule like an atomic glue, knocking an electron away can sometimes reconfigure or cleave molecules in two.

The ionisation line is also the Lyman-alpha line, which is the wavelength absorbed by hydrogen atoms, the smallest atoms. All radiation shorter than hydrogen absorption is known as ionising radiation.
https://en.wikipedia.org/wiki/Ionizing_radiation#Health_effects
Some illustrations.

Thank you for updating your answer with the photochemistry specifics! Apart from the fact that UVB is more reactive, how do photon energies play into this? Is there some threshold wavelength at which photoproduct generation begins, or does it drop off logarithmically with respect to energy after the peak reactive wavelength? To what extent does lower energy light than UV, like visible light, cause these reactions, if at all?

Infrared photons transmit 0.001 to 1.7 eV which can change the quantum states of molecular vibrations and temperature, so infrared can accelerate chemistry including events that lead to molecular instability, and the higher energies make electrons jump multiple orbits upwards to where they are less tightly bound. https://en.wikipedia.org/wiki/Hydrogen_spectral_series#/media/File:Hydrogen_transitions.svg ... Search g.images for the "absorption spectra of DNA", i know blue light can damage DNA, https://www.jbc.org/article/S0021-9258(20)61544-7/fulltext I think it's logarithmic, don't know sorry

@aliential Better to write "to higher energy levels" rather than "multiple orbits upwards to" as technically they're not moving in "orbits" or "upwards".

@Armand The average distance of electron orbitals is a good way to illustrate the energy state, because most biologists will be familiar with the atomic orbital schematics rather than average electron radial distance graphs, the average radial distance tends to rise and electron is further away, and the energy level is also said to rise. https://chemistry.stackexchange.com/questions/15208/difference-between-actual-position-of-electron-and-radial-distribution-probabili

Physics/Chemistry aside, as @mimat and @aliential awesomely explained, it's always good to keep in mind that cancer, in general, is a statistics game, in the sense that at any time, there's a cell suffering mutation in your body, and it is not manifesting as cancer simply because your body evolved to deal with those situations.
You can take a walk on the beach normally without any worries about developing skin cancer, just because this acute dose of UV radiation is minuscule in comparison with your expected lifetime. The real problem is the chronic exposition to those radiations, which leads to more chance of mutated cells appearing, and from those, more of them that would suffer mutations in the specific genes that allow them to trick your cell's defense systems and immune response.
Cancer is a very complex pathology that cannot be explained just by one factor (UV degradation of DNA in the case of skin cancer). There's a lot of variables like the individual genetic predisposition, to cite just one of them.


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Do bears have killer instinct?
For example, all big cats have killer instinct.
They go straight for the throat or neck of their prey, killing it before consuming.
I've seen videos of bears and wolves hunting prey. I've never seen any where they bite the throat or neck deliberately.
Bears just bash their prey till they die or eat them alive.
Wolves eat their prey alive when the prey literally exhausted all of their energy.

I'm a bit confused by your question. Are you asking "why do some species kill by biting the throat and some use other strategies?" A beat beating its prey to death still sounds like an instinct to kill to me...

A bear usually kills its prey by biting it on the back or neck. The bear uses his forepaw to strike very hard, usually breaking the prey's spine so this is why usually his killing instinct is on the back part of a prey. Bears also bite their prey on the snout.
this information can be found at the end of this article: http://www.largecarnivores.fi/species/brown-bear/bears-diet-and-hunting-behaviour.

source: Stack Exchange

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

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Effects of a constant magnetic field on the human body (especially blood circulation and ion channels)?
Recently, while searching for the safety of MRI, I read in several places that hemoglobin and iron in the blood are not significantly affected by magnetic fields, so MRI is safe.  However, since the human body contains many kinds of metal ions, I'm wondering what effect would the long-term exposure to magnetic fields have on the human body, unlike in the case of MRI.

You might be interested to see the video of a frog levitating due to the strong (inhomogeneous) magnetic field. This experiment earned its authors the Ig-Nobel prize... just a few years before they received the real Nobel for discovering a way to obtain single layers of graphene: https://slate.com/business/2014/05/nobel-prize-in-physics-andre-geim-went-from-levitating-frogs-to-sciences-highest-honor.html

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


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Forward or Reverse Strand: Is there a difference when encoding genetic devices?
Background:
In synthetic biology, and also in nature, there are lots of examples of genes in both the forward and reverse orientation. It seems in synthetic biology/bioengineering, most genetic devices are, by default, encoded on the forward strand unless there are concerns of readthrough from one expression unit to another, in which case one of the expression units is included on the reverse strand like below:

It also seems that genes are sometimes in the reverse orientation for no apparent reason, especially in plasmid backbones:

The Question:
My question is, ignoring issues of potential readthrough, does it matter which strand a genetic device is encoded on? So in the example below, would there be any difference between A and B, or does it not matter? Also, does whether it's on a plasmid compared to a genome matter? I'm specifically interested in bacteria here.

This seems like it should be a simple question to answer and I'm sure I'm just missing something, but I can't find anything about it.

I would consider your terminology very carefully, because although your concern is reasonable, the question misuses scientific expressions in a manner that hinders communication. First, genes encode RNA and protein: neither they nor constructs are encoded by anything. Second, each gene has a forward and reverse strand, but almost no genomes do. So what you are talking about is the relative orientation of genes or constructs within a genome, plasmid etc. It would be good if you could reword your question accordingly.

Thanks for the comment, I'll edit based on your first point. For the second point, I think that my incorrect use of terminology for forward and reverse is what caused me to ask the question in the first place, because when I tried to correct them there was no longer a question, and this was also mentioned in the answer, so maybe it's best to leave that in the question so the answer still makes sense?

First, I think you have misunderstood the concept of sense/antisense. These are defined individually for each gene, with the sense strand always referring to the coding (non-template) strand of a gene, and the antisense strand to its complement, the non-coding (template) strand. So in your plasmid example above, all genes are encoded by their respective sense strand, but which of the two strands that is sense for a given gene depends on its orientation. There is therefore no biologically meaningful sense/antisense concept for entire genomes, chromosomes or plasmids. Read more in the Wikipedia article on sense, and the answers to this SE Biology question.
Having said that, it should be clear that the expression cassettes pictured in figues A) and B) are completely identical. If you ignore the context around them (e.g. readthrough), their direction is irrelevant.

It also seems that genes are sometimes encoded on the reverse strand for no apparent reason, especially in plasmid backbones

Many commonly used plasmid backbones derive from vectors that date many decades back, to a time when cloning strategies were far from as flexible as today. Researchers were generally limited by the restriction sites occurring naturally in the DNA sequences. A gene's position and orientation with respect to its neighbouring genes might therefore be the simple result of lack of other cloning options - although I honestly doubt "wrong" orientation would even have been considered an issue. For an example you could read about plasmid pBR322 in this Wikipedia article, and references therein.

Ah yes, of course, I thought I was missing something silly! Thanks for the answer!


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What is the best way from remove background signal from a band when doing Western blot image analysis?
I am doing image analysis of a Western Blot in Image J. I have calculated the total intensity of my protein bands of interest through outlining each band using the rectangle tool in ImageJ, and calculating the area and mean intensity. I have multiplied the area with the mean intensity to obtain the total intensity. However, I want to remove the background signal from each protein band of interest.
The background adjusted protein signal would be calculated as: (protein band mean intensity - background band mean intensity) * (area of protein band). On my blot, I have two isoforms of my protein of interest that were detected by the antibody, and I want to subtract the background from all bands for both proteins.
The way I am calculating the background, is for each lane, making a rectangular selection near the top of the lane where there is no labelling against any protein. The length of the rectangular section is equal to the length of the lane. However I am not sure how wide the rectangle for the background should be. From what I have seen online, there is no fixed method for calculating the background signal.
Are there any ways to determine how wide you want the band for your background to be? E.g. should the width of the band for the background be equal to the width of the protein band of interest, or can it be wider than that?
Additionally, how can you know if you have made the rectangular band for the background too wide?
Any insights are appreciated.

I haven't done immunoblots for years, and didn't do much quantitative analysis of them even then, so caveat emptor. However:
1) "Are there any ways to determine how wide you want the band for your background to be?"
I would say that the central limit theorem is a good place to start. Basically, as the size of your background increases, the precision of your estimate of mean background intensity will also increase (asymptotically). So you want your background sample to be as big as possible.
This does have some assumptions:

Little regional fluctuation of mean background signal

(related) Absence of gel artifacts

So, you want your background sample to be as big as it can be without including any artifacts and as long as it is representative of the blot in the general region of your band. In practice, I imagine that taking a selection the size of your protein band is probably fine in most cases, and probably easier to explain. You just have to pick a representative piece of background to measure.
2) how can you know if you have made the rectangular band for the background too wide?
Wider than the blot is too wide. On an infinitely large blot, I think you can't make it too wide. For practical purposes, you want it to be as wide as you can get it and not overlap obvious artifacts or the edge of the blot. But again, it's probably easier to explain just selecting a piece of background as big as the protein band that is roughly near the protein band, to account for local background variation.


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Why are fairyflies so small?
The Mymaridae are the smallest insects. This video explains their numerous adaptations to being as small as 140 microns yet still complex, such as smaller cells with as little cytoplasm as possible, denucleated neurons, loss of several body parts (including eyes and hearts, depending on the species), and parasitism as an alternative to insects' usual level of nutrition in eggs. My question is why natural selection would favour their being so small in the first place.
Since few extant species have been extensively observed, this question may require some "just so story" speculation, hopefully informed by other examples of organisms becoming unusually, almost prohibitively small for their taxa. On the other hand, their fossil record covers about 100 million years, so perhaps the time and place of shrinking intermediates would suggest specific explanations.

Fairy flies can be so small because they mooch off other insects' eggs, this is one of the reasons why they need to be small, then after that, they don't need to eat as they will die in only a few days. Information can be found on the "how do they manage to be so small" section of this PDF: https://www.cell.com/current-biology/pdf/S0960-9822(18)31343-5.pdf

This poses the chicken-egg problem (no pun intended) of whether they became small due to such parasitism or need such parasitism to be small. It wouldn't surprise me if the parasitism is older, and the host eggs shrank c. 100 Mya for some reason, as is likely if the host species also shrank or adapted to reduced food supplies. But do we know any of that?


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Does vaccination lead to short-term secondary infection suceptibility?
For clarity, here is a summary of my question, per anongoodnurse's comment:
Does a lower peripheral lymphocyte count resulting from recent immunization render us more susceptible to infection by other viruses?

There are many bad-faith arguments circulating that suggest COVID-19 vaccines are doing more harm than good. One talking point is that COVID-19 vaccination leads to a temporary reduction in circulating white blood cells, leaving vaccinated individuals susceptible to infections in the short term.  Former NYT reporter Alex Berenson has been making such claims on Twitter:

1/ The fact the mRNA vaccines transiently suppress lymphocytes after vaccination has come up repeatedly on the feed as a possible explanation for post-vaccination deaths.
Fact check: This is TRUE. @BioNTech_Group
acknowledged it its papers (both 162b1 and 162b2 did so)

2/ By the way, they also lead to a sharp rise in C-reactive protein.
Would love immunologists or virologists to chime in on whether these changes may be in any way clinically meaningful

As sources, Berenson cites two papers detailing the results of phase I/II trials for mRNA vaccine candidates.1,2
Derek Thompson addresses this Tweet and other claims made by Berenson in an article in The Atlantic 3, in which Thompson asks experts to challenge the misinformation shared by Berenson. Regarding the Tweet above, virologist Shane Crotty said the following:

The claim he is making is simply fearmongering, connecting a simple physiological event with bogus claims of deaths ... The observation of lymphocyte numbers temporarily dropping in blood is actually a common phenomenon in immune responses ... The cells are not gone. They come back to the blood in a few days. It is generally a good sign of an immune response, not the opposite.

While Berenson's claims regarding post-vaccination deaths are derived from his (willful?) misinterpretation of the data, Crotty's response got me thinking about the immunological dynamics of vaccination. My question: Does the localization of lymphocytes to secondary lymphoid tissues lead to reduced circulating lymphocytes and a subsequent increase in susceptibility to secondary infections? By secondary infection, I mean a challenge from a pathogen that is different from the one for which the vaccine was received.
For example, a person receives a dose of one of the SARS-CoV-2 mRNA vaccines, then, sometime during the critical period when circulating lymphocytes localize to the site of vaccination, the same person comes into contact with an influenza strain for which they have no adaptive immunity.  Would that person have a lower chance of contracting flu had they not received the SARS-CoV-2 vaccine, all other factors being equal?
I found one publication that shows reduced risk for infection by influenza in patients who already had SARS-CoV-2, though this is attributed to pathogenic competition.4 Considering total pathogen dosage, it is logical to me that challenge with two pathogens is more likely to lead to illness than challenge with a single pathogen, but is there anything in the literature that suggests co-infection by an immunogenic "mock" pathogen (vaccine) and a secondary pathogen leads to a greater incidence of infection by the secondary pathogen?

References

Mulligan, M.J., Lyke, K.E., Kitchin, N. et al. Phase I/II study of COVID-19 RNA vaccine BNT162b1 in adults. Nature 586, 589–593 (2020).
Sahin, U., Muik, A., Derhovanessian, E. et al. COVID-19 vaccine BNT162b1 elicits human antibody and TH1 T cell responses. Nature 586, 594–599 (2020).
Derek Thompson. The Pandemic’s Wrongest Man. The Atlantic, 1 April 2021.
Stowe, J., Tessier, E., Zhao, H. et al. Interactions between SARS-CoV-2 and Influenza and the impact of coinfection on disease severity: A test negative design. medRxiv 2020.09.18.20189647.

Not an answer because I'm no immunologist at all (virologist though...) but the lymphocytes don't localize to the vaccination site, rather to secondary lymphocytic tissues - see here. The lymphopenia is a common occurrence in infection and vaccination and does not affect the antigen presenting cells already present from previous infections, only the pre-differentiation cells

Thanks for your insight, bob1! I'll correct my question. If you're willing to expand on this in an answer, there's a bounty up for grabs.

Unfortunately that's about as far as my knowledge of immunological processes goes. However, I think you will find that the answer is likely no - we are constantly under challenge from pathogens - think of all the bugs in your gut (E. coli) and on skin (Staph infections), inside your throat (strep) etc., and we don't see a sudden rise in these infections with vaccine programs. Note that anti-viral responses (CD8 T-cell) are slightly different to bacterial (CD4), though I don't know at which stage these play a role, though I suspect after the antigen-presenting stage.

@bob1 -  I would imagine that a significant challenge (what I imagine the OP is alluding to) would pertain only to response to another viral illness, not a bacterial infection, though the NYT reporter may not be implying that.

@acvill - Your question is a tiny bit misleading; yes, the number of lymphocytes circulating in peripheral blood decreases, we know that. The question should be (imo), "Does a lower peripheral lymphocyte count resulting from recent immunization render us more susceptible to infection by other viruses?" I can't answer that authoritatively, but decades of clinical experience leads me to lean towards "no". Interferons may be part of the reason. (I'm neither immunologist nor virologist, just a lowly FP/EM.) +1 for a well presented question.

Mechanisms exist that could explain a higher susceptibility to virus B after or during a an infection of virus A, e.g. via targeted inhibition of anti-viral cellular mechanisms. In general, however, these anti-viral mechanisms favor an anti-correlation between infections of different viruses; e.g. up-regulation of interferons drastically reduces the probability of viruses to successfully complete their replication cycles. I once discussed with a leading virologist the possibility to use interferons as a general preventative treatment to temporarily prevent the spread of viral pandemics; I was told that this would theoretically work, but cannot be done due to enormous side-effects associated with them, i.e. ill feeling and depressions.
Similarly, activation of immune cells and the complement system by interleukins and C-reactive protein (CRP), that you mentioned, generally promote resistance against subsequent infections. CRP also promotes chemotaxis to the site of infection, which is why I would, similar to your source, understand chemotaxis as a sign of a good immune response. Examples like this are listed in the paper:

Mold et al. (69) showed that CRP provides mice with protection against infection by the gram-positive pathogen Streptococcus pneumoniae by binding to a PCh determinant of the pathogen cell wall and activating the complement pathway.

The  complement system is also known to be effective in killing cells that are infected by viruses. Unfortunately, I could not find dedicated publication that connect lymphocyte migration with viral susceptibility, but my intuition is that lymphocyte migration should not be problematic when it comes to detecting viruses although it might contribute to the fact, that chronically elevated CRP levels are associated with the risk of cancer.
Importantly, one should not ignore behavioral aspects related to illness and vaccinations: There were reports of statistics, that people had significantly lower chances of being infected with CoV in the weeks between scheduling and receiving their first CoV shot, which was explained by individuals avoidance of risk. Reversely, people might loose their inhibitions concerning social distancing once they feel protected by vaccines, which could show up as a pseudo-susceptibility in statistics.


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

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

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

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

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


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What is background signal in a Western blot?
I have done a western blot and I want to remove the background signal when doing densitometry analysis of my protein bands of interest. I have read some articles online such as this one regarding high background in western blots. I have learnt that there are many factors that can contribute to high background in a western blot. However, I am still not sure what exactly is defined as background. Does it refer to non-specific antibody binding on the membrane, or can it also refer to regions on the membrane where there is no binding to any protein?
Any insights are appreciated.

In this context (and many others), the terms "background signal" and "noise" can almost be used interchangeably, if that helps.
Generally speaking, noise or background refers to any signal that isn't coming from the thing you're trying to detect (typically in reference to how that signal might interfere or be confused with your "true" signal). So non-specific binding could qualify as background, but it can also refer to regions of the membrane that shouldn't have any protein binding (with any number of causes). One exception I can think of in practice is if you have a specific non-target band that consistently shows up, that might technically fit the definition (sensu stricto) of "noise", but a molecular biologist will more likely refer to it as a "technical artifact" rather than "background".
That said, there are still a number of different kinds of "noise" or "background" that may show up on western blots, and the article you referenced does a pretty good job of describing them, but it could benefit from including some images. Here's a similar guide with more images and links to other Western troubleshooting guides. Hope it helps.


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Why is male balding so common in comparison to female balding?
I have heard that over 30% of men will be bald by 30, and that 60% will be bald by 50. However, I hardly ever see a bald woman unless it is a story about a cancer survivor or someone going through cancer, meaning that they lost their hair through chemotherapy rather than natural balding. I do not understand why this is. I do know that women tend to have longer hair than men, so maybe their follicles are more active, preventing them from going bald. If someone could correct my explanation, that'd be appreciated.

Reference please?

I downvoted because this is a question easily answerable by a 10 second google.

Let's start off by saying that "baldness" is a very broad term... it includes not only hair loss but also miniaturization, which accounts for the majority of the phenotypic "baldness" associated with alopecia areata.  While alopecia areata is not the only cause of baldness, it accounts for 4 out of 5 cases in men, whereas in women it only accounts for half.
The reason that it's more frequent in males is the presence of 5α‐reductase in the sebacious glands and the dermal papilla - this enzyme mediates the metabolism of testosterone into dihydrotestosterone.  Dihydrotestosterone, in its turn, binds to androgen receptors and affects gene expression, speeding up the anogen phase.  Consequently more hairs are in the telogen phase, and the hair is shorter. In severe cases, miniaturization can become actual hair loss.
Because males higher levels of androgens, there is more testosterone available to be metabolized in the follicles. Therefore, the incidence of alopecia areata (and consequently baldness) is higher in men than in women.

References

Piraccini BM, Alessandrini A. Androgenetic alopecia. G Ital Dermatol Venereol. 2014 Feb;149(1):15-24. PMID: 24566563.

Randall VA, Thornton MJ, Messenger AG. Cultured dermal papilla cells from androgen-dependent human hair follicles (e.g. beard) contain more androgen receptors than those from non-balding areas of scalp. J Endocrinol. 1992 Apr;133(1):141-7. doi: 10.1677/joe.0.1330141. PMID: 1517703.


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If a person touched an electric eel, would they sustain electrical burns as if they touched a high tension power line?
I've been wondering this, if an eel was continuously shocking someone, would they sustain electrical burns as if they touched a high tension power line due to the high voltage and amps?

Electric Eel
In the electric eel, some 5,000 to 6,000 stacked electroplaques can generate a shock of up to 860 volts and up to 1 ampere of current (1). They can also concentrate the discharge by curling up and making contact at two points along its body. When agitated, they can produce these intermittent electric shocks over at least an hour without tiring.  Eels have been known to jump out of the water to shock prey or dissuade threats in the air (2).
A shock from an electric eel is like the brief, numbing jolt from a stun gun. Normally, the shock can't kill a person. However, the eels can cause heart failure or respiratory failure from multiple shocks or in persons with underlying heart disease. More often, deaths from electric eels shocks occur when the jolt knocks a person in the water and they drown.
Electrical Burn
Electrical injury is the physiological reaction caused by electric current passing through the body, electrical burn is a specific subset of that. For high voltage (above 500V) damage can be very severe but most of the damage occurs bellow the skin. If the voltage is less than 200 V, then the human skin, more precisely the stratum corneum, is the main contributor to the impedance of the body in the case of a macroshock—the passing of current between two contact points on the skin. The characteristics of the skin are non-linear however. If the voltage is above 450–600 V, then dielectric breakdown of the skin occurs.(3) Whether an electrical burn occurs is not always clear cut in the case of electrical injury and will depend on the conditions of the skin (perspiration etc).
Conclusion
It is possible for an electric eel to harm a human even when out of the water. The extent of the harm will depend on the exact voltage, current, hertz, pulse duration, and number of contact points between the eel and human. Whether this harm will included electrical burns depends on further factors and is particularly difficult to answer if you limit 'burn' to injury with a visible skin defect.


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Does gene orientation relative to origin of replication matter on small plasmids?
The recent question about forward vs. reverse strand got me thinking about directionality conventions in synthetic biology.
As noted in the answer to that question, if we consider only DNA in isolation, the strands are symmetric and there is no reason to prefer one over the other. A great deal of work in synthetic biology, however, is done on small plasmids, and there is definitely a directional context for these systems: the origin of replication.
The origin of replication is typically separated from the insertion point in an engineered vector, but the replication process is directional and goes around the whole plasmid. I am thus thinking that there may in fact be a difference in behavior caused by the interaction of transcriptional activity and the replication process, especially for a high-copy plasmid, where replication is much more highly active.
Does anybody know if this is, indeed the case, and to what degree is it worth being concerned about?

I like this question, and I had a similar thought when reading that "Forward or Reverse Strand" post. I've since found a 2005 publication by Mirkin and Mirkin1, which investigates the interaction between the replication fork and transcription machinery in context of an E. coli plasmid.
An excerpt from the abstract:

Studying Escherichia coli plasmids, which carry constitutive or inducible promoters in different orientations relative to the replication origin, we show that the mutual orientation of the two processes determines their mode of interaction. Replication elongation appears not to be affected by transcription proceeding in the codirectional orientation. Head-on transcription, by contrast, leads to severe inhibition of the replication fork progression.

To break this down, replication in E. coli proceeds at approximately 20 times the rate of transcription.2,3 From this, there are two kinds of collisions possible.

"head-on" collisions where replication and transcription complexes proceeding in different directions meet
"co-directional" collisions where the faster replication complex catches up to the slower transcription complex proceeding in the same direction

Mirkin and Mirkin find that co-directional collisions have little effect on the procession of the DNA polymerase III holoenzyme, whereas head-on collisions
cause replication to stall.

One can clearly see that when transcription from the P7 promoter is codirectional with replication, replication was not affected (Fig.3A). Head-on transcription, in contrast, imposed severe constraints on the replication fork progression (Fig.3B).

Altogether, it is a gem of a paper, and I suggest reading the full discussion to best understand the limitations of their experiments and their caveats in interpreting the results. (e.g. the different rates of procession of DNA Pol I and III, and the frequency of polymerase switching.)

References

Mirkin EV, Mirkin SM. Mechanisms of transcription-replication collisions in bacteria. Mol Cell Biol. 2005 Feb;25(3):888-95.
Gotta SL, Miller OL Jr, French SL. rRNA transcription rate in Escherichia coli. J Bacteriol. 1991 Oct;173(20):6647-9.
Hirose S, Hiraga S, Okazaki T. Initiation site of deoxyribonucleotide polymerization at the replication origin of the Escherichia coli chromosome. Mol Gen Genet. 1983;189(3):422-31.

That's a fantastic find!

Nice paper! Strange though that it doesn't mention how such collisions affect plasmid copy number and gene expression levels (quantitaviely speaking). These would be relatively easy things to measure, especially compared to the assays they did do.


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Can anyone identify this spider? (greater Poland region)
This is in Poland, in the Greater Poland area, found a few days ago by a garage in the city.
I didn't have any coins on me to give a sense of scale, but the body is roughly 1.5cm long. It was dead when I found it.
I'm curious because I haven't seen any spider like this one during my stay here, they're all tiny specimens normally and this one really stuck out.

That looks like a Funnelweb Weaver (family Agelenidae), specifically Tegenaria atrica,  based on the patterning of the abdomen and thorax.

Female Tegenaria atrica, picture by Jørgen Lissner

Their range includes Poland:

Range: Andorra, Austria, Belgium, Bulgaria, Croatia, Czech Republic, Denmark, Faroe Islands (introduced), Finland, France (Corsica), France (Mainland), Germany, Great Britain (Channel Islands), Great Britain (Mainland), Great Britain (Northern Ireland), Greece (Crete), Greece (Dodecanese Islands), Greece (Mainland), Ireland, Italy (Mainland), Latvia, Liechtenstein, Lithuania, Macedonia, Netherlands, Norway (Mainland), Poland, Portugal (Mainland), Romania, Slovakia, Spain (Mainland), Sweden, Switzerland, Ukraine, Yugoslavia (van Helsdingen 2009.1).

Source: http://www.jorgenlissner.dk/families.aspx

These giant house spiders (atrica/duellica etc) were moved into the Eratigena genus 7 years ago, along with the Hobo spider (E.agrestis). Tegenaria includes the barn funnel weaver and similar.


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How do cilia beat?
From what I have learnt, the mechanism of the beating of cilia is: movement of dynein towards the (-)-end i.e. towards the microtubule-organizing center (MTOC), causing the 2 pairs of microtubules to (supposedly) slide. This is prevented by linker proteins anchored in the adjacent pairs of microtubules. Therefore, when dyneins move, the linker proteins become skewed hence and bending of cilia.
My question is: As far as I know, dynein can only move in one direction (towards (-)-end) i.e. the cilia can only move in one direction, which is forward beating action. I would like to ask how can the cilia move back to the original position (backward movement) and initiate the next beating?
Edit: I have checked Wikipedia, it says there is a process called intraflagellar transport (IFT), which is bi-directional and allows the retrograde transport of cilia (backward movement?) by dyneins, which seems contradictory to what I have learnt, so how can this process actually happen?


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How do G proteins move?
G proteins consist of an alpha subunit and a beta/gamma subunit. These proteins are involved in various cellular signalling process.
From what I have understood, the alpha and gamma subunits have covalently bound lipid tails. That is, they seem to be directly connected to the cellular membrane. If this is the case, how do these protein subunits move?
I understand that the cellular membrane is flexible but I'm currently imagining a flying fox type scenario. This is where the alpha subunit is covalently bonded to one phospholipid and is now gliding down a cell membrane. I kind of find this hard to believe because it seems ridiculous (but fun!).
How do alpha and gamma protein subunits move if they are covalently bonded to the cellular membrane?

Interpretation of the Question
The question asks how the G-protein α- and βγ-subunits move, but does not state the context or circumstances of the movement. I assume that the question is, in fact:

How do the G-protein α- and βγ-subunits move apart and migrate
from receptor to target enzyme when their interaction is prevented by
the binding of GTP to the α-subunit?

False premise in the question
The problem envisaged in the question is that as the α- and γ-subunits have lipid moieties covalently bound to their amino acid chains, they are somehow part of the lipid cell membrane. This non sequitur may arise from a misunderstanding of lipid chemistry: the cell membrane is a bilayer the main constituent of which is individual molecules of phopholipids containing two long fatty acid chains and one polar organic phosphate (e.g. phosphatidyl choline) attached to a glycerol backbone. Other hydrophobic molecules (cholesterol, proteins with hydrophobic amino acids on their surfaces) can interact with these phospholipids.

The lipid moieties attached to the G-protein subunits are, in contrast, single palmitoyl or myristoyl fatty acid chains (in the case of the α-subunit) or farnesyl or geranyl (substituted fatty acid) chains (in the case of the γ-subunit). So the idea that they are somehow equivalent to the membrane phospholipids is incorrect.
How do they move?
As the lipid bilayer is fluid, its constituents can move within it, like ships on the sea. A review by Wedegaertner discussing G-protein trafficking illustrates this as shown below:

When the interaction between the subunits is prevented by GTP, they are free to drift apart in the membrane, like a boat cut loose from a ship at sea. The illustration shows them attached to the membrane by a single line representing the lipid group, but also considers evidence that they may move away from the membrane, presumably because the interaction is weakened on dissociation. Their movement is presumably random thermal motion in each case, as is that which leads to their reassociation after the GTP is hydrolysed.
However, as @BryanKrause mentions in his comment, it should be emphasized that the ability of the subunits to ‘float’ through the membrane (rather than ‘sink’ into the cytoplasm) facilitates their mode of action. They must first associate with the hormone/agonist receptor to receive the initial signal (or first messenger) and then move to interact with the target enzyme/protein which transmits the signal within the cell (e.g. through the second messenger cyclic AMP produced by the enzyme adenyl cyclase). See, for example, this Nature Scitable article.


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Trying to identify a plant with pain-killing properties from northern Vietnam
My mother-in-law uses this plant to alleviate her pain caused by a severe case of spondylitis. This is a plant used in traditional medicine in her village near Hanoi, Vietnam. She doesn't know the name of the plant, even in Vietnamese. I'm interested in identifying this plant mainly to find out its exact pharmacological properties (if any) and possible side-effects.
This is a climbing plant that can easily become as tall as a big tree. It is present year-round in this region.
To use it she just cuts it longitudinally and let it dry in the sun before boiling it and drinking the resulting decoction.
Here is a picture that she took of the plant in the wild. This is the one with the heart-shaped leaves.

And here is another picture where she removed the leaves from the plant.

Is the plant she uses the one with the heart-shaped leaves?  There are several plants in that picture near the vine stem, just want to make sure we are looking at the right plant.

Yes, the plant with the heart-shaped leaves is the one she uses. Sorry for the ambiguity. I have edited my question to clarify this.

it might be this plant https://en.wikipedia.org/wiki/Telosma_cordata it looks like some of the uses fit your description.


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What are the uses of centrioles and matrix of centrosomes?
In centrosomes, the gamma-tubulin ring complexes (gamma-TuRC) located on the surface are essential as the nucleation site for the growing (with polarity) of microtubules.
However, I see that there is also a centriole (made by 2 centriole units in T-shape structure) and a centrosomal matrix. According to Wikipedia, it seems without centrioles, the cells can still function normally and grow (please correct me if I am incorrect), and it seems I cannot find much information in the internet suggesting the use of both centrioles and centrosomal matrix.
Therefore, I would like to ask what are there functional significance? And I would like to ask if we are able to make a synthetic sphere with many gamma-TuRC on its surface (without any rejection), can the cell perform a normal cell cycle?

THis was too long for a comment.
It would be helpful for you to indicate what exactly you mean by "cells can still function normally and grow".
There are a few observations related to your question about absence of centrioles (from your wiki page):

In Drosophila mitosis and development can occur to some extent in centriolar mutants, but "they die shortly after birth" due to flagellar and ciliar defects.

Some organisms do not have centrioles and use other mechanisms (e.g. angiosperms).

So, in the sections of your wiki page "Fertility", "Ciliogenesis", etc., those list the functional significance of centrioles.
If what you mean is "what is the role of centrioles in mitosis", then we of course have a separate question. You can find a lot of resources on this topic via google searches.
As for your last question, about the synthetic sphere, you will have to spell out the experiment in much more detail- for example, what do you mean by "synthetic sphere"? A sphere defined by a lipid bilayer with gamma-TuRC (for example) on its surface and no other features is not a cell and won't go through a cell cycle.


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How do physics notions of fluid dynamics relate to pressure gradients in circulation?
I'm having a hard time comprehending why sometimes physiology notions seem to contradict each other and contradict physics teachings.
More specifically I don't understand why aortic coarctation causes the pressure gradient to increase. In this condition the radius of the blood vessel decreases which should mean that pressure decreases too. According to Bernoulli theorem ΔP+Δvp/2=o
where v is velocity and p density. This theorem and the fact that velocity has to increase to maintain a stable flow through the coarctation should mean that the pressure gradient drops. Moreover in every textbook I've found it is said that tension on the aortic wall increases too but this seems even more counterintuitive, because if the radius decreases due to La Place T=Pr tension (T) should decrease too.
Then the most puzzling thing to me is the pressure drop when there vasoconstriction of  the arterioles, this is fine according to my reasoning so far (except it seems to contradict aortic coarctation) but resistance is supposed to increase too with vasoconstriction, and because of this equation: ΔP=Q*R (where Q is flow and R is resistance) the pressure gradient should go up. Now I think I understand that it increases because of the successive drop in pressure, correct? What am I missing with aortic coarctation? I'm sure it has to do with confusing the PTM in that specific place and the pressure gradient but I can't figure it out.

As far as we know so far, biology isn't able to break any laws of physics.
However, biology isn't passive: biological systems react to changing environments to maintain some level of homeostasis. Arguably this is one of the defining characteristics of life.
If you narrow the aorta, you will always get compensatory changes. Ultimately, the circulatory system is tasked with delivering sufficient blood to the body. It might be a bit of an oversimplification, but let's assume that blood flow stays constant, because flow is a good measure of the ability of circulatory system to deliver enough oxygen/nutrients to the periphery.
Blood flow is pulsatile, which also adds some challenges in understanding things simply, but let's simplify and think in terms of mean pressures. Again, this is wrong, but it's not terrible, kind of like when in a physics class you discuss a "uniform spherical cow" or something like that.
We can start with an equation you mentioned:
ΔP=Q*R
You write:

In this condition the radius of the blood vessel decreases which should mean that pressure decreases too

This is false. If we keep flow (Q) constant, but R increases due to a constriction, then ΔP, the change in pressure, must increase.
Consider:
ΔPaorta=Q*Raorta
If Q stays constant, but R (resistance) increases due to the decreased radius, then ΔPaorta must increase: there is a larger pressure drop. Perhaps you've confused the larger change in pressure with a "decrease in pressure" because there is this larger pressure drop?
Consider also that we can consider the rest of the parallel vasculature (all branches off the proximal aorta) in series with the aorta. If we think of the vasculature after the aorta as:
ΔPdistal=Q*Rdistal
then you can think of the whole system as:
(ΔPaorta + ΔPdistal) = Q*(Raorta + Rdistal)
If only the aorta is constricted and the distal vasculature keeps the same pressure and flow, then ΔPdistal must also not change. Therefore, the total pressure drop (equal to the difference in pressure between the aorta and great veins, the sum ΔPaorta + ΔPdistal) will be larger when ΔPaorta increases.

As far as Bernoulli:

This theorem and the fact that velocity has to increase to maintain a stable flow through the coarctation should mean that the pressure gradient drops. Moreover in every textbook I've found it is said that tension on the aortic wall increases too but this seems even more counterintuitive

Due to Bernoulli, if you go from large (A), to small (B), to large (C) diameter in some vessel, yes, you will have less outward pressure in the segment (B). You will also always have decreasing energy from A to B to C. However, think about what we were just talking about: if you want to keep the perfusion of the rest of the vasculature constant, that means you have to keep the energy at C (interchangeable with pressure in this context) constant, despite the constriction. You shouldn't be thinking about A B and C here when comparing a vessel with and without stenosis, you have to think about the non-stenosed case where you have large (X), large (Y), large (Z). In this case, you still have decreasing energy from X to Y to Z, but without the stenosis, you don't lose as much going through segment "Y". It is segment A that requires more energy/pressure/tension on the vascular wall compared to segment X.
There's some simplification here regarding vascular compliance, non-Newtonian fluids, and vascular permeability but these can be mostly ignored for these purposes. I think this website will help you a lot:
https://www.cvphysiology.com/Hemodynamics/H001
especially
https://www.cvphysiology.com/Hemodynamics/H012
for the part about Bernoulli's principle.

First, you are misapplying Bernoulli's law.  At each point, Bernoulli's law says that $$\text{constant}=P+\frac{\rho v^2}{2}$$  But remember, that constant is not constant in time for unsteady flows; it is constant in space.  To make use of Bernoulli's law, we should consider two different points in the fluid flow.
I will call the one closer to the aorta "upstream" and the one closer to the superior vena cava "downstream."  Since the constant in Bernoulli's law is the same for these two points, it cancels if we subtract.  Thus $$0=\Delta P+\frac{\rho}{2}\Delta(v^2)$$  (In fact, this is still not true, but it's a good place to start — see below.)  If the fluid returning to the heart is faster than the the fluid pumped out, then $\Delta(v^2)$ will be positive, but the vena cava will have lower pressure than the aorta, so that $\Delta P$ will be negative.
So yes, if the change in velocity increases, then $\Delta P$ will "decrease", but decreasing a negative number gives it a larger magnitude.
Now for the technicality: it might seem peculiar that I assumed $\Delta(v^2)$ is nonzero.  If fluid flows faster out of region than in, then either the density changes, or, before long, there will be no fluid left there!  So if $\Delta(v^2)$ is nonzero, either the heart will soon exsanguinate, or the blood is somehow rarefacting and compressing.  Is that the case?  Of course not!
Bernoulli's law does not apply to blood flow, because Bernoulli's law assumes viscous forces are negligible.  If viscous forces were negligible, you wouldn't need a heart; your blood would just flow on its own, a perpetual motion machine.  Instead, each millimeter of blood vessel has a boundary layer of slow-moving fluid at its edges — slowed down, because it touches the capillary walls.  Keeping this fluid moving absorbs some of the hydraulic head.
Since blood vessels are largely homogenous, the amount of head absorbed is proportional to distance traveled.  This means a good model for blood flow is actually pumping against gravity: we can consider "downstream" points as "pretend higher" than upstream points.
Bernoulli's law in the presence of substantial altitude (or "altitude") changes has another term: $$0=\Delta P+g\Delta h+\frac{\rho}{2}\Delta(v^2)$$  To translate between our model (in which fluid is pumped up) and blood flow, $h$ describes the length traveled by a blood cell and $g$ describes the viscous drag per millimeter.  Decreasing the arterial thickness increases the cross-sectional proportion of blood flow in which the viscous drag from the capillary walls is relevant.  In short, it increases $g$.  So capillary constriction has much the same effect as an increased $\Delta(v^2)$: it must decrease $\Delta P$ to compensate.  But now the same analysis as before shows that we are decreasing a negative number, giving it a larger magnitude.
(I've assumed in my formulations of Bernoulli's law that our density $\rho$ is constant.  This is not true, but a reasonable approximation, as Bryan Krause's answer says.)


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Permission for Figure Reuse
I was wondering how I can go about gaining permission for reuse of a figure in this post. I was hoping to reuse the image that is exemplifying the cross section of the retina. If anyone know please let me know I appreciate the help!

This question is off-topic here, because it is not about biology. It is on-topic in academia.stackexchange. I can migrate it if you want.

I’m voting to close this question because it is about figure reuse and not biology.


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Why isn't the ovum reabsorbed into the body (like sperms) if it is not fertilised?
I have read that when sperms are not ejaculated out of the body, they are broken down and reabsorbed. Why can't the ovum be reabsorbed into the body instead of shedding it out during menstruation.

Are you referring to menstruation?

yes, why do females go through menstruation instead of just reabsorbing the ovum?

Apparently they are
Technically speaking, the ovum is not shed because it does not exist unless and until fertilization occurs.  Development leading up to the ovum otherwise stops before the final division of meiosis.
Now, you can ask why the body doesn't reabsorb oocytes, but then the answer is that it does, in a process called follicular atresia, with one or a few exceptions per  month.
Now what about that secondary oocyte that isn't fertilized?  Well, it's time to pull out a lovely article from 1917 (Harry Carleton).  Why are we so unable to match such prose today?  The paper describes a mouse study, giving quite recognizable descriptions of membrane blebbing and nuclear fragmentation characteristic of apoptosis in a decade during which it is usually said to have been forgotten.  (A 2005 work reports this for unfertilized human oocytes) Carleton likens the apoptotic changes he observed to atresia in the ovary, and says that the oocytes are reabsorbed by phagocytic cells.

Menstruation is not the shedding of the ovum, it's the shedding of the uterine lining, which prepares for fertilization even if fertilization does not occur. If there is no implantation of a fertilized ovum, the prepared lining is shed. That an ovum might be included in this shedding event is completely inconsequential (a human ovum is about 0.1 mm in diameter).
In most species, the lining (endometrium) is absorbed. The evolutionary reasons why some animals do not absorb the lining are unclear. Some speculation in the Wikipedia article includes that building a thicker lining ahead of possible fertilization is the actual beneficial trait being selected, and that the inability to reabsorb the endometrium is merely a consequence of not being able to reabsorb the thicker lining quickly. Evolution isn't perfect, and just because something could happen differently doesn't mean it will, especially if there isn't strong selective pressure for or against it. There is also previous Q&A on this site about the evolution of menstruation.


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Does the term 'protein expression' refer to the production of proteins only or also their regulation?
I am learning about molecular biology and I have come across the term 'protein expression' in a research paper. I have searched the definition of this term online and on the Thermo Fisher Scientific website it states that "Protein expression refers to the way in which proteins are synthesized, modified and regulated in living organisms". However, on the National Cancer Institute website it states that protein expression "Refers to the production of proteins by cells".
I was wondering, between these two definitions, which one is more correct? Can protein expression also be used to refer to how proteins are regulated (e.g. can you use the term protein expression when discussing how one protein regulates the activity of another)? Any insights are appreciated.

I like MattDMo's answer, but I would add that the two definitions you cite are likely meant for two different audiences. The Thermo Fisher site is primarily a source for scientists and students of science (i.e. those that may buy TF products), and the definition is therefore more technical.  The cancer.gov site is likely meant to be a resource for cancer patients and laymen interested in better understanding cancer biology, and thus makes no reference to protein regulation or modification.

There are no formal definitions accepted in science for ambiguous
phrases such “protein expression”.

If you wish to know what a particular author who uses such a shorthand phrase means you need to examine the context. If you wish to write scientific reports that are comprehensible to others you must express yourself precisely, defining any shorthand phrases that are necessary to avoid clumsiness.
In the context of the question, all that “protein expression” means to me is “expression of protein” — the synthesis of the protein from some entity that has the potential to do so. It a fundamental level that would be a gene or mRNA that encodes a protein (or proteins — that too is unclear), in which case this might be less ambiguously expressed as, for example:
“…expression of protein from gene X inthe plasmid construct Y…”
“…expression of proteins from mRNA in vitro…”
(I would generally retain the preposition. Be kind to it, poor little thing!)
To indicate that one was interested in the potential of tissues to synthesize proteins, then (with all due respect NCI, who are probably simplifying for the layman) one would need to write something like:
“…expression of protein in liver cells (after prolonged starvation etc.)…”
Under no circumstances would I imagine the term “expression” to imply or include “regulation” or “post-translational modification”. To illustrate why, consider the following example of a perfectly valid use in this sentence:
“A problem with expression of mammalian proteins in bacteria is that the required post-translational modification does not occur.”
If I wished to indicate I was also writing about regulation I would say so specifically:
“The expression of haemoglobin in reticulocytes and its regulation”
(and expect others to do so too.)
The fact that, as a professional molecular biologist, I disagree with @MattDMo, who is likewise a professional scientist, only demonstrates that the term is ambiguous. We would both like the context.

You made some good points about context - I was assuming one when we really don't know what it is without more info.

The Thermo Fisher definition is more explicitly accurate, although one could argue that the term "production" in the NCI definition implies regulation and post-translational modification (PTMs) as well. Either way, protein expression definitely includes regulation. Typically, when you measure protein expression, such as via Western blot, you are looking at the total amount of your target (regardless of whether you're using an antibody for total protein or PTM-specific) at a single timepoint. That amount has been influenced by regulation of various kinds.
EDIT
As David talks about in his answer, context is key. Given your recent questions about Western blotting using mammalian extracts, I implicitly assumed that context in my answer above, when in fact there could be other, very different contexts (such as bacterial or cell-free protein production where there is no regulation other than the promoter(s) present).

Adding a third viewpoint, I'm primarily an electrophysiologist in neuroscience. In my corner of the world, I have to say we can be a bit sloppy about terminology from molecular biology.
There might be more precise meanings intended in other areas, but when someone writes "protein expression" I typically translate this roughly to "we measured protein". It's sometimes presented as a contrast to "gene expression" which roughly translates to "we measured mRNA", or as "activation/activity" of some protein which means "we measured phosphorylation/we measured enzymatic activity by looking at products/reactants".
In this way, like in MattDMo's answer, "protein expression" includes everything leading up to translation of proteins and everything after in terms of modification and regulation, because what's actually being measured is protein level at some moment in time. That also might be all we care about, if the goal is to infer something about that protein's role in some cellular process. The details of how exactly you got to those protein levels might be important to someone else, but are left out when using a vague term "expression".
If this is what is meant, why not just say "protein", instead of "protein expression"? I think this is because it shifts the "agency" of what's going on from protein molecules to a more wholistic view of cell biology. When we talk of changes in protein expression, it is meant to imply that there is a regulatory change, not just some stochastic variation in protein levels: it's an active process that the cellular machinery is involved in, even if the specific steps involved are not mentioned. Additionally, this terminology leaves open the possibility that an observation involves other downstream effectors.


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Identifying an insect in Cambridge UK
I have come across an insect in Cambridge UK that I could not identify.
I tried to find this in various catalogues of local insects without success. The insect was about 1-2cm in length and didn't move at all until it was disturbed. I found it around 11am. We are currently experiencing high temperature variations (8C-20C).
Could someone please help identify it and point me at any useful resources I can use in the future?

It's a greater bee fly, Bombylius major, a nectar feeder and generalist floral pollinator which pollinates hundreds of species of flowers. It lays eggs near real bee nests and it's larvae feed from the bee larvae.
https://en.wikipedia.org/wiki/Bombylius_major

Thank you!! What a fascinating creature, can't belive I have never come across it before.


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Identify a large wasp (?) from southern Poland
This insect has appeared "out of nowhere" in one of my rooms. Can you help me identify it?

Details:

location: Katowice, Upper Silesia, southern Poland, eastern Europe (46.42 N, 17.78 E),
date: April 3rd, 2021 (early Spring, approx. 3:10 pm).

At first I was more than sure that this is large male bee / wasp / Apidae family member. But I was surprised to see absolutely no signs of yellow or orange strips, only gray ones, if I am not mistaken.
The windows were closed tightly at the moment of its appearance and were not open too many times in the days before, as we still have kind of cold early Spring here, in Poland right now. Though I must admit that we had a very warm previous weekend (March 27th/28th) with temperatures of up to 19°C / 66°F. But, I am still unsure, if it appeared just "these days", or if it was able (in some magical way) to survive somewhere behind wardrobe since past Autumn (very not likely?).
It was very weak at the moment of finding it. It was certainly unable to fly though its wings seemed OK. It was looking like it had at least one leg broken. He was moving very slowly and attaching itself to any surface it found (piece of paper, ruler etc.). I moved it gently to my balcony / piece of grass and let the nature do the rest.

it is not a wasp it is a bumblebee,i did see this years first bumblebee a coupe of hours ago here in norway,they do wake up now in the start of spring to start a new hive.i do not know what type you have there but it shoul be fairly easy for you to find a listing for your country.

the bumblebee might be https://en.wikipedia.org/wiki/Bombus_ruderarius or it might be bombus subterraneous but this last one is rare to find in the north of europe.


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Why is movement of water through cell walls considered the apoplast and symplast pathway?
Why would the movement of water through cell walls be considered the apoplast and symplast pathway? I understand why it's considered the apoplast pathway (as the water is moving through a non-living part by diffusion) but should it not be considered symplast since that is only for when water moves through living structures? Thanks in advance.

Your question could be a bit more clear, but I think you are referring to this-

The apoplast is the space outside the plasma membrane consisting of intercellular spaces where the material diffuses freely; it includes parts such as the cell wall and intercellular spaces.

The symplast consists of the cytoplasmic network of plant cells interconnected by plasmodesmata.

I suppose, in the motion of the upper stream of water (as indicated by the blue arrow in the diagram) you can see that to enter the symplastic pathway, the water has to first pass through the apoplastic pathway, in a sense. That is, it cannot 'teleport' directly into the cell's protoplasm, it has to pass through the cell wall.
Hope that clears things up.


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What made this pile of tiny poops at the base of an old oak? Eastern Long Island, NY
I ran across three trees (all with cavities) that had mounds of these small droppings at their base. These were approximately 50-100 meters from the shore of a salt marsh on the east end of long island.
We don't have porcupines, and I've never seen such piles associated with squirrels, so my first thought was bats. Any ideas?

What is the size? perhaps something is living in the tree and that's the resulting midden. Bats dump under their roost. I think it's some social rodents.

They are quite small. In the middle photo you can see an acorn for scale.

This has been identified as scat from flying squirrels (Glaucomys volans) by several biologists in the county. It is apparently the first documentation of the species in this area.

UPDATE: I was not paying close enough attention to size. If the feces is as small as the OP mentions in the comment below this post ("20+ of these scat in an acorn"), then this is very unlikely porcupine!! Instead, the size and shape suggests the feces belong to either a rat (perhaps wood rat) or some type of squirrel.

I await an update form the OP with more specifics before diving deeper...

Hollowed-out tree? Pile of pellet-like feces? End of Winter/start of spring?
Almost assuredly these belong to a porcupine.

 Source: user Thomas at http://livingprimitively.com/2012/05/
The North American porcupine (Erethizon dorsatum), which can be found throughout Canada and much of the northern US, is present in New York.

 Source: NH PBS

Animaldiversity.org suggests that porcupines are primarily tree dwellers in the state of NY.

For a suburban example like yours, see here.

Although porcupines do not hibernate, they reduce their range significantly during the winter and will tend to accumulate large piles of scat in and near their winter den (or suite of dens -- source). Although caves are ideal as they keep porcupines warmer, they also will frequently use hollowed-out trees as winter dens.
Since the inner bark of trees is a favorite food of porcupines (source), they will linger quite a bit around their den tree or other nearby trees if available.
Porcupine scat matches what you've found. Scat is oblong, slightly curved, and composed mostly of sawdust (due to their high wood diet) [Source: here]. According to Northwoodguides:

Wood fibers are evident in their scat. Scat may be piles of pellets varying in length from 1/2 to 1 inch long or it may be present in a chainlike pattern connected by wood fibers. Color varies from season to season depending on diet but is usually brown to black.

This site also has some good info, photos, and videos.

It is unlikely your scat belongs to another mammal such as a flying squirrel. Although flying squirrel poop looks similar and is smaller, their feces will not be notable woody as they eat lichens, fungi, berries, leaves, and other non-woody foods. Source. This site suggests that flying squirrel scat can accumulate at the base of a tree, but I have not seen this nor do the other characteristics match your almost textbook example of a porcupine "poop tree."

Perspective and scale are really difficult in images like this, but doesn't it seem like the scat in OP's picture is far smaller than 1/2 inch? Certainly seems smaller than that in your picture.

I am confident we do not have porcupine in the area.

Also I'd estimate that you could fit 20+ of these scat in an acorn - second photo

@Bryan yeah, I guess after viewing these photos on my computer screen, the scat does seem quite small. I had not really focused much on the OP's middle picture. Hmm, perhaps flying squirrel, then. That Idiot, can you describe the scat? Was it dry and woody/saw-dusty, or moister and seemingly made out of other food stuffs?

@ThatIdiot wow, ok, if they're that small, then definitely not porcupine. Feces that size and shape likely belongs to either a rat (wood rat) or some type of squirrel. You could look into the snag to see if there's any sign of a nest or drey that might help with ID. Getting an exact scat size and more commentary about its texture and contents could also significantly help.


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What is the number of synaptic vesicles in an axon terminal?
Is there any research as to the average number of synaptic vesicles per axon terminal in a human neuron's axon? On top of that, what percentage of those vesicles are used in a single action potential cycle i.e. membrane depolarization, hyperpolarization and return to resting potential?

Let us continue this discussion in chat.

Short answer
Several to thousands of vesicles per synapse. In the cortex, 0-1 are released per typical synapse. At neuromuscular junctions or specialized CNS synapses there can be more.
Longer answer
It doesn't make much sense to talk about an "average", since there are different types of synapses with very different properties, but we can talk about some examples from synapses used as models. In Rosenmund & Stevens, 1996 they estimate about 10 readily releasable vesicles at one synapse in hippocampus. Rizzoli & Betz, 2004 count hundreds at a frog neuromuscular junction.
In hippocampus and neocortex, for a typical synapse there are from 0-1 vesicles released per spike. Higher release probabilities to activation of single cells are achieved by making multiple synaptic contacts; in a typical cortical synapse, there's really just one active site so a max of one vesicle released (Silver et al 2003; Auger & Marty 2000 and Abbott & Regehr, 2004 also discuss this a bit).
Short-term plasticity can strongly influence release probability (Abbott and Regehr 2004 is a good reference to thinking about synaptic computations like this). Multiple action potentials occurring quickly can cause a sustained increase in calcium concentration in the presynaptic cell, increasing release probability at otherwise low-probability synapses (short-term facilitation). Alternatively, many spikes over a longer time period or at higher probability synapses can exhaust the pool (short-term depression). Rosenmund & Stevens used this to estimate the readily releasable pool size of about 10: they triggered a ton of rapid-fire spikes and counted release events, finding only 10. Rizzoli & Betz mention that 10 seconds of 30 Hz stimulation (300 pulses) depleted the available vesicle pool.

Abbott, L. F., & Regehr, W. G. (2004). Synaptic computation. Nature, 431(7010), 796-803.
Auger, C., & Marty, A. (2000). Quantal currents at single‐site central synapses. The Journal of physiology, 526(1), 3-11.
Reyes, A., Lujan, R., Rozov, A., Burnashev, N., Somogyi, P., & Sakmann, B. (1998). Target-cell-specific facilitation and depression in neocortical circuits. Nature neuroscience, 1(4), 279-285.
Rizzoli, S. O., & Betz, W. J. (2004). The structural organization of the readily releasable pool of synaptic vesicles. Science, 303(5666), 2037-2039.
Rosenmund, C., & Stevens, C. F. (1996). Definition of the readily releasable pool of vesicles at hippocampal synapses. Neuron, 16(6), 1197-1207.
Silver, R. A., Lübke, J., Sakmann, B., & Feldmeyer, D. (2003). High-probability uniquantal transmission at excitatory synapses in barrel cortex. Science, 302(5652), 1981-1984.

Sorry for not being specific. My focus is the neurons in the celebral cortex, will the answer still apply for that?

@Peter Neocortex and hippocampus are two parts of what is referred to as cerebral cortex.

Yeah, just seen that. I wrote the comment immediately after reading the first paragraph in second section :D


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How do honeybees requeen themselves?
It is said that beehives once queenless try to rear a new one by themselves. Beekeeping resources, books, websites, youtube videos, etc. have a very pragmatic human-centered view to the issue: what should the beekeeper do and don't. Some say, that the beehive can potentially rear a new queen on their own. I've also heard from beekeepers that they can be helped by introducing an extra brood comb from another hive.
I am interested in knowing the details on how this re-queening process takes place without human intervention.
Queens, like workers are female, hence they must come from diploid eggs. Hence only a mated queen can provide the egg needed to produce a new queen. Also it is known that queens are reared inside special queen cells which lie in vertical position in the comb.
It is known and it can be easily observed, that if the queen dies unexpectedly, the hive prepares for a substitute by building queen cups (will be queen cells).
But I wonder how do they actually get a queen from those cells.
The workers must either

carry an egg, previously laid by the former queen, from a worker cell into the cup,
or build the queen cup around a cell that already has an egg, or a young larva.

I can't imagine any other possible way.
So, how does exactly the requeening processes takes place?
Update. To be more specific about the details of the process of requeening I would like also to add the following questions:

Do they start breeding a queen from an egg or a young larva?
Do they choose this egg/larva at random?
Do we know a probability distribution for queen hatching dates? ie. the probability of a queen emerging (starting from a 0-day egg) after 15 days, 16 days, 17 days, etc.
What's the attitude of worker bees with respect to queen cells? Can a queen cell be destroyed by worker bees under certain circumstances?

Hi @Lagrange.el.Ciencia - very interesting question indeed! Unfortunately, I'm afraid though that you can easily find a satisfactory answer with a search engine. Could you please show us an attempt at trying to understand this, perhaps we could help you with understanding the parts you don't understand?

@SPr I couldn't find the answer anywhere on the internet, that's why I posted the question here. Can you post a link here to prove your point?

Does this or this not answer your questions? They would at least help focus your questions, I would advise to do that to increase the odds of getting a nice answer. Good luck!

There are two potential circumstances where a bee colony loses its queen.
Scenario 1
The queen is old.  She is not laying eggs well anymore, which means that many, most, or virtually all of her eggs are left unfertilized, resulting in drones (males) instead of worker bees.  This scenario requires urgent attention, because the hive will not survive without a steady brood production, and once all of the queen's fertile eggs are gone, there can be no possibility of replacing her.
Worker bees are able to lay eggs--though few are aware of this, and it seldom occurs in the wild.  A worker bee's eggs would all be drone (male) bees from infertile eggs because the worker is not sufficiently developed to have even the possibility of mating with a drone.
Queen bees mate once, and lay hundreds of thousands of eggs over the next as many as six or seven years before reaching the end of their productivity.  They store the sperm in their body and are able to choose whether to lay a fertilized or unfertilized egg--at least, up until those stores are gone.
So when it becomes apparent within the hive that the queen is at the end of her useful life, it is urgent that she be replaced.  The workers will take some of her last remaining fertile eggs and place them in the special queen cells, fed by extra royal jelly (all bees get some, but queens just get a bigger dose of it, and the hormones in the royal jelly help the queen to mature).  Whether before or after the workers have done this I am not certain, but the worker bees themselves will turn traitor and, for the good of the hive, kill the aged queen to make way for a new queen.
Scenario 2
The queen is lost to some unforeseen misfortune.  If this occurs during the winter hibernation period, the colony will perish, having no possible recourse.  But during the breeding season, worker bees can take emergency measures to produce a queen from the last eggs laid.  If there are existing downward-hanging queen cells on standby, they will likely relocate those eggs to them.  If not, I have seen a few queen cells positioned horizontally like all of the rest of the brood, but made larger to accommodate a queen's size.  This may be what the Wikipedia article references.
Beekeepers do not usually appreciate the sight of queen cells, and tend to destroy them whenever they are discovered, for several reasons: 1) They do not wish to have rival queens develop that might fight with and kill their special hybrid queen (queens can be purchased from various breeds, including Carniolan, Italian, etc.) by which the beekeeper has sought to balance the temperament of the hive with the environmental conditions at the site; 2) beekeepers know that bees naturally will split, with a large part of the colony following a new queen to start a hive in a new location, if new queens emerge.  This will set back the production of the original hive as many worker bees are lost to the emigration; and 3) queens which fight well (there can only be one queen in a hive, so queens will battle it out to the death) are not necessarily the best egg layers--therefore, if a queen must be replaced, the beekeeper would prefer to take charge of this.
Additional Answers
Regarding the specific questions under the main one--and, again, these are answered according to my understanding:
Worker bees will move an egg that is not more than about three days old.  Beyond this it might be impractical to move it.  This is why action must be swift if there is a loss of the queen.  As eggs progress through the larval stages, they increase in size within the cell.  They are fed, cleaned, and generally pampered (climate controlled, etc.) throughout the process.  But a large larva could not be easily moved.
I've never heard of a drone emerging from a queen cell, and believe the worker bees must be able to distinguish fertilized eggs from unfertilized eggs.  That is the only point of significance to egg selection.  Any fertilized egg could become a queen.
In order to become queens, the larvae must consume adequate quantities of royal jelly.  A larva that had been fed on the worker-bee fare for a week or two already could hardly play catch up to join the royal ranks so late in the game.  Queens must be fed more of this royal jelly from the early stages onward.
I have never observed worker bees taking any interest or initiative in destroying queen cells.  Worker bees would be happy to use those cells, as needed, or leave them empty when not needed.  I have often seen empty queen cells.  The existence of the cell does not mean it must always be in use.  If any member of the hive would have a wish to destroy them, it might be the queen, who does not desire competition.  But queens do not do manual labor of any kind beyond their task of egg laying.  The worker bees actually control or greatly influence even the egg laying--by how much they feed and pamper the queen.
[NOTE: I used to do beekeeping as a hobby, and before that I worked for a beekeeper--moving bees, splitting hives, requeening/adding new queens to hives, installing queen excluders to keep the honeycomb brood-free, extracting honey, etc. This knowledge of bees comes in large part from actual observation of them and from anecdotal evidences, rather than from scientific papers. If papers (second-hand science) are preferred here above actual observation (first-hand anecdotal evidence), then perhaps this answer may come up short of the site requirements.  I am new here, and uncertain as to how rigid the rules might be; nevertheless, I am more familiar with the bees themselves than with papers written about them.]

thanks for the answer. I like to hear from first hand experience as well. I'm a hobbyist beekeeper with just one year experience. And in the recent spring I discovered that one of my colonies had lost the queen, in fact there was no brood in any form: larvae, capped cells, etc; except for a couple of queen cells. Based on the reasoning that the queens emerge after 16 days, hence before workers and drones, I concluded that those cells could not possibly contain a queen. Therefore I came up with the hypothesis that they could be rearing (out of desperation) a drone there, maybe laid by a worker.

This is an informative answer, and firsthand experience is often very useful. I don't particularly mind posting an answer largely based on your experience, but (as it seems you understand) I think it is still worth trying to track down a couple of related citations that at least roughly corroborate your answer. I don't know that you need technical literature, e.g. wikipedia or similar resources is fine.

Thanks to @S-Pr I found the answer on wikipedia. On the Supersedure section of the article it is written the following:
If a queen suddenly dies, the workers will attempt to create an "emergency queen" by selecting several brood cells where a larva has just emerged which are then flooded with royal jelly. The worker bees then build larger queen cells over the normal-sized worker cells which protrude vertically from the face of the brood comb. Emergency queens are usually smaller and less prolific than normal queens.
Although, There is no reference to a source. Maybe one of the citations at the end of the page has the answer.

This is interesting, but it doesn't answer all questions. First of all, how does a replacement queen get mated?


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Why is DNA replication not 100% accurate
I've been reading about DNA mismatch repair (MMR) and how this process improves DNA fidelity. However, I was wondering, what is stopping MMR from correcting all mistakes in the daughter DNA with 100% fidelity? Why is the error rate still around 1 in 10^9 base pairs? Is it because the MMR proteins aren't present in cells in a high enough concentration? What would you have to change about this process to achieve 100% fidelity?

Have you researched all the other questions on DNA repair and errors in DNA replication on this site? Please do, and then tell us why your question is not covered by them if you still need an answer.

Nothing is 100% precise - any measurement or process allow for some error, the only difference is how often such errors occur (i.e., the probability of an error). These wildely range in biology - e.g., it is about 1 per $10^4$ in HIV replication, but only 1 per $10^9$ for human DNA (due to the repair mechanisms).
Note that $1$ in $10^9$ for human DNA means pretty much that there is about 1 error per each copying of the genome (which has the size of about $3\times10^9$). One could therefore still pose a question of why the error rate is so high? E.g., Human body consists of about $15\times10^{12}$ cells. Thus, if the error rate were about 1 per $10^{22}$($\approx 3\times10^9$ by $15\times10^{12}$), we could have human organisms consisting of the cells with identical DNA.
The answer to this is that errors are not necessarily bad: the copying errors are the source of the mutations driving the evolution! Note also that many of the errors have no effect at all on the well-being of the organism. Thus, it is fair to say that the existing error rates were selected by the evolution for assuring the appropriate rate of the evolutionary change/adaptation, without causing immediate harm to the organism. (One could even speculate that 1 error per genome copy is the appropriate rate across the organisms, but for a moment I cannot support this assertion by references).

Just out of curiosity, what would be some ways to artificially decrease the error rate of DNA replication? Would increasing the concentration of MMR proteins do this?

I do not have sufficient background in biochemistry or molecular biology to answer this - my field is more population genetics. Exposure to toxic substances or radiation are certainly important factors increasing the mutation rate (hence the cancers).