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Greyish spots behind a peach's stone, what could they be?
I'm sorry if it's a silly question, but what are those greyish spots behind the stone of this peach (or whatever this is)? What are they for? Are they safe to eat? The fruit is ok from the outside

it is some type of mold,you should probably not eat that one.

I concur, looks like it has a yeast or bacterial-infection - a very common thing in fruit.

Callus can develop inside peaches (https://www.tasteofhome.com/article/peach-callus-tissue/), between the mesocarp and the endocarp. Callus is edible and harmless. It's a tissue composed of unorganised parenchyma cells, which in turn are multi-purpose cells that can be found in a number of "soft" tissues with metabolic purposes including, but not limited to, the mesocarp and the endosperm. Callus' main purpose is to seal damaged tissues, see for instance:

this blogpost that explains the difference between mold and callus in a peach where there actually is a mold infection (which you should not eat)
its counterpart where there is no mold, but a considerable amount of callus (way more than you have there) was produced because the stone had split open; this one would be safe to eat, once you've ascertained that there is no mold, although callus may contain pieces of hard tissue from the stone.

Small quantities of callus can appear as leftovers form older and smaller lesions.

Which begs the question, how could that peach get "wounds" from inside?

A peach is not waterproof you know ;)


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What is the difference between BSA fraction V and the initial fraction?
I am preparing a supplemented culture medium and I need to use BSA. There is fraction V of BSA that we normally use for immunocytochemistry and there is another type named the initial fraction that is specific for cell culture but we don't have enough amount in the lab currently.
I want to know whether or not I may use the fraction V for cell culture as well.

Welcome to Biology.SE. Who is the manufacturer/provider and have you tried looking this up yourself? I searched using "BSA fraction V" and this was my top result.  Please note that the expectation on this site is that you will demonstrate that you have done some prior research before posting. Please take the [tour] and consult the [help] starting with [ask] for details.

For an extremely specific question like this, I think you will increase the probability of getting a helpful response if you include the actual details of the reagents.  In other words, for me to order those same two types of BSA I would need to know at least the manufacturer's name(s), and the catalog number(s).  From that one could possibly bootstrap their way to an answer. Also, after clicking on the link from @tyersome, I did a quick search and found this Wikipedia entry: https://en.wikipedia.org/wiki/Cohn_process that describes the steps.

Thank you for your comments.
Yes. I checked the manufacturer's protocol, the datasheet, and research gate beforehand but I could not find anything specific. I also asked my supervisor's idea but I was not convinced to use it so I kept on looking for more information. Thank you for the links you shared. I will check them.
By the way, I used the fraction V BSAfor supplementing my culture medium and so far the cells are fine.
The ref number for BSA's:
Bovine serum albumin fraction V REF10735086001, ROCHE
Albumin, Bovine initial fractionation by heat shock, A7906, Sigma
Thank you.

source: Stack Exchange

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

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Is ampicillin a good choice of drug to treat a urinary tract infection caused by E.coli
Is ampicillin a good choice of drug to treat a urinary tract infection (cystitis) caused by E.coli? How does the environment of the urinary tract effect its ability to treat the bacteria.
When cultured on a CLED agar plate and an ampicillin disk is placed in the centre it appears to work well, but will it work this well in the human body?

Hi ! This seems like a homework question. The users of this site will gladly help you, however we will not do your homework for you: it is required that you show your attempts at answering the question first.

In this instance, the question text should lead you down the right path to the answer: try to summarize the difference between the in vitro antibiotic test (CLED agar) and the in vivo conditions in the urinary tract, and consider the consequences of these differences.

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


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Did bilateral symmetry evolved just once?
If I understood correctly, all bilaterians come from a single organism (the Urbilaterian) that showed this type of body plan for the first time at the end of the Ediacaran.
Does that mean that bilateral symmetry evolved just once in the entire history of life? Is it correct to say then that bilateral symmetry is not a feature of convergent evolution? That this is indeed a thing that evolution explored just that time in history and never again?

It's currently hypothetical. pre-cambrian fossils are necessary from the 1bn-600 million region to find protostome - deuterostome ancestor. Genetic data is also inconclusive. some information if you search for bilateral common ancestor. i.e. https://dev.biologists.org/content/129/13/3021 indeed the common view is that there is a common ancestor.

@com.prehensible Let me see if I got it right. One can then say that bilaterality is a feature that appeared only once in life's history and that this is what we think right now? Even if there is no enought evidence to flasify this idea yet and we wouldn't be very surprised to see that it happened twice or more times during the evolution of life.

Yes, all the baliteria are classed in the common clade which have a similar cell attributes and physiology, they all have hearts whereas starfish and jellyfish don't, there are various genes that suggest common ancestry. There is currently no evidence of bilateral from parallel evolution, although it's very possible or probable that there were some previously and perhaps even today, i.e. tardigrades don't have hearts, so perhaps some species one day will be found to be convergeant species.

@com.prehensible I'm not a biologist at all so I would like your opinion on this. I've found that the Sea Cucumber has "weak bilateral symmetry" while been an Echinoderm (and thus a descendant of radially symetric creatures). Could this be considered bilaterality? If so, then we have some evidence for convergent evolution right? Source: https://en.wikipedia.org/wiki/Sea_cucumber#Body_plan

Sea cucumbers and sea anenomes both have a bilateral juvenile stage, so they have perhaps evolved from bilateral ancestors, check google scholar for "bilateral sea cucumber". https://www.researchgate.net/profile/Taha_Soliman4/publication/262415405/figure/fig6/AS:281720105521180@1444178715416/Light-microscopy-image-of-larval-development-of-Apostichopus-japonicus-red-variants-a.png A new fossil of a bilateral animal has been found from 550mn years ago: https://phys.org/news/2020-03-ancestor-animals-australian-fossils.html squids are starfish with mollusks on them, there are hybrid symmetries.

@com.prehensible Interesting, If you are willing to make of this a full answer I would accept it.

Ok, i collated the comments to an answer. thanks

A lack of strong evidence causes the field to be mostly hypothetical. Detailed pre-cambrian fossils are necessary, from the 1bn-600 million years ago, to find a protostome - deuterostome ancestor.
Genetic data is also inconclusive. A search for bilateral common ancestor gives i.e. dev.biologists.org/content/129/13/3021 It's a summary of research, where the accepted view is that there is a common ancestor to all known bilateral organisms.
All the baliteria are classed in the common clade which have a similar cell attributes and physiology, they all have hearts whereas starfish and jellyfish don't, there are various genes that suggest common ancestry. There is currently no evidence of bilateral from parallel evolution, although it's very possible or probable that there were some previously and perhaps even today, i.e. tardigrades don't have hearts, so perhaps some species one day will be found to be convergeant species, although they are thought to be miniaturized lobopodia.
Sea cucumbers and sea anenomes both have a bilateral juvenile stage, so they have perhaps evolved from bilateral ancestors.
researchgate.net/profile/Taha_Soliman4/publication/262415405/…
A new fossil of a bilateral animal has been found from 550mn years ago: phys.org/news/2020-03-ancestor-animals-australian-fossils.html squids are starfish with mollusks on them, there are hybrid symmetries.


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Could Sars-CoV-2 vaccines make the immune response less effective against new variants?
Some viral diseases (e.g. influenza and dengue fever) are thought to exhibit original antigenic sin.
The immune system remembers viruses that it has been previously exposed to, allowing the body to mount an effective defense if the same virus is seen again.  However, in some cases, this immunological memory can be overly specific.  When the body is exposed to a new variant of a familiar virus, it produces antibodies against the old variant rather than the new variant.  If these antibodies are less effective against the new variant, the infection can be more severe than it would have been in a person with a naive immune system.
Is there reason to believe that the same phenomenon could occur for Sars-CoV-2 and its variants?  In particular, could people who were infected by or vaccinated against the original strain be more vulnerable to Omicron or other future variants?

here is a good place to learn about the imune system https://www.youtube.com/watch?v=LmpuerlbJu0

"If these antibodies are less effective against the new variant, the infection can be more severe than it would have been in a person with a naive immune system." What is the reasoning behind this statement?

The wikipedia article for Original Antigenic Sin (OAS) oversells it a bit, in my subjective analysis. While the effect is experimentally verified - e.g. patients with a Dengue type 4 infection will produce antibodies that bind type 1 much more strongly than 4 if they were first infected with type 1 (source) - there is no evidence I'm aware of that proves the resulting immune response is less effective than a naive immune system of the same age would mount. From Original Antigenic Sin: How First Exposure Shapes Lifelong Anti–Influenza Virus Immune Responses:

Although OAS has often historically been depicted as a problematic response, recent data have demonstrated that, in certain contexts, eliciting OAS may also be beneficial.

It's not obvious that the poor match of OAS antibodies to the second infection is enough to make up for the much more rapid response compared to that of a naive immune system. Mismatched antibodies generally still neutralize other strains, it's just that a higher concentration is required.
A big confounding factor here is another mechanism, Antibody-Dependent Enhancement. ADE is most infamous in Dengue, which causes mild disease the first time but can be deadly after that if later infections come from a different strain than the first virus. ADE arises in this case because Dengue virus can infect the white blood cells that envelop and attempt to destroy antibody-bound particles. This results in accelerated virus production and a dysfunctional immune response. Despite the fact that immune cells do not display the ACE2 receptor that their spike protein needs to bind before it can fuse with the cell membrane, both SARS and SARS2 have been found to also infect macrophages when spike-binding antibodies are bound. Unlike Dengue, though:

Macrophages infected with SARS-CoV, however, did not support productive replication of the virus.

and

SARS-CoV-2 infection thus produces antibodies that elicit ADE of infection, but these antibodies do not contribute to excess cytokine production by macrophages.

Which, together with the protective effect observed for SARS2 vaccination and prior infection, we can conclude ADE isn't an issue for COVID severity, even if variations arise that can escape antibody neutralization.
Finally, there is some important context here that is not obvious to the casual investigator. The new omicron variant of SARS2 has been described as "highly mutated" because it has more than 30 mutations in the spike protein, out of 1250 amino acids in the full sequence. In other words, the other ~97.6% AA are identical. For comparison, I looked up and ran a BLASTp analysis of hemaglutinin (analogous receptor binding protein in influenza virus) from H1N1 and H3Nx strains of influenza. (uniprot accession nos. P03452 and F1KLX3, respectively) These two antigens have only 42% identical amino acids. So they are far more dissimilar than different variants of SARS2. COVID is not likely to reach similar levels of differentiation anytime soon, and we can expect any potential OAS effects to be mild for a long time as well.

No.
Let's approach this issue from the beginning. At first, we have what is called innate, nonspecific or natural immunity... many synonyms to say that it is

" the body's first line of defense against germs entering the body " quote

Now, one important feature that this mechanism has is that it will be the first to contact with the target antigen and thenceforward do another specialty of them that is Antigen Presentation (dendritic cells are the most famous for that)

APCs may interact with two classes of lymphocytes: the B or bone marrow-derived lymphocytes, but especially with the T or thymus-derived lymphocytes.  quote

From here adaptive immunity appears which includes everything you have refereed.
In that sense, all that will matter here and related to the subject is that if Ig's will have affinity for the antigen.

Let's assume they have cellular immunity, which is

a protective immune process that involves the activation of phagocytes, antigen-sensitized cytotoxic T cells and the release of cytokines and chemokines in response to antigen. Cellular immunity is most effective against cells infected with viruses, intracellular bacteria, fungi and protozoans, and cancerous cells. It also mediates transplant rejection nature

Let's assume they don't have affinity to the antigen

In that case (that could be due to a mutation of virus surface...) your immune system will  not recognize that epitope (fancy word to say antigenic determinant, it's the fragment that the immune system will recognize).
As a result of that a new Antigen Presentation must be done. In parallel HIV is a good example of that, the virus that infects a person at first is continuously suffering mutation after mutation (due to the inefficient reverse transcriptase enzyme), and thus when the body has Ig's to attack the infection, there's already another virus to attack, and so on, and so on..


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Values of the blood tests pancreatic amylase and lipase
Anyone know what is considered slightly elevated, moderately elevated and strongly elevated values of pancreatic amylase and lipase?
Many different laboratories in my country divide between these categories for interpretation, but they don't specify which values qualify for each category.
Hope this is the right place for this kind of question.
Thanks in advance.

It is not necessary a fixed value. I think it depends on the doctor that interprets it. For e.g if amylase's normal value is 70, and laboratoy value is 80, i would say it is slightly elevated. A value of 300 is strongly elevated.

The poster asks for a range that has some official or formal basis. What you consider normal etc. is of no relevance if it is not backed up by evidence that it is based on a scale that is in operation. Please read the Help on answering questions for this site.


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Mercury intoxication in cats
I was not sure if this question is more appropriated to be here or in Pets Exchange. I'm posting here first.
I accidentally broke a thermometer in my bedroom and, by my lack of attention, have spread mercury along the house. I cleaned the most part before the spread, so what I found after was only really tiny drops of mercury. However, I have four cats and I'm afraid that one of these tiny beads could possible be stuck in them paws while they are walking and they possible lick it, swallowing the beads.
I'm maintain the house ventilated most part of day (except when I go sleep) to minimize mercury vapors and I already search for possible symptoms of mercury intoxication in cats and found weakness, vomiting, diarrhea and difficult walking. Until now, I didn't observe any of these symptoms, but I would like to know what I should to if I notice some of them.
Because COVID-19, reach my veterinarian maybe will be difficult.
PS: I live in a country which doesn't have a service to come to my house to check the mercury amount in the ar neither get rid of it.

Unlikely that you have a mercury problem. I have had about 6 mercury thermometers broken in my house over a few years ( the places I kept them were not safe from a housekeeper).I don't know if she did anything to clean up; I except only sweep up broken glass. These were laboratory thermometers ,so typically over 12 in. long. No cats but dogs, no symptoms yet.

I don't have sure if your case applies to mine because, as much as I know, dogs don't lick themselves. If the drops of mercury were sufficient tiny, I guess the dogs and cats were not even be able to seen it. My worries about my cats is exactly because they lick them paws.

@Mycroft The oral toxicity of elemental mercury (the kind in thermometers) is very low in humans and laboratory animals, and it is likely not of much concern in your case. Liquid mercury is very poorly absorbed across the GI epithelium, so your cat's licking behavior isn't going to contribute much to overall risk of toxicity. The main health concern with elemental mercury exposure is inhalation of the vapors.

@MikeyC Could you send the source or reference? I would appreciate that.

It is soluble mercury compounds that are harmful if ingested.


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What is the latest possible point during a pregnancy when a fetus can merge with another fetus?
Background
A Chimera is an organism that is composed of two or more zygotes.  There are several documented incidences of this happening in humans as shown in the cited link.
Since chimeras primarily arise early in pregnancy when one fetus absorbs another, I wanted to know....
Question
What is the latest point in pregnancy at which a human fetus can absorb another human fetus?


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Is self-fertilization in hermaphrodite animals an asexual or sexual reproduction?
There are various Hermaphrodite animals, which can self fertilize.
So can this be called sexual reproduction because  there is fusion of gametes though from the same individual
? Or asexual because the involvement of a single parent(characteristics of asexual reproduction)?
There is a similar question-
Can Self-Fertilization in flowers be called asexual reproduction?
Can I extend the same logic mentioned in the  @Hawkeye's answer to the given question link on the animal case above and say that it is a case of sexual reproduction?

You can (and should) extend the logic in Hawkeye's answer. Self-pollination is sexual reproduction.


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Do we come to know which allele is dominant by seeing family genration tree only?
I know that a Gene has Alleles (variation) and one is Dominant over Other i.e the Other Recessive.
Then I got a Thought that How can we tell whether an Allele is Dominant or Recessive...... and I came across this Site while Googling, and It says we can tell this by Observing Patterns in the Family Generation Tree.
So, my question is that can we only describe an Allele by observing pattern? Is there any other Method or by looking at the Molecular level and tell?
Please extend this "How can we tell whether an Allele is Dominant" to a Special Case where a Gene has 3 Alleles.....can we have 2 Dominant Allele?

Addressing Your First Question
We can tell whether an allele is dominant or recessive based on patterns in family trees, that is true, and it is very helpful! However, that is not the only way, since by looking at the molecular function of the alleles, the dominant and recessive relationship between alleles can be assessed without needing to look at family trees!
I think a deeper understanding of what it means to be dominant versus recessive would be helpful, because usually biology isn't just that simple! In most scenarios where there is a distinct recessive and dominant trait, it is because the dominant trait causes some specific activity/functioning protein while the recessive trait does not. Let's look at an example of this:
Let's choose eye color:1
There are multiple genes that affect eye color but let's just look at one: the one that codes for the brown pigment (melanin) to be produced in the iris [specifically the HERC2 gene]. As you probably already know, brown eyes are dominant and blue eyes are recessive.
Let's call the dominant allele B and the recessive allele b. The only way for blue eyes to be the phenotype is for the allele combination to be bb. Now think about why this would occur on a molecular level. Alleles are just forms of genes, which then in turn code for some protein. Think back to what we said earlier about how most of the time dominant alleles cause some certain activity within the cell and recessive alleles do not. We can now use that knowledge to uncover the molecular basis of this eye color scenario: The B allele codes for the brown pigment to be produced in the iris, while the b allele codes for a dysfunctional protein that does not lead to melanin being produced, leading to a blue-ish color seen. So, if the B allele causes the production of melanin and the b allele does not, it makes sense by the B allele would be dominant in this case. In the case of Bb, melanin is still being produced (even if it is because of just one allele), so there still would be brown eyes! Therefore this makes sense by bb is the only allele combination that results in the blue-eye phenotype, because it is the only combination with no allele still producing melanin. This is why brown eyes are dominant to blue eyes, because blue eyes can only exist without the presence of any B allele.
So, by knowing how an allele actually functions on a molecular level, that can help us to understand if it is in fact dominant or recessive to another allele. We should also acknowledge that genes do not necessarily need to be in this black-and-white relationship of recessive or dominant. There is also incomplete dominance and co-dominance!
Now to Your Second Question
When talking about three alleles, it is important to understand that allele dominance only is used when comparing one allele to another allele. So with three alleles, the dominance, recessiveness, co-dominance, or incomplete dominance is between two of the alleles.2 So if we are talking about alleles A, B, and C. We could say things such as:

A is recessive to B, B is dominant to C, C has in-complete dominance with A, etc...

However, it is really up to the molecular function of each of the alleles and to determine how those interactions would take place. But to answer your question directly of "can we have 2 dominant alleles," the answer is sort of. Allele B and C can both be dominant to allele A, but that says nothing about the interaction between Allele B and Allele C.

1 This is a simplification of the actual molecular mechanism of eye color, but at a simplified level this works to illustrate our point. You can read more into the genetic/molecular basis of eye color here.
2 This article is very good at discussing alleles and clarifying the point that dominance is only between two alleles.


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Can Euchromatin convert into Heterochromatin?
I know that Heterochromatin can convert into Euchromatin but is the reverse possible? If yes, then How?

I would suggest in the future doing a small amount of research before asking. For example, the wikipedia page for euchromatin says this:

Euchromatin participates in the active transcription of DNA to mRNA products. The unfolded structure allows gene regulatory proteins and RNA polymerase complexes to bind to the DNA sequence, which can then initiate the transcription process. Not all euchromatin is necessarily transcribed, but in general that which is not is transformed into heterochromatin to protect the genes while they are not in use. There is therefore a direct link to how actively productive a cell is and the amount of euchromatin that can be found in its nucleus.
It is thought that the cell uses transformation from euchromatin into heterochromatin as a method of controlling gene expression and replication, since such processes behave differently on densely compacted chromatin, known as the 'accessibility hypothesis'. One example of constitutive euchromatin that is 'always turned on' is housekeeping genes, which code for the proteins needed for basic functions of cell survival.

Facultative heterochromatin is chromatin which converts back and forth depending on circumstances. This occurs through (de)"condensation" or (de)"compaction" of chromatin:

Among the molecular components that appear to regulate the spreading of heterochromatin are the Polycomb-group proteins and non-coding genes such as Xist. The mechanism for such spreading is still a matter of controversy.[19] The polycomb repressive complexes PRC1 and PRC2 regulate chromatin compaction and gene expression and have a fundamental role in developmental processes.

I would suggest reading those pages a little bit and coming up with a more specific question if they don't answer it.

I am truly sorry and thanks for the advice and help, will see it in the future and I actually read the Wikipedia article and some other websites and my mistake, i didn't read it well and got them all mixed up and confused.  Thanks a lot for help.

@Cerebralcortex No worries. Like I said, in the future. I know that it is not always obvious how to follow the rules. Just quoting from the sources you have explored is always a good idea, even when it's trivial, as it helps us out at least that far.

I understood your point. Thanks a lot.


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Is "Cloning" exact or almost similar to parent?
I was studying "Reproduction in Organism" as an interest of my own and there was a line

offspring produced through single parent are exact copies of their parent. Also, they are genetically identical.

So, in here, it says, "genetically identical" (I assume that identical here implies exactly same) but then the next line quite confused me.....

The term clone is used to describe such morphologically and genetically similar individuals.

Here, the term "genetically similar" is used.
So, clones (offspring produced through asexual reproduction- involvement of one parent) are "genetically exact" to their parents or genetically similar?
If "genetically exact", Then how is it possible since, there is 'No 100% efficient DNA Replication' that can be achieved?

Aren’t you splitting hairs rather?  I have no idea what book you are reading — you should always give a reference and preferably a link in questions — but the author of a book, like a lecturer in front of students is trying to communicate the essence of a concept, and if he hedged ever statement with disclaimers he’d never get his message across. Is it really important for what is being described and the distinction being made that there can be mistakes in DNA replication?

Biology is a lot messier than pure math, so if you insist on the same level of perfection and rigidity in definitions you are going to be very frustrated. You are correct that DNA replication is never 100% efficient, so "genetically similar" is probably a more literally accurate description of a clone.  However "genetically similar" is a very vague term, which we might apply (depending on context) to two cells from the same individual, clones and parents, two siblings, a child and a parent, two unrelated members of the same species, or even two members of the same biological kingdom. It is sometimes useful to distinguish different levels of similarity, even if we acknowledge that the boundaries of our definitions are fuzzy and arbitrary. Saying two individuals are "gentically identical" is really a short-hand for "in the context of the phenomena we're looking at, genetic differences are so small as to be irrelevant"
If you look at the level of DNA base pairs, it's estimated the average number of base pair differences between two humans is about 20 million or 0.6% of the 3.2 billion base pairs in the human reference genome. Clearly that 0.6% difference can generate a lot of variation in readily observable traits. During development some cells in an individual will undergo somatic mutations, so even two cells from the same individual may not be literally genetically identical. For the most part (excluding catastrophes like cancer), these differences will be in only a handful of bases out of the 3.2 billion, and won't cause any observable difference in the two cells. The difference between a parent and their clone will mostly be these somatic mutations, probably with some additional mutations caused by the cloning process.


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What are the methods to quantify the bacterial adhesion rate for the biofilms grown on coupons in CDC or annular bioreactor, non-invasively?
I'm interested to know that if I grow the biofilm on coupons in the CDC bioreactor at a particular shear stress, and after say 48 hours, I take out the coupon from the bioreactor to quantify the bacteria attached to it; what are the commonly preferred 'non-invasive' methods that I can use to do so? Can LIVE/DEAD staining be used in this case?
Additionally, if I want to know the bacterial adhesion rate (when the coupon is still inside the CDC bioreactor, and the baffle plate is rotating at say 80 rpm) at different time intervals (say after 1 hour, 4 hours, 8 hours), without disturbing the coupons, can I do that by using any Imaging technique?
Please let me know. Thank you for reading my question.
Regards,
Grishma

By "non-invasive", do you mean you want to quantify the bacteria in the biofilm in such a way that it can be re-insterted into the bioreactor and continue growing? What exactly are you to accomplish with this experimental design?

Thank you for your response. By non-invasive I mean to imply that can taking the images (without taking the coupons out of the bioreactor) at different time instances be possible. By knowing the growth at different time instances, I'm working towards figuring out the optimum time instance when we can introduce the disinfectant treatments.


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What is a general timeline to replace stainless steel SS 316 pipes in food industry?
Does the dairy and/or food industry (specifically but not limited to the USA)considers to replace their stainless steel SS 316 or SS 304 pipes after say 30 years or so? Could someone please share their experience or opinion.
I have this question because I wanted to know if the cleaning in place procedures stand ineffective after say 30 years because the metal's surface roughness, hydrophobicity, corrosion resistance would change.
If you have an idea about any beverage industry besides dairy or even meat industry, please let me know. It will be very helpful.
Thank you in advance.

I’m voting to close this question because it is about industrial practices and metallurgy, which are not on-topic for this site. Please consult the [tour], [ask], and other [help] pages for more information.

I would appreciate if this question is still visible. I'm new to this website and all I'm interested in is the knowledge that some users are willing to contribute.I would like to defer and say that this question is not just industrial practices and metallurgy based but it also aims towards people contributing to the food industry. I see one useful response.

Stainless does not "wear out" or deteriorate in general food service , so no replacement. There may be some unusual service that causes corrosion . If that occurs I expect a more corrosion resistant alloy replacement is quickly installed. Keep in mind if there is corrosion ,there are traces of Cr, Ni, Mo going into the food . That would bring lawsuits regardless of any harm. It is hard to imagine any surface texture change ;possible exception of raw foods with entrained sand which might cause polishing of the stainless.

Thank you. I agree with the points you have mentioned, I was thinking if there is a general timeline for the SS 316 pipes, where we can say that after say 3 billion production cycles (or say after transferring 20000 liters of milk per hour for say 50 years) of service in the food processing plants, they start to corrode and needs to be replaced; as opposed to replacing them after say 5 years, where they are not showing any signs of possible mechanical failures or alterations in their roughness. I understand that there are no set guidelines. Your response is greatly appreciated.

There is no deterioration: Infinite life ( as an engineer I  cringe when I use that word). I am sure there are buried carbon steel pipelines that have been in service over 75 years ; much higher corrosion potential inside and outside than SS in food service.

Thank you once again for your response. In that case is there a specific timeline that the industry follows for inspecting the presence of corrosion inside of the pipe? That looks like a reasonable thing to do in this situation. Can you share your experience with any inspection technique used and its timeline followed by the food industry?

In a refinery with carbon and low alloy steels metal loss is expected. So very detailed surveys are documented  both for the refinery and various government agencies.  Usually ultrasonic ; it is important that the UT tests be made at the exact same spot as there are some original variations in wall thickness.  Today very accurate inexpensive UT units are available "off the shelf", Frequency of inspection is determined with experience , from a few month to a few years. For SS food piping , likely every 5 years will be enough.  .

I expect there are organizations that have written requirements and/or guideline for examination.Likely they concentrate on organic contamination but may have NDE for equipment integrity. ASNT American Society for Nondestructive Testing might have something you can use.

Thank you for your helpful responses. Much appreciated.


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Can someone identify this bug?
I am looking for some help identifying this bug. I am in southern New Mexico, US. There are a handful of these on the inside and outside of all the window panes on one side of my house. They are about 3mm long. They appear this time of year (late April/early May), stay on the windows for a a week or so and then disappear.  Hard to get a clear picture as they are so small. Any assistance would be greatly appreciated. Thank you!


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What is this insect? And does it eat aphids on plants?
I found this insect that looks like a praying mantis on my plant which was infested with aphids. I sprayed neem oil and most aphids died, even one of these praying mantises did. But here in this picture is one and I want to know if it is going to eat the aphids so I can stop spraying neem and killing every bug in the process.
The insect is around 2 centimeters long.
This is in a hot and humid area in the middle east. The plant, I guess, is from the jasmime family. It produces small scented roses (hasn't flowered yet due to the aphids problem).

Based on the head morphology and the upper limb visible on the first picture, I would say it looks like a mantis. The length of the abdomen also confirms the same.

The internet is also full of several non-scientific sources that seem to confirm they eat aphids. Animals will normally learn to avoid bitterness in food as it's a sign of toxicity. I haven't found a lot of information about how bitter are aphids, however mantis are sit-and-wait predators, so they will try most things that crawl their way. Judging by the following pictures (and the article linked at the end), I would say it's very likely:

Indeed, catching every prey would be a beneficial strategy because of uncertainty in encountering another prey due to a sit-and-wait strategy. By holding prey with its forelegs and gradually eating the prey by chipping away at it, the mantis has enough time to find edible parts of prey and reject unpalatable parts/prey (Reitze and Nentwig 1991).

Sources:

https://en.wikipedia.org/wiki/Mantis
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5882761/
https://praying-mantis.org/what-do-praying-mantis-eat/


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Identification and odd leaf anomaly
We're in the process of welcoming sheep, thus setting up the fences, now inside on of the areas, there is a small tree. Never seen leafs like this before. I suspect this to be some sort of anomaly/disease ?.
I identified 2 oddities : the branches are chorros-like and some leafs have small, vivid red appendices growing on them

Could anybody identify the tree?
are the branches and leafs 'normal'
3 is there any danger for the sheep? (toxicity) ?

Region : South-west France
Size: About 2 meters
Overall picture :

Details :

Closeup:

Not sure about the tree identification. But regarding the oddity I had to think about galls

Could you post it as an answer so I can accept your answer? it's indeed galls on a Ulmus minor.


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How is in-vitro fertilization technically achieved?
I failed searching on Google technical details about how in-vitro fertilization is achieved. I'm referring to the toolset and its use, rather than the chemical or biological aspects of the process. I often watch on TV how a needle penetrates into a human egg to fertilize it with sperm, but provided that a human egg sizes about 100 microns, I come up with the following questions:

Do there really exist needles so thin to penetrate a 100 micron cell? In such case, how are these needles manipulated without breaking or losing them in the lab?
How do technicians manipulate the needle with such micrometric precision?
How do technicians keep the human egg still so they can break into it with the needle without pushing the egg away?

Not sure if these questions sound naive, but I haven't been able to find any simple answer to them on the Internet.

Have you read the Wikipedia article on Microinjection and followed up the references there? Remember the word needle does not imply any particular material or mode of construction, and of course the first needles were used for sewing (rather than injection) and made of bone.

@David, thank you! Actually Google never dumped the result for this Wikipedia's page and I also didn't come up with the "microinjection" word. I will check it out and follow up the references. Thx again!

After following user David's hints, I have collected some videos that answer the questions I posted:

Regarding to needle manufacturing, there exist machines able to create micropipettes (this is how the needles are actually called) by heating glass cilinders and pulling them to create very thin tubes (capillaries). Click for featuring video.
Regarding to the high-precision manipulation, technicians use mechanical devices able to convert macroscopic motion (eg: human manipulation) to microscopic motion (eg: using reduction gears). Click for featuring video.
Regarding to how they keep the egg still, technicians use another type of pipette that slightly "sucks" the egg in a vaccuum-cleaner style. For a full-feature video of how the egg and sperm are manipulated, check this video out.


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How fast could the Amazon rainforest regrow after deforestation?
We hear a lot about clear-cutting of the Amazon rainforest and how that affects climate change. However, are there any studies on how fast areas of rainforest can regrow or the ecosystem can recover if left alone after logging or slash and burn agriculture? It is often discussed how many ecosystems can rapidly recover after human exploitation stops (e.g., temperate forests). However I don't know if that would apply to the Amazon because rainforest soils are so nutrient-poor after slash and burn agriculture.

depending on the type of deforestation possibly never. slash and burn rainforests often don't recover.

Plants can regrow in a matter of weeks, months, years, depending on species. However, I encourage you to review secondary succession as well as second growth forests vs old-growth forests. All forests are not created equal. Just b/c plants regrow, doesn't equate to the Amazon "forest" (in its current state) having returned. Its current (perhaps already former) state will likely never regrow (in fact, there is almost 0 chance). But any similar analog would take 100s or more likely thousands of years to establish.


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Have orcas ever been observed to be eaten by another species?
Orcas are well known to prey on just about everything that lives in the ocean, even including great white sharks. Yet in a lot of cases I know that the food chain is not unidirectional, there are many cases where even so-called apex predators will get attacked and eaten if they are weak and let their guard down (the eternal rivalry between lions and spotted hyenas comes to mind).
My question is this, are there any known cases of orcas being killed and eaten by another non-orca marine mammal (i.e., not humans)? Such as a lone adult without a pod being attacked, or a calf being taken when it's mother wasn't looking?

Since orcas are difficult to observe, such an event has likely not been observed even if it happens. For example, members of even relatively well-observed pods like those in the Salish Sea area (Pacific Northwest) are almost never observed to die. Rather, they are deemed dead after not being observed for perhaps a year or two.

This Orca Network births and deaths page may be useful: https://www.orcanetwork.org/Main/index.php?categories_file=Births%20and%20Deaths

No, there are no known cases (unless anecdotal evidence from lifelong marine mammal observers exists, which is possible).
The best candidate for such a phenomenon would be the sperm whale due to its large size and the presence of teeth. Baleen whales could potentially injure an orca, but would not be able to eat it. However, I think even in the case of sperm whales, killing and eating an orca would be very improbable for a couple of reasons.
1 teeth size and function sperm whales have external teeth only in the lower jaw, and generally swallow prey whole 1. They cannot effectively grasp or tear prey, which would make it very difficult for them to eat an orca even if they wanted to.
2 previous accounts of interactions Accounts of interactions between sperm whales and orcas suggest that orcas are not scared of sperm whales, and that sperm whales avoid orcas when possible and engage only in defensive behaviors during interactions. This article in pictures documents an interaction between orcas and multiple male sperm whales in which the sperm whales are successful at avoiding the orcas, but do not attack them. Playback experiments such as this one have noted that playing orca calls cause sperm whales to stop foraging efforts and spend more time at the surface, again suggesting that sperm whales are more likely to try and get away from orcas than they are to ever willingly attack them.


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Floats of Algae, a house-made conjecture
Background
In North of Scotland there are many seaweed types. One is a green algae (chlorophyta).
They are full of 'bubbles'. According to web searches one of those bubbles (there are two types you can notice by sight) are spores; the other ones are called floaters.
According to searches, Kelp (or brown algae) floaters are full of gases. But we find most of the Chlorophyta full of water, some of them contain bubbles but tiny ones.
Conjecture
The water inside could be of a lower density than the sea water, instead of air bubbles.
Question
Any information on this respect?

One consideration is the energetic costs to the organism. It's going to be energetically more favorable for an organism to be in osmotic balanced (isotonic) with its environment than to constantly work to maintain lower internal osmolarity through active transport of water or solutes. Second thing to consider is cell size and density differentials. Air at sealevel is several hundred times less dense than water, so even tiny gas bubbles would create significant buoyancy for a cell. On the other hand, pure water is only about 2.5% less dense than sea water, which means a much (much) larger volume would be needed to generate equivalent buoyancy.
All that said, there seems to be some plausibility to your conjecture, as there are some large marine phytoplankton that use active water transport to maintain vacuoules at lower density than that of seawater (Source).
This paper discusses some other competing mechanisms as well, but as the author of the article states:

"... most of the cases of positive buoyancy in phytoplankton not
  generated by gas vesicles concern diatoms..."

That's not an incontrovertable refutation of your conjecture, but it seems to me that gas vesicles are a much more efficient means of generating buoyancy, and would probably be energetically favored over other biological means of generating buoyancy.

I really appreciate your knowledge, thanks. (I can't yet upvote answers.) Where do you take the energetic considerations from?

My reasoning is this. For the water in a cell compartment to be less dense, it would need to have a lower solute concentration than the surrounding seawater. Maintaining that disequilibrium between the cell and its environment requires constant energy expenditure to overcome the constant osmotic diffusion of water across the cell membrane.
Full disclosure, I'm a microbiologist, so there may be some aspect of algae cell physiology I'm overlooking. I tend to think of every problem from a bacterial POV.


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Regarding different nucleotides on a DNA strand
I am not a biologist therefore, it might seem as an elementary question. I retrieved rodent sequences from UTR database:
http://utrdb.ba.itb.cnr.it
And I know there are supposed to be four nucleotides namely: A,G,C, and T. However, on this database I get sequences that have 'n' nucleotide in several locations, 'm' and 'k' as well. What does these letters mean? I haven't been able to find anything regarding it. Does it mean these positions in UTR are undefined or they are some 'intermediate' nucleotides if there are any?

These are IUPAC codes for so-called "degenerate" or ambiguous bases, alternatives to the usual A, T, C, and G nucleotides (for DNA). The N code represents any base, while M and K map to A or C, and G or T, respectively.

Okay. Thanks. That makes much more sense to me now.


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Do all anabolic reactions involve condensation?
I know that condensation is one example of an anabolic reaction (building macromolecules from monomers), but do all anabolic reactions involve condensation? Or is there an example of an anabolic reaction which isn't also a condensation reaction?
Could anyone elaborate on this please?

Assuming that all valencies of the reactants are satisfied, an anabolic reaction will always involve condensation as some bonds will be broken when a new bond between the reactants is formed.

We (or at least the school of biochemists with which I associate myself) do not talk about individual reactions as anabolic or catabolic, but use these terms for the overall  metabolic pathways. The classification of enzymes by the International Union of Biochemistry is solely by their chemistry — see https://www.qmul.ac.uk/sbcs/iubmb/enzyme/rules.html. Individual reactions in an anabolic pathway will differ chemically.


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Why do we have both on and off bipolar cells?
I have a question regarding the reason behind the 2 bipolar cells.
So, from my understanding we have both on and off bipolar cells and from the numerous diagrams I have seen, I find that most show a single cone attached to both an off and a on bipolar cell.
The on bipolar cell reacts in an inhibitory manner to glutamate and so if light hits a photoreceptor attached to this bipolar cell, less glutamate is released and so the bipolar cell will become depolarised.
The off bipolar cell is the opposite as it finds glutamate to be excitatory and so it will become depolarised in the dark.
My question is, in the light if a single cone has light presented to it, it will become hyper polarised and so will release less glutamate. If the bipolar cells attached to this cone have opposite effects as in one will become depolarised and one will become hyper polarised what is the reason for the off bipolar cell, why would we need that cell if it only becomes depolarised and doesn't result in anything?
A second question is, do the bipolar cells connect to corresponding ganglion cells for example, on bipolar cell connects only to on-centre ganglion cell? If so why is this?
Lastly, we also have single cones that connect to single bipolar cells. Are these cells on or off bipolar cells I assume they are on because if they were off we wouldn't be able to sense anything as the cell would be hyper polarised and so wouldn't cause the ganglion cell to reach an action potential. Is this thinking correct?


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Why is the blood thick in Wet Cupping / Hijama
I have just witnessed the wet cupping procedure being performed and have questions regarding the blood that is seen in the cups. I understand there are no studies that show cupping is an effective treatment for many diseases as some claim it to be but my question is regarding the blood that is released.
The procedure aims to eliminate the 'bad blood' which leaves clean blood to circulate the body, the practitioner pointed out the difference between the clean and bad blood and there was a substantial difference in how it looked and flowed. The blood was very clumped up and thick and didn't flow well at all whereas some of the blood was a lot more fluid and was able to flow easily. I was told this runny blood is clean blood and is what we want in our bodies.
My questions are what is the thick clumpy blood and why is it like that?
Is it actually bad blood?
Thank you in advance!

This is very good question indeed as I spoke to someone who said that he had it done and he could literally feel the difference in stress levels and blood pressure. I couldnt find correlation between the two so this is interesting topic to explore.

I believe the reduction in blood pressure maybe due to the removal of blood so with less blood circulating the pressure would drop but I may be wrong. I have also spoken with many people who have had the procedure done and they claim it massively helped with reducing pain such as back pain. I was really shocked at how thick the blood was, it was like a solid and many videos show this same thing and I was curious as to why the blood is that thick and how it doesn't cause the blood vessels to block.

Are you familiar with clotting?

Clotting occurs at the site of damage and this causes the blood to thicken right? If that is correct, then I do understand clotting but my question occurred because some of the cups had little to no thick clotted blood whereas others had the blood completely clotted and some cups had a mixture. Why does this occur if it is only due to blood clotting, shouldn't all cups have a similar amount of blood and shouldn't the blood all have the same viscosity also?

@James That would happen if all the cups were placed at the same time (since clotting takes some time). Did you observe any pattern—e.g. cups placed earlier had thicker blood?

We had a demonstration of blood coagulation/clotting in a biology lesson with the school nurse. She just took half a test-tube of blood sample from a class pupil and we waited a moment, and the blood became a solid lump inside the test-tube.
The process is there to protect you from leaking blood if you cut yourself, the process uses fibers and platelets and complex proteins.
https://www.youtube.com/results?search_query=blood+clotting
wiki: Coagulation
Blood letting is a very ancient practice that used all sorts of methods like annelids/leeches, which has not been proven to have any benefits. The blood in your body does not seperate into good blood and bad blood by sitting in a jar.

let's all downvote everything on the site :) that would be positive :)

Exactly, someone is fooling around by downvoting most of the questions.

What an awesome answer! Thank you! I too don't understand all of the downvotes, I showed research in my question and I believe it to be a good biological question and one which may help someone who had a similar question. 3 downvotes seems a bit excessive maybe if the downvoters explained what was wrong with the question it would help me and others avoid such mistakes in the future, helping the site the improve.


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What's superposition and thread in RosettaCM?
I'm a beginner in structural biology.
I had a question while reading a paper on RosettaCM.
What does RosettaCM's superposition and thread mean?
I googled it.
As a result, the following results were obtained.

The term structural superposition refers to rotations and translations performed on one molecular structure to make it match another structure or structures. Inherent in the definition of structural superposition is an assumed measure of structural similarity. The optimal superposition is the one in which this similarity measure is maximized. Alternatively, one can define superposition in terms of a difference measure, such as root-mean square deviation ( RMSD ). In this case, the optimal superpositon is one in which the RMSD is minimized. The program ASH uses the former approach with similarity defined by the NER score.
Also, implied in any superpositon is an alignment, or mapping, between points in one structure (usually atoms) and those in another. Sometimes alignment and superpositon are used interchangeably.

Is this correct?
I also think of threads as part of a protein segment, is this correct?
In other words, in Rosetta CM's 1-step Global Superpotion, after aligning, the templates are stochastically determined, and the unselected templates are superposed so that RSMD is smallest.
Furthermore, the superposed template is a thread.
Is the above correct?

I’m voting to close this question because it is not about a biological process or mechanism.


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How does the DNA cross through bacterial cell wall during electroporation?
There exists a lot of literature on electroporation of Gram-positive and negative bacteria. Most of it gives an explanation that electroporation works by creating transient pores in cell membranes of bacteria for the DNA to pass through.
Both types of bacteria have a cell wall as well (differing in thickness). How does the DNA pass through the cell wall that it encounters on the way?

The bacterial cell wall is quite porous, and is not considered a permeability barrier for most small molecules. It mainly functions as structural support and to resist turgor pressures.
The average pore size of relaxed peptidoglycans were measured to have a radius in a range of about 2.0 to 2.5 nm, regardless of thickness (i.e. Gram + and Gram - bacteria have similar pore sizes), but when stretched under turgor pressures, peptiglycan is permeable to globular proteins of 50 kDa or more, while hyperosmitic shock of bacterial cells can trigger the release of proteins up to 100 kDa in size (Vollmer et al., 2008). That equates to ~6.5 to 8.5 nm in diameter by one method of estimation.
A single strand of DNA double helix is around 2 nm in diameter, so it stands to reason that even a circularized plasmid could potentially pass through pores just a little more than 4 nm wide.
Reference:
Vollmer, W., Blanot, D., & De Pedro, M. A. (2008). Peptidoglycan structure and architecture. FEMS microbiology reviews, 32(2), 149-167.

Good answer (+1) and you've done a nice job of providing a relevant supporting reference. However, in the future please include the complete reference information since links can break. One easy way to get that information is to search for the paper on Google Scholar and click on the ‟ symbol to get reference information. I've formatted your reference in way that minimizes changes to your answer, but this is another good example of how to format references.


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Hardy-Weinberg principle
The following paragraph on Wikipedia about the Hardy-Weinberg principle is bothering me.

It should be mentioned that the genotype frequencies after the first generation need not equal the genotype frequencies from the initial generation, e.g. f1(AA) ≠ f0(AA). However, the genotype frequencies for all future times will equal the Hardy–Weinberg frequencies, e.g. ft(AA) = f1(AA) for t > 1. This follows since the genotype frequencies of the next generation depend only on the allele frequencies of the current generation which, as calculated by equations (1) and (2), are preserved from the initial generation:

Why is it so that the genotype frequencies are dependant on the previous generation, but not in the case of the first as compared to the inital generation?
https://en.m.wikipedia.org/wiki/Hardy%E2%80%93Weinberg_principle#math_1

I can't think of a more succinct way to phrase it than the explanation in your post.

"...the genotype frequencies of the next generation depend only on the
allele frequencies of the current generation..."

The genotype frequencies still do depend on the initial generation, they just depend on the allele frequencies of the previous generation, not the genotype frequencies. For example, an initial generation consisting of only (XX) and (xx) genotypes will produce F1 offspring with (XX), (Xx), and (xx) genotypes through random mating. Since the (Xx) genotype frequency was 0% in the initial generation, and >0% in the subsequent generations, it can't be equal that of the initial generation. But it will still be a function of the relative frequencies of the two alleles in the population, (X) and (x).


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Why is selection less effective in small populations than in larger?
I can understand that the genetic drift has a higher impact on smaller populations, but what does it mean for the selection to be less effective in small populations than higher?

Hi Gljiva, could you please specify what kind of selection you are talking about, as well as the context to better understand what "effective" means?

@F16Falcon e.g. this sentence on Wikipedia "In small populations, selection is less effective, and the relative importance of genetic drift is higher because deleterious alleles can become more frequent and 'fixed' in a population due to chance." https://en.m.wikipedia.org/wiki/Small_population_size

This question seems to be about negative/purifying selection, judging by the wikipedia quote. Positive selection can often (but not always) occur more slowly in smaller populations, but 'efficiency/effectiveness' of selection generally means the rate at which deleterious variants are purged from the population, so I'll skip out taking about positive selection (unless you did mean that).
First, genetic drift: Genetic drift is the stochastic change in allele frequencies caused by random differences in the survival of different individuals. For example, a mouse might get struck by lightning and not transmit any of its genes to the next generation. Whether or not it was struck by lightning probably wasn't related to its fitness, it was just 'bad luck'. As population size increases, genetic drift becomes weaker because the larger the population, the smaller the proportional impact of each random event that concerns just one individual
Negative selection tends to be less effective in smaller populations because random fluctuations in allele frequency (drift) may lead to deleterious alleles reaching higher frequency. The rate at which deleterious alleles are removed from a population depends on mutation, dominance, linkage, and demography and can vary across populations. Therefore, the average fitness over time may become reduced. Kimura in 1963 was one of the first people to show this.
In reality, 'low efficiency of selection' and 'strong drift' in small populations are the same thing.


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Reasons for the existence of symporters and antiporters
I'm wondering what is an evolutionary adaptation to the evolution of symporters and antiporters instead of just uniporters.
Antiporters might help preserve electrical neutrality by pumping in/out an ion of the same charge as is the case in H+/K+ ATPase, and perhaps transporting 2 ions at the same time is more efficient than just one.
But the same can't be said for Na+/K+ ATPase, which actually contribute to a net negative charge, so why not instead use a uniporter here?
Additionally, could the efficiency hypothesis also be applied to symporters or are here other reasons at play?
Hence in brief, what justifies the existence of symporters and antiporters as compared to uniporters?

The Na/K ATPase hardly contributes to any charge. The (lack of) importance of the 2/3 ratio is often misleading to students. There are many questions here about this.

Uniporters function as passive transporters and can not achieve concentrative accumulation. Symporters and antiporters are examples of active transport (they couple the movement of a subtrate to an additional process that yields energy). Since some solutes are present at very low concentrations on one side of the membrane (e.g. in the blood) systems had to evolve which can achieve concentrative uptake (as opposed to equilibrative uptake as mediated by passive transporters). Therefore, it makes sense that not only uniporters exist, but also symporters and antiporters (and primary active transporters as well).

For me the more interesting question is, why do uniporters have to exist when you have pores and channels? (Uniporters differ from the latter two in that the function according to the alternate access mechanism and are not open to both sides of the membrane)

Uniport: a membrane transport process in which a single kind of sub-
strate is transported across the mem-
brane, either by the mechanism of mediated diffusion where the
substrate equilibrates at the two membrane sides (e.g., monosac-
charides in mammalian erythrocytes; TC 2.A.1.1.12), or by active
transport where an external source of energy is used to achieve
movement against a chemical potential or an electrochemical po-
tential gradient (e.g., plasma membrane H+-transporting ATPase
TC 3.A.3.3.1 or EC 3.6.3.6). Such transport systems may be designated as uniporters.

The above quote comes from Oxford Dictionary of Biochemistry and Molecular Biology and according to this definition active uniporters seem to exist.

@RtoR Most channels are specific to certain very small molecules and ions like sodium. If there were channels that were large enough to accommodate molecules like glucose, many other molecules would be able to pass through as well and the membrane would lose its selective permeability, and would be unable to maintain concentration gradients.


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Can the basement membrane of blood capillaries expand?
I have been doing some rudimentary research into the basement membrane and found the it contains collagen fibers which are known for their elasticity.  Does this mean that the basement membrane can expand in capillaries?

It's a good question.
Though there is hardly some evidence to answer your question.
However I will share what all I found.
So in capillary basement membrane, mostly collagen type 1 and 4 are  present.
Now collagen type 4 aids in elongation of the new capillaries-

in the ex vivo rat aortic model of angiogenesis using a type I collagen matrix, type IV collagen promoted new vessel elongation and survival in a dose-dependent manner compared with controls (no type IV collagen), which grew until day 9 and then regressed during the second and third week of culture (treatment with 3, 30, 300 g/ml of type IV collagen in 43, 57, 119% increase in microvascular length) [139]. In all then, type IV collagen seems important for stability of blood vessel formation.

The collagen in capillary basement membrane impart mechanical stability to the vessel.
Also elastin is a component of the basement membrane. Reference
Now though I couldn't find that it's the elastin of basement membrane only, but-

Comprising 50% of the dry weight of major arteries, elastin is the most prominent ECM protein in arteries [43]. In vessels, elastic lamina alternate with rings of smooth muscle forming a strong, flexible part of the arterial wall [43, 44].

Here is the article


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Are all antibodies against a common antigen identical?
I understand that when some antigen (e.g., virus, bacteria, etc.) is recognized in the body, antibodies specific to this antigen are produced that, in turn, bind to the antigen and effectively neutralize them as a potential threat to the organism.
Are all the antibodies that are produced against a specific antigen necessarily identical?  Either within a single organism (e.g., a single person), or between different organisms (e.g., between different people, different species, etc.)?  If two people get sick with the same disease, develop antibodies, and recover, are these antibodies the same?  If a human and some other animal get sick with the same disease, will the antibodies each develop match?
Key to the operation of the antibodies is their specific recognition/binding of the antigen.  I assume that the structure and composition of the antibody is tuned to bind to specific exposed moieties on the antigen.  I can imagine that there are many different potential binding sites on the antigen to target and many possible combinations of ways to recognize those sites by the antibodies.  I would think that it would be a remarkable coincidence (highly unlikely) if separate organisms both, independently, happened to develop the same “molecular strategy” for recognizing a particular antigen.  This outcome seems to be implied in this question,
How are antibodies specific for a disease detected in the blood if everybody produces a different antibody for the same antigen?

Alright, there are two major questions:
(a) Are all the antibodies that are produced against a specific antigen necessarily identical?
Not in most cases. Antigens can either be monovalent or polyvalent, meaning that they can either have one epitope or various different epitopes (an epitope is the site of the antigen that binds to a T-cell receptor or a B-cell receptor). Most antigens are polyvalent, which implies that a single antigen may interact with several different T and B cell lineages. Each B cell lineage is only able to produce and export one type of antibody. Because the antigen will interact with different lineages, it will promote the production of different types of antibodies. These multiple antibodies produced against one antigen are called polyclonal antibodies, since they arise from multiple clonal lineages. When the antigen only has one kind of epitope, it will induce the production of only one type of antibody, which are called monoclonal antibodies, because they arise from only one clonal lineage.
(b) Do the antibodies produced against a certain antigen differ between members of the same species or between species?
Yes, in both cases. There is an important genetic variability surrounding immunoglobulins and T cell receptors.
Reference: Karp, G. (2009). Molecular and Cellular Biology: Methods and Concepts. Wiley. New York.


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Can there be traits which aren't possible objects of selection, e.g. beneath a "threshold of genetic noise"?
Is it possible that there are traits that might not be possible objects of the selection because of highly sensitive dependence on genotypes? The context of my thought came when I was having a discussion, more philosophical/political, with someone who was asserting individual characters (e.g. being good or bad) are innate in some sense. My impression is that, to whatever extent genetic determination of observable personality is the case, it'd be a highly complex phenomenon that could depend on many genes, and such matters are very much up in the air. This led me to thinking more abstractly about whether there could be such a thing as a trait that depended on so many genes-- to make it simple, let's say the entire genome-- and depended on in in a way that made it essentially a random trait.
For example, let's say there's a trait T, and we are looking at a creature that has a genome of only three base pairs, and to make it simple let's suppose the genetic code was binary, 1s and 0s (so eight possible genomes). So 100 represented an entire genome for whatever this is. And suppose that T was completely determined by genome (or else, that probability of T was determined by genome), and that the trait T was distributed over genomes such that T={000,110,101,011} and not T={100,010,001,111}. Visually, one could picture the genomes as corners on the unit cube in three dimensions, and T has been distributed so that any two corners separated by a single edge are opposite with respect to T, or, equivalently, that any two corners that can be connected by a minimum of two edges are of the same class with respect to T.
If there is no copying error in genomes then we can have selection for T; for instance, we can have pressure that favors one of the four genomes that cause T. But suppose there is always some random genetic error when a new individual is made. Say, for instance, the third spot is always randomly 1 or 0 with probability .5, and that there's no reducing the genetic randomness below this threshold. Then it seems impossible for there to be selective pressure for or against T, for any non-random distribution on the first two digits still just moves probability around genomes that give a net 50% probability of T being instantiated or not, because in the way I've assigned T, it is statistically independent of the value of any particular (or even any two) genes.
In essence, the trait is so very sensitive to changes in genome-- changing any single gene completely changes the trait-- that whether or not it is instantiated is swings back and forth with any random genetic changes. This is reminiscent of chaos in classical mechanics; some systems are simply so sensitive to underlying conditions that they are no subject to control and prediction in the fullest sense (though that doesn't mean they have to be fully random like the thing I've made here). Just on this basis a phenomenon like this seems formally possible, but my question, as someone who doesn't actually know the field, is whether it's in fact a known or theorized phenomenon, and if so what it would be called. Do there exist, or is it possible there exist, traits that are so sensitive to changes in genome that they can't be objects of selection because they fall under some barrier of genetic "noise," or perhaps things that at least start to look like that on a spectrum? Or are genomes always more "continuous" than this, so that, for pretty much everything, a small change in genotype leads to a small change in phenotype? If that were the case for some reason, then I think what I'm describing couldn't happen.
My apologies if my question is amateurish and my use of the language isn't quite right; I've never posted here before, and I'm a mathematician who's only just beginning to go back and self-educate on chemical and biological sciences, and this was a random thought I had while brushing my teeth, and didn't have the vocabulary to successfully search for and recognize answers.

some people suggest that the entire genome does affect certain traits and these traits are still the target of selection: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5536862/

Don't want to get too down into the weeds here, I think you are making things rather complicated (thus someone else's downvote), but here are a few notes:

I would recommend looking up epistasis, which is a fundamental concept in genetics. (https://en.wikipedia.org/wiki/Epistasis). There are many ways in which a trait can be non-responsive to selection, one way is complex epistasis, which can have an effect on selection similar to what you say, in the case of (for example) sign epistasis.

Another way a trait can be not affected by selection is just not being important - if the selection coefficient (https://en.wikipedia.org/wiki/Selection_coefficient) is smaller than the inverse of the population size, selection will not work.

When I was first learning to code I made a toy model of a genotype:phenotype map here that can simulate both cases I think: https://github.com/maximilianpress/teaching_code/blob/master/EvoSim.r. It won't win any prizes but it illustrates the issue rather clearly IMO.

I would suggest reading a bit and maybe playing with the toy model to think about this more.


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Tree-pest coevolution
Many trees first reproduce decades after germination.  Many pests of trees reproduce in under a year.  It would seem that the pests have an advantage in the evolutionary arms-race, as they can evolve a means of attack far faster than the tree can evolve a defense (cf. Does an increased reproduction/mortality rate provide an evolutionary advantage?).
I once read a speculation that trees might mitigate this by varying the genetics (or perhaps only epigenetics?) of different branches within an individual.  The branches that do better produce more seeds.  The seeds produced by a branch carry information specific to the branch.  This means evolution (or the epigenetic equivalent) happens at the level of the organ, not the individual.
Is there any research supporting this speculation?  If it has been refuted, how do trees compete effectively in the arms-race?


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Is magnetic resonance microscopy appropriate for investigating ion-channel flow?
I've been looking into ways to characterize the elecrophisiology of neurons for cell signaling and I came across magnetic resonance microscopy as a tool for gaining images of neuronal activiy at a large scale.
This made me question, is it possibly to take a timeseries video of an active neuron and view the actual signal flow through and outside of it?

Clarification
I am unclear of your aim. What feature of elecrophisiology do you want to characterize?
What do you mean by large scale? E.g. Micrometers (μm),  Milimeters (mm) or Centimetres (cm).
Magnetic resonance microscopy imagings at Micrometers (μm).
Answer
An established way to observe neuron propagation is the use of calcium imaging. You can take a video under a fluorescent microscope to observe (Not measure) elecrophisiology. Also I believe this technique may provide the 'larger scale' you are seeking.
More On Calcium Imaging:
https://www.cell.com/neuron/comments/S0896-6273(12)00172-9

Ah I wasn't aware of calcium imaging I will look into it. To clarify yes, I wanted to know if it is possible to inspect/observe signal propagation through a single neuron.

Excellent, I admire your curiosity.


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Does the coast of California support a larger population of marine mammals than Maine?
Visiting the Maine and California coasts, I've noticed that it is much more common to see marine mammals from the coast in California, including seals, dolphins, and whales. I've been hypothesizing about reasons that this might be the case, and have come up with several ideas.

I'm a tourist, not performing a formal population study. Maybe the numbers are similar, but my measurement method is flawed. I've looked up some better numbers in the NOAA Stock Report:

Seals:

Harbor seals, Maine (75,000) vs. California (27,000),
California Sea Lions, California (257,000).

Whales:

Gray Whales, California (27,000)
Humpback Whale, Maine (900) vs California (15,000)

Dolphins:

Common Short-Beaked Dolphin, Maine (170,000) vs California (839,325)

There are many other species, but these numbers seem to confirm that California has a larger population. Of course, the coast of California is also much larger than the coast of Maine. I'm not sure how to correct for that.

Maybe the fishery in the North Atlantic is more overfished. Wikipedia says that 71% of fish capture comes from the Pacific vs 20% from the Atlantic, but that the Pacific has only twice the volume of the Atlantic[1]. This is much more general than California vs Maine coast, but it suggests that the Pacific has a larger fish population than the Atlantic per volume which could support a larger mammal population.

Maybe there are more protected habitats in California. 15% of the south coast region is protected from fishing. Whereas in Maine, I was able to find information about proposed Marine Protected Areas, but no information about currently protected areas.

Does the coast of California support a larger population of marine mammals than Maine? If so, what factors support the larger population?

You might consider the California coastal current as one possible factor: https://en.wikipedia.org/wiki/California_Current

Assigning whales to a particular coast seems particularly difficult given the large territories that many (most?) species associate with

Also why limit to Maine? There's nothing particularly special about Maine vs, say, New Brunswick and Newfoundland and Nova Scotia, besides political boundaries

@BryanKrause Maine is simply the location where I have visited the coast. If you would prefer to answer for a larger section of the North Atlantic coast, please do.

@BryanKrause NOAA fishery stock report specifically assigns Humpback Whales in the Gulf of Maine as a "relatively  discrete  subpopulation(s),  fidelity  to  which is determined matrilineally"


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Number of "mutations" in Omicron variant
Currently in the media they say that the Omicron variant has more than 30 "mutations", ie changes in spikes. I find this confusing, because the way I understand a single change in the virus can alter more than one spike in one go. I assume there is some randomness to mutations. So one mutation (new copy) can change 2 spikes, another can change 0 or 5.
Is it misleading?

Welcome to Biology StackExchange! I don't think I understand what you mean with "a single change in the virus can alter more than one spike in one go". All of the spike proteins that build a virus particle are (more or less) identical, because they are a product of the same gene – there is only one gene for S protein in the SARS-CoV-2 genome. Therefore, if there is a mutation in the S gene, all the spike proteins produced will carry this same change.

I think the OP does not understand what spike means in the context of a coronavirus. Spike is the name of one of the important proteins of the virus and it is around 1200 amino acids long. Three copies of this protein form the characteristic surface structures of the virus well known from cartoon drawings.

Mutations are generally random, yes, but the "30 mutations" referred to are not random among omicron-variant virions, but rather 30 differences between the omicron variant and the reference genome they are comparing to from early in the pandemic. Most omicron virions will have the same 30 "mutations" as all the others, because that's why that group was given a name. These are not new mutations in every virion, they are mutations that happened earlier in the lineage that were passed down to all the descendants of that lineage. They are only "mutations" in comparison to the reference genome. If it helps, substitute the word "differences" for "mutations": Omicron has 30 differences in the genome coding for the spike protein compared to the reference strain of SARS-CoV-2.
For a single virion, the cell it infects is going to produce all spike proteins that are the same, because they are built from the same genetic template. You wouldn't typically have multiple spikes of different types in the same virus particle (theoretically possible with errors, etc, of course).
Since the pandemic started, an incomprehensible number of different mutations have occurred in SARS-CoV-2 virions replicating in human hosts. However, most of these mutations are not consequential because they did not spread in the population. For ones that do spread, you can track their origin in a sort of "family tree". See for example on NextStrain:
https://nextstrain.org/groups/neherlab/ncov/21K.Omicron

Bryan Krause has the answer, but I wanted to add a note about the connotation of the word mutation and what it actually means.
The word mutation just means genetic change that a cell (or virus) doesn't fix by the time it replicates itself. That's it. There are a few different ways to skin this cat, but the situation you're imagining is if the virion (viral genes) copied itself multiple times, called polyploidy. The thing is that mRNA viruses don't really have the ability to do that, because they can't self replicate, and so the required mechanism is off limits until they infect someone. When you say that a mutation could double the number of spike proteins, it makes me think that you assume that more genes = more proteins. While this is sometimes the case, what determines how many proteins (called protein products) come from genes is their level of expression and regulation.
So, what determines how many spike proteins a virus makes depends on how well the virus can convince the host to make more spike proteins, which might come from a mutation in a gene, but having multiple genes is not always the source of multiple copies of a protein. If we want more protein, we need more mRNA, which means we need more expression of a gene. You might say, well more copies of the viral mRNA would produce more proteins right? Yes, true, but again in a situation like that, you're really describing a higher viral load (just more of the same virus) than an instance where an entire viral genome has spontaneously doubled itself.
Some people interpret mutations, because of entertainment, as the source of genetic change responsible for dramatic differences that are cartoonish and comical. Think of the cyclopes from Futurama, for example. But no, mutations are often no so exaggerate in their appearance. Most mutations, in fact, are unhelpful and depending on how often mutations are produced in a species, are typically selected against quickly. This is an indication of two things:

The 30 or so mutations you report are the source of differences in traits that give the virus an advantage. Yes a mutation in a Hox gene for example could result in drastically different results. But more often, mutations that are helpful come in more subtle and less dramatic forms.

A variant of the virus is identified based on its genetics. Each variant of the virus is classified by its genome. So yes, the Omicron variant might produce a slightly different antigenic site than the Delta variant. We're not changing the number of spike proteins, we're changing the identity of the virus.

As it’s currently written, your answer is unclear. Please [edit] to add additional details that will help others understand how this addresses the question asked. You can find more information on how to write good answers in the help center.


text:
Where can I find a cannabinoids profile of hemp strains?
For my web article, I need to find out the content of individual cannabinoids in hemp strains, specifically for Kompolti, Carmagnola and Purple Haze. I mean the content of all the components, not just THC and CBD.
Do you know of any website that provides this information?
Thank you for answer


text:
How can the layperson test whether a UVC light sold as "germicidal" is a fake or probably the correct wavelength?
Are there simple ways to test whether a light is likely short wave / UV-C, or at least whether it is probably a fake?
Real Example:
2 lights are allegedly germicidal and supposedly emit germicidal 254nm radiation.

Light 1 darkens transition glasses and emits the smell of chlorine / ozone.
Light 2 does neither but appears much brighter than Light 1.

Does the ozone smell of Light 1 entail that it at least emits radiation within the UVC band?
Assuming the glasses do darken outdoors and do darken in response to Light 1, given that they do not darken with Light 2, is it safe to conclude Light 2 emits no UV at all?

I’m voting to close this question because it isn't about biology — please consult the [tour], [ask], and other [help] pages for details.

@tyersome will this question be a better fit on one of the other SE sites,if so it should be migrated.i think the question is important to get answered as there is a lot of fake gemicidal lamps on the market and we are in a pandemic at the moment.i do not disagree wit this question beeing a poor fit here on biology but what are the alternatives.

@trondhansen — If I had a good suggestion I would have made it — since this seems to be fundamentally an optics question there might be a place for it in physics. However I'm not familiar with that site, but since this is a "how do I do this at home" question rather than one about fundamentals of science I'm skeptical whether it would be a good fit there. I think there is also a site about DIY/home repairs. Finding the right site is ultimately the responsibility of the poster. Also note that there is no guarantee that there will be a SE site for any particular question!

Sometimes Physics SE is very helpful, but not always. I think if you have a little patience and the question is closed and then migrated by a moderator, there's a good chance it will receive an answer, though I don't know if it will be helpful.

FYI: a "blacklight" LED will darken transition glasses (Don't ask me how I know!)

Transitions lenses darken with exposure to UV-A light, so they do not indicate whether a bulb is emitting UV-C or not.

You can do the banana test to identify if it is real or fake.
Get a green banana and cover parts of it with a sticker you now need to expose the banana with the uv light for about one hour,the green banana will get brown/yellow at the exposed part and stay green under the sticker if the uv-c light is genuine..
It is best to do this in a dark room and the banana can not be in a plastic bag or any covering as this might stop the uv-c light.
The uv source needs to be close to the banana for this to work.
If the color of the green banana stay the same after the test your uv-c light is fake.
Never look directly at the uv-c light and do not shine the light on your bare skin.
source https://www.reddit.com/r/BigCliveDotCom/comments/gj9ymb/uvc_the_green_banana_test/

Re, "Never look directly at the uv-c light." UV-C exposure will hurt your eyes alright, but it doesn't matter whether you "look at" the light or not. The UV-C rays will never reach your retinas. All of the damage will be superficial. Don't expose any part of your body to UV-C if you can avoid it, and also, don't breathe the ozone.


text:
Is a "Nerve" a cell or a tissue?
Nervous tissue includes Neurons and Glial cells. Neurons have soma and other projections (neurites) namely Axon and Dendrites. Axon or dendrites of a nerve cell covered with endoneurium
is called nerve fibre, a bundle of nerve fibres covered by perineurium is called
nerve fasciculus, many nerve fasciculi covered by epineurium form the "nerve". Is the "nerve", which is present in the PNS, will be regarded as a tissue or a cell?

Welcome. As far as I can see, you've answered your own question.

I'm new to the subject, can you please elaborate, if you don't mind?

What kind of response is that?

I advise you to scour google and search for "cell versus tissue" - the thing you need to get clear for yourself is the distinction between these two terms. Then this question will be answered quite easily.

I think you are clear that nerves are not cells. Your question should be more precisely: Do nerves have the propierties to be consider a tissue?


text:
Adaptive radiation vs divergent evolution
What is the difference between divergent evolution and adaptive radiation? People have Said different things
Divergent evolution is when species from a common ancestor evolve differences by adapting to different environmental conditions
Adaptive radiation - species evolve differences due to the different environments
Are they essentially the same thing also I’m confused with the terminology niche
Could someone please tell me the similarities and differences between the two

Welcome to SE.biology & thanks for your question. It's helpful for people trying to answer your question if you include links to sources for the statements made, rather than saying 'People have said different things'.

They are similar, but distinct, concepts.
In divergent evolution, selective pressure causes differences within a single species to accumulate, eventually leading to speciation. Speciation can be caused by a variety of factors, such as geographical, reproductive, behavioral, or temporal isolation, etc.
In adaptive radiation, typically several niches are present in an ecosystem, leading to several species evolving from a single common ancestor. A niche is essentially an opportunity for a species in an ecosystem to evolve, to where there is little to no competition. Darwin's finches tend to be the prime example for adaptive radiation. Since there was little competition when the finches first arrived at the Galapagos islands, they speciated into multiple distinct species to specialize in consumption of seeds, fruits, insects, etc. Eventually, each species evolved to have distinct traits, such as in their behaviour and reproduction, making mating between species close to nill.

There is not a hard, clear distinction between the two.  In divergent evolution, accumulation of differences as a result of selective pressures amounts to adaptation to different "niches" defined by behavior, environmental role, etc.  The two terms are useful and have different meanings as you've describe, but their meanings overlap.

I agree, their meanings do overlap. However by distinct I meant the terms are generally not interchangeable; as I understand adaptive radiation is only used for several speciation events occurring from a single ancestor. But yes, I believe this would still be considered divergent evolution.


text:
Why do I get cytosine to guanine/adenine transitions in bisulphite treated sequences?
I got my sequencing results (bisulphite treated and non treated sequences of same species Allium cepa) and now I have to do analysis in Cymate online tool. I prepared all sequences as it is written in original Cymate paper (master sequence and clones - aligned in ClustalW, blunt ended).
My problem is that I got gaps in results (image is attached, it is from Cymate Result) on positions 27, 50, 58 etc.

When I looked back at my original alignment FASTA file and compared those positions, I noticed that those gaps are from C to A, or C to G transitions (and obviously Cymate outputs only C to C, and C to T cases).
Does anyone know why do I get those C to A, or C to G, are those some mismatches, should I manually remove it from alignment, or did I made some other mistake?
Any advice from you would be very useful for me!
My FASTA file alignment, which I uploaded to Cymate, is here (if anyone wants to check). First sequence is master sequence (non-treated, orifinal sequence) and the rest are clones (bisulphite treated sequences).

Consensus_cepa__(289_bp)
GAAAGCCAACCACCACATCCGCCATCCCTCACAGTATGCCAACGAGCAGCTGAATGACTCCGAACAACGCAAAGCATGACGCCCAAACCGACGAACACCCAACCGAAAGGCCACAAGCGCAACGTGCATTCCAAAACCCCATGAACCACCGAATCCTGCAATGCACACCACGCTCGACGCCATTCGCTACAGACCACATCGACACGAGCGCCAAGCCATCCATCACCCGAAGCCATCCACCCACTCACAAACATACCACGAAGCACAGCAAATATGAAGACAAACCCTC
MV_A_SP6_izrezani_s_primerima__(295_bp)
AAAAATCAATCTCCACATCCGCCATCACTCACAGTATATTTAC-AGTAGATAAATAA-TTAAAATAACGCAAAACATAACGCCCAAACAGACGTACTCTCAACCTAATAACCTCGAACGCAACTTACATTCAAAAACTCGATAATTCACGAAATTCTGCAATTCACACCAAA--TATTGCATTTCGCTACGTTCTTCATCGACACGAAAACCAAAATATCCATTGCCAAAAATCATTCAGACGCTCACTGAAATAACACAAAACACATCAAA-ATAATAACAAACTTTC
MV_B_SP6_izrezani_s_primerima__(295_bp)
AAAAATCAATCTCCACATCCGCCATCACTCACAGTATATTTAC-AGTAGATAAATAA-TTAAAATGACGCAAAACATAACGCCCAAACAGACGTACTCTCAACCTAATGACCTTGAACGCAACTTACATTCAAAAACTCGATGATTCACGGAATTCTGCAATTCACACCAAA--TATCACATTTCGCTACGTTCTTCATCAACACGAAAACCAAAATATCCATTACCAGAAATCATTCAGACGCTCACTGAAATAACACAAAACACATCAAA-ATAATAACAAACTTTC
MV_C_SP6_izrezani_s_primerima__(291_bp)
AAAAATCAATCTCCACATCCGCCATCACTCACAGTATATTTAC-AGTAAATAAATAA-TTAAAATAACGCAAAACATGACACCCAAACAGACATACTCTCAACCTAATAACCTCGAACGCAACTTACATTCAAAAACTCGATAATTCACGGAATTCTGCAATTCACACCAAA--TATCGCATTTCGCTACGTTCTTCATCGACACGAGAACCAAAATATCCATTGCCAGAAATCATTCAGACGCTCACTGAAATAACACAAAACACATCAAA-ATAATAACAAACTTTC

Welcome to SE.biology. This is a nice question, but I think you might get a better answer in https://bioinformatics.stackexchange.com/

how did you generate these sequences? are they e.g. sanger sequences or did you go through a complex workflow (not familiar with cymate)? what proportion of bases carry this error?

Also, your cymate data is not linked.

I quickly aligned your sequences, and as far as I can tell, the answer is that your "consensus" sequence is a poor match for the 3 other sequences:
CLUSTAL format alignment by MAFFT L-INS-i (v7.310)

Consensus_cepa_ gaaagccaaccaccacatccgccatccctcacagtatgccaacgagcagctgaatgactc
MV_A_SP6_izreza aaaaatcaatctccacatccgccatcactcacagtatatttac-agtagataaataa-tt
MV_C_SP6_izreza aaaaatcaatctccacatccgccatcactcacagtatatttac-agtaaataaataa-tt
MV_B_SP6_izreza aaaaatcaatctccacatccgccatcactcacagtatatttac-agtagataaataa-tt
                .***..***.* ************** **********... ** **.*. *.***.* *.

Consensus_cepa_ cgaacaacgcaaagcatgacgcccaaaccgacgaacacccaaccgaaaggccacaagcgc
MV_A_SP6_izreza aaaataacgcaaaacataacgcccaaacagacgtactctcaacctaataacctcgaacgc
MV_C_SP6_izreza aaaataacgcaaaacatgacacccaaacagacatactctcaacctaataacctcgaacgc
MV_B_SP6_izreza aaaatgacgcaaaacataacgcccaaacagacgtactctcaacctaatgaccttgaacgc
                 .**..*******.***.**.******* ***. ** *.***** ** ..** ..*.***

Consensus_cepa_ aacgtgcattccaaaaccccatgaaccaccgaatcctgcaatgcacaccacgctcgacgc
MV_A_SP6_izreza aacttacattcaaaaactcgataattcacgaaattctgcaattcacaccaaatattgcat
MV_C_SP6_izreza aacttacattcaaaaactcgataattcacggaattctgcaattcacaccaaatatcgcat
MV_B_SP6_izreza aacttacattcaaaaactcgatgattcacggaattctgcaattcacaccaaatatcacat
                *** *.***** *****.* **.* .*** .***.******* ******* .. . .*..

Consensus_cepa_ cattcgctacagaccacatcgacacgagcgccaagccatccatcacccgaagccatccac
MV_A_SP6_izreza --ttcgctacgttcttcatcgacacgaaaaccaaaatatccattgccaaaaatcattcag
MV_C_SP6_izreza --ttcgctacgttcttcatcgacacgagaaccaaaatatccattgccagaaatcattcag
MV_B_SP6_izreza --ttcgctacgttcttcatcaacacgaaaaccaaaatatccattaccagaaatcattcag
                  ********.  *. ****.******. .****. .******..** .**..***.**

Consensus_cepa_ ccactcacaaacataccacgaagcacagcaaatatgaagacaaaccctc
MV_A_SP6_izreza acgctcactgaaataacacaaaacacatcaaa-ataataacaaactttc
MV_C_SP6_izreza acgctcactgaaataacacaaaacacatcaaa-ataataacaaactttc
MV_B_SP6_izreza acgctcactgaaataacacaaaacacatcaaa-ataataacaaactttc
                 *.***** .* *** ***.**.**** **** **.* .******..**

I would suggest trying to come up with a different, more appropriate consensus/reference sequence. This one does not appear to be appropriate.
Granted, I have no idea how you came up with this consensus sequence (it certainly is not a consensus of the other sequences you show), and possibly there is something else going on that I am not understanding.
This does not seem to have anything to do with the bisulfite conversion, as the data also include changes that cannot be attributable to bisulfite, gaps, etc.
Knowing more about the whole workflow would help.
UPDATE
Also, while I'm not familiar with the workflow, could such gaps not be related to methylation on the opposite strand? E.g. CGTA-->TACG.
Is there a particular methylation context that you are looking at? CpGs only?
In some cases there is support for weird variants (e.g. consensus is not an outgroup).
If it's sanger data, it's always a good idea to directly inspect traces.


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Reproduction in animals
Humans have acquired knowledge about their environment through many observations. Today, humans have wide variety of resources to gain knowledge about reproduction in human beings and other reproductive processes. This knowledge does not come from genes. But on the other hand the animals example pig don't have any kind of resources which teach them about reproduction, still they can perform their reproductive processes. Even an isolated mice can do so if a mate comes in his vicinity.
But the isolated mice doesn't have any knowledge about reproduction then how can they perform it?
https://animals.mom.com/how-a-pig-reproduce-2607021.html
https://oacu.oir.nih.gov/sites/default/files/uploads/training-resources/mouserepro.pdf

TL;DR: instinct. Even humans don't require any knowledge to reproduce. If you just do together what feels good, there is a good chance that it ends with sex. Behavior of most mammals is much more strongly triggered by pheromones than that of homo sapiens. You probably should start with reading about the vomeronasal organ and the response triggered in rodent brains by reception of sex pheromones.

Animals don't have any great knowledge about the processes of digestion, yet they manage to eat.  Consider that if animals (or plants, bacteria, &c) had to be taught how to reproduce, and understand all the biological details, they would never manage to reproduce at all :-)

Arguably, humans, upon learning in detail about reproductive processes and their control, seem to tend toward avoiding those processes reaching their biological ends rather than seeking them out.

Instinct
What is instinct, instinct is any behavior which did not require cognition or consciousness to perform or innate behavior that does not require learning.
BY the nature of building a brain it is possible to build in behavior by laying out neurons and connections in preset patterns. Thus some behavior can be encoded genetically.
Simple examples of Instincts include reflexes and fixed action patterns, but there is a whole spectrum of behaviors ranging from pure instinct to pure learned and everything in between.