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Did we evolve from Africans?
I learned about The Theory Of Evolution in middle school and our teachress told us that we evolved from African People. Is that true? How?

Did your teacher say that we came from africa or african people? There's a difference there.

Because you are young, you can see most simply from this list of images accompanied by the time in years, Ma means millions of years... https://en.wikipedia.org/wiki/List_of_human_evolution_fossils#Pleistocene Some of the people 's bones are at least 250,000 years old, if not older. If it takes 25 years for a generation of father to son, that means that we have skeletons from great-great-grandfather * 10,000 great.

Welcome to Biology.SE!

Did we evolve from Africans?

Who is "we" in your sentence?
Although, it might not have been your intent, you seem to exclude Africans (and people of recent African descent) from the "we" (which would be rather insulting)!
I will rephrase your question. I will pick "caucasians" (thinking that you might be caucasians and by "we" you may have had "Caucasians" in mind) to rephrase your question but I could have picked Han Chineese, Polynesians, Micronesians, Mongolian or any other (big or small) extant human lineages that currently lives mainly outside of Africa. I will rephrase your question as Did [caucasians] evolve from Africans?
What does "evolve from" mean?
No extant lineage is the ancestor of another lineage. An extant species of lizard is not the ancestor of an extant species of mammal, just like an extant species of mammals is not the ancestor of an extant species of lizard. The same hold true for any two extant lineages. Extant lineages share common ancestors. Their Most Recent Common Ancestor (MRCA) may have lived a long time ago or only relatively recently. This answer might help you to understand these concepts.
If you mean to ask Did [Caucasians] evolve from current Africans? as in Is Nelson Mendela the ancestor of Kurt Cobain, then the answer is (obviously) "No".
So, when you ask Did [Caucasians] evolve from Africans?, I am assuming, you meant Did [Caucasians] have descendants who lived in Africa?
Did Caucasians have ancestors who lived in Africa?
Yes. All modern humans (aka Homo sapiens or Homo sapiens sapiens) are descendent from first humans that lived in Africa. The MRCA of all modern humans lived in Africa.
To reiterate the above, this in no way suggests that modern Africans are "ancestors of" or "more primitive than" or "less evolved than" any other human lineage. However, interestingly, because early split among human lineages happened in Africa, the majority of genetic diversity among humans is found in Africa still today.

I learned about The Theory Of Evolution in middle school [..]

If you want to learn a bit more, you might want to have a look at a simple and very introductory source of information such as evo101 by UC Berkeley
EDIT
Comments shows that the OP did not quite get it yet. Here are some more info...
First, please have a look at this answer (already indicated under the section What does "evolve from" mean? above). Make sure to read it fully. Did you read it?
H. sapiens is a monophyletic group (for simplicity, I will make abstraction of horizontal gene transfer here). The MRCA of this group used to live in Africa. Some of the sub clades of this group have moved elsewhere in Africa, and some have moved elsewhere outside of Africa (there has been a fair amount of back and forth too and a fair amount of secondary contacts as there is no reproductive isolation among H. sapiens). That's all!
Your confusion comes from the fact that you call "Africans" both the MRCA and the current lineages that live in Africa. It may make you feel that people currently living in Africa and the MRCA of all humans who lived in Africa are somehow more related just because they live on the same continent but that would be wrong. All human lineages have evolved from this MRCA (who lived in Africa), whether the lineage you want to consider is currently living in Africa or not.

Or to reduce it to one sentence: All humans, including modern Africans, evolved from ancestors who lived in Africa.

Hmmm, interesting. If I understand your theory correctly, we evolved from the MRCA African People and NOT the extant African People because there is a difference between extant African People and the MRCA African People? We're two different lineages?

@Hierarchist I don't believe that's correct- properly speaking all the major lineages of humans are "African" lineages, which includes your "we". Some of these major lineages gave rise to people who left the African continent, but they still arose in the African continent. The MRCA of any group of people is different from the current people, was I believe what Remi.b was trying to communicate, so no one alive "evolved from" anyone else who's alive. More simply, the MRCA of "African people" is simply the MRCA of humans; all "non-African" humans are part of "African" lineages.

I'm trying to understand your theory: if the MRCA of us and African People is different from African People, then we're a different lineage from African People? Or are we the same lineage as African People because there's no difference between the MRCA of us and African People and African People? Moreover, you seemed to say that we split off from African People all the way back when we were Africans? I'd appreciate an explanation of your theory.

@Hierarchist Please see the Edit section which will hopefully clear things up for you.

@Hierarchist Please stop saying "we" when you mean "caucasians" (or something else). 1) it is unclear who is included in the term "we". 2) You clearly exclude current Africans from the "we" (which sounds rude) and for all you know I might be Nigerian and hence it would make the conversation very confusing.

Also, it there any reason you repeated your theory three times? It make it sound like you have an incorrect view of the legitimacy of the modern evolutionary synthesis (which is the name of what you call the theory of evolution). See the post Is evolution a fact? for more info.

@Hierarchist I think the issue is that the idea of a coherent group of humans different from "Africans" is not scientifically well-supported. Talking about people by their continental birthplace and/or physical appearance is, at best, misleading. "Non-Africans" are still "Africans" in that they are part of one lineage among many lineages that arose in the African continent. "Non-Africans" are quite closely related to many "Africans". A "non-African" person is much more closely related to many "African" people than randomly selected people of "African" descent are, on average.

"Did Caucasians have descendants who lived in Africa?" Do you mean "Did Caucasians have ancestors who lived in Africa?" few caucasians have african descendants, they all have african ancestors. A parent is an ancestor of their offspring a child is a descendant of their parents. you confuse the two several times.

@John Thanks for the correction. I fixed the error.

@John: Though if you want to get into linguistic confusion, there are a good many (several million, at least) Caucasians who have descendants who were born & live in Africa :-)

What you could do is to take a look at diagrams such as this one:
You can make a google image search for "Cavalli Sforza" and get a lot of similar diagrams. This diagram is using a concept known as genetic distance by fixation index. This is a way to measure how different different ethnic groups are genetically. From the diagram it is easy to see that there is a large genetic gap between the current sub-saharan Africans and the rest of humanity. The genetic distance between sub-saharan africans and any other ethnic group is almost twice as large as the distance between any two non-african ethnic groups. It is from measurements such as these that scientists are able to tell that humans first must have been living in Africa before we took off to the rest of the world.
The people who were living in Africa 50000-70000 years ago, before the "split", were probably on average very different from modern African people although they probably were adapted to the hot climate. I do not now if you are familiar with the so called "Bantu-Expansion" that occured in several waves in the last 4000 years? This is what wikipedia says about the populations in africa before the bantu-groups took over:

"Before the expansion of Bantu-speaking farmers, Central, Southern and
  Southeast Africa were populated by Pygmy foragers, Khoisan-speaking
  hunter-gatherers, Nilo-Saharan-speaking herders, and Cushitic-speaking
  pastoralists."

From very recent research we also know that all non-subsaharan groups are a result of interbreeding with Neanderthals/Denisovans. I think that current estimates says that people from western Eurasia has 2 percent of there genes from these groups, east asians has around 3 percent and people from Papua/New Guinea around 4 percent, but this is new research so those numbers might change.

Here are two other genetic distance by fixation index diagram, from this page, also based on the work of Cavalli-Sforza, more focused on how different ethnic groups in Africa are related:

There are also some more modern approaches that might not be so easy to comprehend, see for instance this article from Nature.

I find this figure somewhat misleading. Specifically, Cavalli-Sforza represents "Africans" as one clade, when in fact there are at least dozens if not hundreds of clades in that one leaf that are more distantly related than the other leaves are from each other. If you drew all those clades in, you'd see that all other clades are a rather tight group nested in the African clade.

You mean like this diagram on this page, which is also by Cavalli-Sforza, but I do not know if it is free of use, the other diagram was from wikipedia commons.

yes that one is better (URL is slightly broken)- it is still using the distance-based tree, which make it look like there are two clades, which we know isn't the case, but it is at least showing the huge diversity within the continent. From a cursory google, Figure 1 from this paper [https://www.nature.com/articles/srep29890] is much closer to the current scientific understanding.

On my current level of understanding the nature figure is a bit difficult to understand. The guy really just wanted to know why we think the "out of Africa" theory is true. Can you find some simple clues pointing in that direction in the Nature figure?

I think that OP had a somewhat different motivation for the question, though it's hard to be sure from his phrasing. We need to be very specific in this case because there is a lot of pseudoscience and bad stuff (racism, obviously) around human origins. The figure I linked is more accurate because it shows that "Africans" are not monophyletic. That is, there is not a common ancestor of "Africans" that is not also the common ancestor of "non-Africans", because "non-Africans" arose out of Africans. Cavalli-Sforza drew his figure to make the two groups look monophyletic, which is wrong.

@MaximilianPress, so we arose out of Africans? What's the difference between "around out of" and "evolved from"?

A couple things: 1) The people currently living in the continent of Africa and the people who lived there 100,000+ years ago are not the same people. This is why the term "Africans" is pretty meaningless in your question. You need to be more specific or your question is unanswerable. It's like thinking that Moctezuma I and Pancho Villa are the same person because they both had political power in Mexico (except 200+ times less accurate). 2) not saying what you mean by "we" is starting to look like trolling. 3) I don't know what you mean by "evolved from". Humans are all the same species.


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Can you identify this bug

This was found in my home in Mojave county Arizona. It was about 1/8 inch long. I have a cat. Hoping not a flea.

Definitely not a flea. It has the mouthparts of a true bug, order Hemiptera. I can't tell beyond that.

If the specimen is still at hand, adding a top view photo would help get an answer as to what true bug we're seeing here (but if the primary concern was flea or not, that's been dealt with).

I don't have it anymore. I Would like to know what it is, but yes my concern was flea. Me and my cat keep getting bit up. I have seen lacewing and thrips in house and on me. I know the larvae stage of both feed on blood. Also thrips are known to lay eggs under people skins. Pretty sure all these stupid little bugs are tearing us up. Just trying to identify  everything I see. So I can prevent as much as possible

source: Stack Exchange

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

sort: votes


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Need help to determine % difference between DNA-strand from two different haplotypes. Known nucleotide diversity and more
Backround:
229 DNA sequences
493 bp in length
Haplotype diversity: 0.9956
Average  number  of  nucleotide  differences: 12.50544
Polymorphic sites: 145
Nucleotide diversity: 0.02426
Is it possible to determine how many percent difference there is, on average, between DNA-strands from the different haplotypes?
The answer may be quite obvious, but this is new to me.

No, unless you have the distribution of haplotype frequencies. In that case you could compute the expected difference in nucleotide across haplotypes based on the average number of nucleotide difference conditioned on that H distribution.

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


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Ideal examples of Magnoliophyta Lilianae
What are the ideal examples of Magnoliophyta (Lilianae-to be precise) for a teacher to show students?
And, does anybody know exact name of this flower? Picture


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Immunoprecipitation compared to western blotting
Immunoprecipitation and western blotting are both used to locate a specific protein within a sample and to isolate it.  In immunoprecipitation, a specific antibody and agarose beads ( or other insoluble beads) are used to precipitate the protein. In western blotting, SDS-PAGE is carried out and primary and secondary antibodies are used to locate and isolate the proteins on the nylon membrane.
My question is: which technique should be used when? what is the difference between the two? is one of them "better" / does one of them have advantages over the other?

The two techniques serve different purposes:
IP: purifies a protein
WB: visualizes or quantifies a protein
Most often when I have done IPs (in the hazy past) I have turned around and run the protein out on a WB, so one will frequently combine both techniques. Sometimes a protein is very low abundance so you will not see it in a small volume of crude cell lysate on a WB, and you have to IP it from a large number of cells to get enough protein to visualize on a WB.
Note that IPs will also co-purify associated proteins, so a good way to know whether two proteins stick together is to IP one of them and probe for the other on a WB. This "co-IP" analysis is a very common use case for both techniques.
Hope that helps.


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How many electrons does the b6-f complex need to pump one proton into the thylakoid lumen?
In photosynthesis, photons are used through photolysis to split water molecules and retrieve their hydrogen ions and electrons in the water-splitting complex. For each four photons, two water molecules are split and four electrons are retrieved.
The electrons will go on to pass into chlorophyll a in photosystem II and after being excited by another photon, pass through a series of electron carriers and drop energy along the way. One of these electron carriers is the cytochrome b6-f complex which uses some of this energy to help pump hydrogen ions from the chloroplasts stroma and into the thylakoids lumen.
However, I'm unsure of exactly how many electrons the b6-f complex needs to pump each hydrogen ion across the membrane. Is it 2? 4? I've been unable to find an answer anywhere so far.


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Why is Cannabis Sativa considered a distinct form of Cannabis?
My understanding is that the word Sativa is Latin and means "cultivated." See here: https://en.wikipedia.org/wiki/Sativum
Since all cannabis consumed by people is cultivated and grown from seed, shouldn't all Cannabis be called Cannabis Sativa? And so isn't Cannabis Indica also Cannabis Sativa? If taking a cutting of a plant grown from seed and rooting it means that "clone" isn't considered to have been grown from seed then maybe those plants shouldn't be called Sativa, although this would still seem to qualify as cultivation. But either way I fail to see what bearing it has on phenotype or alkaloid profile. How has it come to mean having thin leaves and high THC content?

A ver energetic recent document from 2016 demonstrates that no scientists have used the recent genetics technology to see which are the oldest populations of cannabis and if they diverged 5,000 years ago or 50,000 years ago. indeed in Mexico and Russia there are varieties 1 foot tall and in Thailand 20 foot tall, which suggests there may be differences 50,000 or 5000 years old, a future PhD or Research group can find out. https://www.frontiersin.org/articles/10.3389/fpls.2016.01113/full

Be careful with over-interpreting etymology, especially in the context of biological terminology. There are hundreds of cultivated plants, very few of which have any reference to 'cultivation' in their names. This would be like complaining that someone named their child Amber and she grew up to have blonde hair, and then further arguing that everyone else with brown hair should have been named Amber. The distinction between indica and sativa strains is an interesting one, but it has nothing to do with etymology.

@BryanKrause ok, so I should not expect scientific names to have any concrete relationship to the plants they are naming?

Just recognize that names are names. They typically are based in something, but they need not follow a consistent system nor be entirely accurate nor are names describing a trait indicative that the trait is not shared with other species.

@BryanKrause i see. It seems strange to me that science, which normally values consistency and accuracy for obvious reasons, would not value either of those things when it comes to naming plants. I guess it probably is pretty difficult in this area tho, what with there being so many plants and so many subtle differences and new information being added all the time. Still, it sounds like real science has been influenced by stoner science rather than the other way around. Anyway, thanks for the information!

@dev_willis A name of a plant is just a name, that's it: it's a reference so we can all talk about the same plant. Each plant has too many characteristics to describe them all in a two-word name. Sometimes names come when other information is missing: you might name a plant based on where it is first discovered, and then find out it is more widespread than you first realized. You might name a plant based on a feature that is so far unique to it compared to similar relatives (maybe a different color?), and then find other relatives that also have that feature.

C. sativa was originally named by Linnaeus in 1753, long before the plant was commonly used for recreation (in Europe, at least), so the name probably reflects the fact that that species was cultivated for fiber (hemp), just as many plants have the Latin name Officinalis or officinale, meaning that they were used in medicine.  Later botanists considered other varieties to be sufficiently different to be different species or subspecies. (Including some interesting reasons based in the laws of the 1970s: https://en.wikipedia.org/wiki/Cannabis#Taxonomy )
It's also not true that all Cannabis is cultivated.  It can be found growing wild, either native or as a introduced plant, in many parts of the world.

Thanks for the link. So it sounds like it was named this way to make a distinction between wild plants and plants cultivated for industrial use and later when Westerners discovered it being grown in India they felt like it was different enough to need a distinct name? And from there the vagaries of language enabled the words to drift away from their original meanings to the totally unrelated meanings we have today?
BTW, I'm aware that it grows wild. Everything does, or did. But few if any people are consuming those plants. All I said was that the plants people consume are cultivated.

@dev_willis: No, I don't think Linnaeus was really making a distinction.  Nor do the Latin names given to plants (or animals) always (or even frequently) have an exact, literal meaning.  Consider all the species, or even entire genera (like Fuschia or Wisteria), that are named after people, for instance.  One of my favorites is Dichelostemma ida-maia: https://www.wildflower.org/plants/result.php?id_plant=DIID


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Recombination due to crossover, outcome?
Garden peas normally have 7 pairs of chromosomes (n=7, 2n=14). Please calculate how many different types of gametes can be produced through the meiotic process if no crossover happens. If cross-over happens regularly, how many different types of gametes can be produced and why?
I have tried the question, I would suppose the answer to be 2 ^ 7 = 128 for the types of gametes that are produced( that is without crossing over).
However, I am not sure what is the solution what is the answer if cross over does happen. appreciate any solution to the problem.

The question asked for the number of gametes, not the recombination frequency (which cannot be 128 by the way, a frequency is by definition bounded between 0 and 1). For crossovers, the question is unclear as it depends on the crossover frequency and if recombination hotspots are present.


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Why are bees attracted to Stag Hides in Lime bath
A friend has some stag hides in lime-water solution. He noticed the stag hides were covered in bees of several different species. He also noticed that the nearby sheep hides in a similar bath have no bees. What attracts the bees to the stag hides? Alternatively, what repels them from the sheep?
There are a lot more bees when the sun shines. The bees principle seemed interested in the hairy side of the hides. There is a small stream and a dried up pond nearby, so probably other places if they just wanted a drink. There is no noticeable scum on the water of either container.

Photos of the stag hides:

Photo of the sheep hides:

Short answer: They are probably looking for minerals from the lime
Explanation:
Insects from time to time need minerals (salt) they can't get from there floral diet. Because they can't chew these directly of rocks, they suck these up from puddles or occasionally from human sweat. This behaviour is well known from butterflies, but also from honeybees
Notice BTW that there are indeed several bee species (Probably Apis mellifera, Bombus terrestris agg. and Bombus lapidarius), but also several flies including Eristalis cf. tenax, a hoverfly.
Why not from the sheep hides? I'm not sure, but the water around the sheep hides looks awfully brown, suggesting there are a lot of humic acids un the water. That might be less attractive to the insects.

So a combination of attracted to both and repelled from the sheep. I shared this post and answer with my friend and he is pleased with the answer and will be letting the other people he was discussing with know.


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Could bacteria and phages be found in tissues?
in the literature, there are several studies of the gut virome and microbiome, for instance Reyes et al. on Nature (https://www.nature.com/articles/nature09199?error=cookies_not_supported&code=f5201dbe-3cda-4e09-ba17-688d0352ef81).
Now, it makes sense to find bacteria (hence phages) in stools. However, there are other studies reporting bacteria from tissue, for instance Kostic et al. on Genome res (
Article Genomic analysis identifies association of Fusobacterium wit...
). In this specific case, the identified bacterium (Fusobacterium nucleatum) is an endocellular parasite and has virulence factors that allows it to penetrate tissues. But my question is more general:
Would be normal to identify bacteria and bacteriophages INSIDE human tissues?
In particular, would whole genome sequencing metagenomic experiments be likely to identify bacteria genome from human tissues? And if yes, how can we explain the presence of bacteria inside loci that are supposed to be sterile?
Thank you

Do you mean in healthy or diseased tissues? There are some bacteria, viruses or parasites in healthy tissues.

in both cases, there are differences in abundances and species between diseased and healthy tissues but in general, in the absence of an obvious infection, tissues should be sterile. Or not?

Tissues within the organs are usually sterile, but not necessary 100%. Theoretically, sterile means zero microbes, but in practice, sterile means no microbes detected by usual medical tests. So, yes, there can be few microbes in healthy tissues. And there are a lot of microbes in the gut, saliva, on the skin as part of normal flora. But you are probably asking if there are microbes "in the tissues" not only "on" the skin or in the body cavities.

correct, I am talking deep solid tissues such as muscles

@Gigiux If there is not enough specificity in your question such that you need to clarify your intents in the comments, your question is not specific enough and you should edit it.

It seems this question was also asked on ResearchGate.  There are already some answers there.

Per my comment to the question, here is an answer to the same question asked on ResearchGate:

Whole genome sequencing of human tissue samples often results in reads aligning to bacterial references, and this is actually a method used in the diagnoses of infectious diseases.
Understanding the Promises and Hurdles of Metagenomic Next-Generation Sequencing as a Diagnostic Tool for Infectious Diseases
Identification of low abundance microbiome in clinical samples using whole genome sequencing
However, because pathogen DNA may be present at a much lower abundance than host DNA, it may be difficult to distinguish true infections from contamination and false positives. Steven Salzberg addresses these concerns and offers a computational solution in a recent publication:
KrakenUniq: confident and fast metagenomics classification using unique k-mer counts
"Usually, the vast majority of the reads match (typically 95–99%) the host, and sometimes fewer than 100 reads out of many millions of reads are matched to the target species. Common skin bacteria from the patient or lab personnel and other contamination from sample collection or preparation can easily generate a similar number of reads, and thus mask the signal from the pathogen."

To expand on this answer, it is important to realize that accurate identification of low-abundance organisms in metagenomic reads requires very good reference genomes.  A separate paper from the Salzberg group discusses a startling discovery:  many high-copy repeats in the human genome have been incorrectly annotated as bacterial proteins in the NCBI RefSeq database.
Human contamination in bacterial genomes has created thousands of spurious proteins
This suggests that researchers should be careful when attempting to infer the presence of low-abundance bacteria or phage in human tissue sequencing data, particularly when the presence of those organisms is not corroborated by other analyses.

NERVES and BRAIN
After chickenpox infection, some Herpes viruses travel along the nerves and may remain dormant in the dorsal root ganglia of the spinal nerves...they can be activated later and cause shingles.
According to (jvi.asm.org):

Herpes simplex virus 1 (HSV-1) establishes latency in neurons of the
  brains and sensory ganglia of humans and experimentally infected mice.

INTERVERTEBRAL DISCS
PubMed:

Our findings further validated the presence of low-virulence anaerobic
  bacteria in degenerated IVDs, and P. acnes was the most frequent
  bacterium.

sorry, I should have specified that I was referring to tissues not directly in contact with the environment, such as brain and muscles - blood is out because there is compelling evidence for viruses in the bloodstream such as Anelloviridae.

OK, what about Herpes simplex virus in the nerve ganglia after chickenpox infection? I updated my answer.

sure, those I know about. My data from WGS from tissues indicates the presence of non-human viruses and plenty of bacteriophages. Would it be normal to find them inside tissues?

Most people probably have Herpes simplex viruses latent in their nerves and, some, even in the brain, as I wrote in my answer. Other possible candidates are Mycobacterium tuberculosis (in latent tuberculosis), Epstein-Barr virus (in chronic infectious mononucleosis), Borrelia burgdorferi (Lyme disease). I mean, these bacteria can persist inside the brain, bone or other tissues after healing. It's called latent asymptomatic infection.


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Is returning cholesterol to the liver really performed by HDL?
Various answers in biology SE, including two quite upvoted ones (1, 2) claim that (in humans) returning cholesterol to the liver is done by HDL.
If I understand correctly, Wikipedia's Reverse cholesterol transport page also says this is done by HDL.
However, this blog post (by Peter Attia) says:

Historically this process of returning cholesterol to the liver was
  thought to be performed only by HDL’s and has been termed reverse
  cholesterol transport, or RCT [...]
This RCT concept is outdated as we now know LDL’s actually perform the
  majority of RCT. While the HDL particle is a crucial part of the
  immensely complex RCT pathway, a not-so-well-known fact is that apoB
  lipoproteins (i.e., LDL’s and their brethren) carry most of the
  cholesterol back to the liver.  In other words, the “bad” lipoprotein,
  LDL, does more of the cleaning up (i.e., taking cholesterol back to
  the liver) than the “good” lipoprotein, HDL!

Which is right?

According to Reverse Cholesterol Transport: Molecular Mechanisms and the Non-medical Approach to Enhance HDL Cholesterol (Frontiers in Physiology, 2018), both HDL and LDL are involved in reverse cholesterol transport.

In short: HDL takes cholesterol from the blood (from lipid-laden macrophages) and delivers it to the liver 1) via scavenger receptors (SR-B1) or 2) via LDL and LDL receptors (LDL-R). (For a detailed explanation of the diagram, see the Figure 1. in the linked article. There's a similar diagram (Fig.1) in Journal of Cardiology.)
Petter Atti says in his blog (emphasis mine):

Historically this process of returning cholesterol to the liver was
  thought to be performed only by HDL’s and has been termed reverse
  cholesterol transport, or RCT [...]
This RCT concept is outdated as we now know LDL’s actually perform
  the majority of RCT. While the HDL particle is a crucial part of
  the immensely complex RCT pathway, a not-so-well-known fact is that
  apoB lipoproteins (i.e., LDL’s and their brethren) carry most of the
  cholesterol back to the liver. In other words, the “bad” lipoprotein,
  LDL, does more of the cleaning up (i.e., taking cholesterol back to
  the liver) than the “good” lipoprotein, HDL!

He says that LDL does "more of the cleaning" than HDL, which may be technically correct in the sense that more LDL than HDL particles may be involved, but this alone does not change the concept of good or bad cholesterol. In the image, you can see that the initial cleaning (step 2 and 3) is done only by HDL, so without HDL no cleaning might occur at all.
Low HDL and high LDL levels in the blood are known risk factors for atherosclerosis (NCBI Books, 2019). Not all LDL particles are bad, though, the most harmful are oxidized small dense LDL particles (Hindawi, 2017).

I don't think your quote of Peter's blog supports your claim, as Peter only said that more cholesterol is returned to the liver by LDL (than the amount of cholesterol that is returned to the liver by HDL, which is non-zero). The sentence before the one you quoted says, if I understand correctly, that LDL returns cholesterol to the liver..

@OrenMilman, I edited the answer completely.

Can you elaborate on the difference between uptake of LDL by either Scavenger-Receptor "SCR-B" or LDL-Receptor on liver cells. Must I read "the most harmful are oxidized small dense LDL particles (Hindawi, 2017)", first? Can you expand your answer, as most people I guess do not know that liver cells have the LDL receptors and have never heard of Scavenger Receptor on liver cells (me, only yesterday, before I read you excellent answer).

Great answer!  It's pretty much focused on the question, so why not elaborate more about the concept of "cleaning up": those words may not be used for LDL carrying  cholesterol that might become oxidized while being carried on LDL? Then, that would be the SCR-B, not the LDL-receptor on liver cells?

Re critique by Oren Milman above:
Your last link out, Hindawi, says: "Oxidized LDL is recognized by a number of receptors, including CD36 and TLR-4", thus "cleaning up" in a literal sense you apply seems not to be "done" by LDL. When LDL becomes messy from O2, it does not do any reverse transport any more - itself, needs to be cleaned up, by receptors presumably not located on the liver but on immunce cells. I think that's very interesting, why don't you elaborate. Quote is very difficult to find, as very relevant,  reading through the source you gave.


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Why does muscle blood flow decrease during exercise?
My questions semi-relates to these two items: Where does extra blood come from to fill your muscles during exercise? , and Blood pressure during exercise .
While reading Exercise Physiology by Dr. Brooks, I've come to the following quote, which is a bit puzzling to me:

Muscle blood flow increases exponentially with metabolism. At maximum exercise, some vasoconstriction occurs in active muscle in order to maintain blood pressure. Maximum muscle blood flow is largely determined by the amount of active muscle. The larger the portion of active muscle mass, the less total muscle blood flow.

Questions:

Why is it that the larger the active muscle mass, the lower the total muscle blood flow? I'd expect it to be greater.
Say that I am doing the bench press, does that qualify as an exercise with large active muscle mass?

I think that vasoconstriction from the quoted part refers only to maximum exercise. Because, in general, blood flow in the active muscles during exercise increases.

Re #2, think about the difference between doing it with heavy weight & few reps, vs light weight & many reps, or in the extreme, a highly aerobic exercise like rowing where endurance rather than strength is needed.

@jamesqf not sure I am following the comment james. Are you saying that Q#2, only applies to endurance / aerobic exercise? i.e anaerobic exercises like bench press would not necessarily qualify?

@angryip: No, I'm saying that apparently (I have never seen detailed studies) blood flow increases during aerobic/endurance exercise, but doing things like a bench press with heavy weights gets the muscles "pumped", which seems to decrease the blood flow.  (This is just my casual observation, of course, and could easily be wrong.)

@jamesqf interesting. I'll try to dig it up in this book and observe

I think there might be some missing context here leading to confusion of which muscles are being referred to in that passage.
During exercise, blood flow increases in active muscle due to local vasodilation. Cardiac output also increases, which ensures that total blood flow in the body is sufficient to meet the increased demand.
At higher levels of exercise, there is also systemic vasoconstriction. Systemic vasoconstriction acts to maintain blood pressure. You simply have too much total muscle for maximum cardiac output to supply all the muscle with full vasodilation plus the rest of the body without a loss of pressure. For an athlete with greater maximum cardiac output, it would be possible to fully perfuse more muscles at high effort than for someone untrained.

At maximum exercise, some vasoconstriction occurs in active muscle in order to maintain blood pressure

Because vasoconstriction is systemic, it has an influence on all the muscles, including the active ones. You should think of this vasoconstriction as relative to already dilated vessels, not necessarily compared to rest.

Maximum muscle blood flow is largely determined by the amount of active muscle.

This sentence could be rewritten as:

Maximum blood flow through a given muscle is largely determined by how much muscle is active in the rest of the body.

That is, the maximum blood flow through an arm muscle would be greatest if your legs are resting.

The larger the portion of active muscle mass, the less total muscle blood flow.

This is I think the most confusing sentence...I believe what they are referring to is the total muscle blood flow for a given muscle (total meaning over time rather than over space), which will be maximum when fewer other muscles are active at the same time.
Joyner and Casey 2015 explain all this in more detail; their Figure 8 is most directly related to the question but the rest of the background is also useful.

Joyner, M. J., & Casey, D. P. (2015). Regulation of increased blood flow (hyperemia) to muscles during exercise: a hierarchy of competing physiological needs. Physiological reviews, 95(2), 549-601.

that makes a lot more sense! thank you! the wording in ch 16&17 of the book is a bit challenging to understand.


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Why don't materials and methods describe culture media in volume?
After reading several materials and methods sections of cell culture experiments, I have not seen the recipe for culture media ever described in terms of volume.

Human adipose tissue was obtained from six samples of abdominal fat from female donors (age range: 20–45 years) after receiving informed consent and cultured as described in a previous study.[15] Briefly, samples were washed extensively with sterile phosphate-buffered saline (PBS) to remove contaminating debris and red blood cells. Washed aspirates were treated with 0.075% collagenase type I in PBS for 30 min at 37°C with gentle agitation. The collagenase I was inactivated with an equal volume of DMEM: F12/10% fetal bovine serum (FBS) and the infranatant centrifuged for 10 min at 800 rpm. The cellular pellet was resuspended in DMEM: F12/10% FBS and plated at 20000 cells/cm2 in T75 flasks in DMEM: F12 medium supplemented with 10% FBS and %1 Penicillin/streptomycin. After 24 h, it removed the nonadherent cells and expanded the adherent ADAS cells by serial passage. In this study, we used cells at passages 3–5 for all experiments and all experiments repeated at least in triplicate.

In this excerpt from the paper, Efficient transdifferentiation of human adipose-derived stem cells into Schwann-like cells: A promise for treatment of demyelinating diseases by Razavi et al, there is no mention of the volume of media used to culture the cells.
Moreover, there is no description of the height of the media in the dish, so it seems to me that from most cell culture descriptions, there is no way to properly reproduce the experiment simply by reading the paper.
Why do these sections fail to specify volume information?
Is there something that I'm missing here?

Have you checked reference 15?

@canadianer yes

The volume of media would be different for different culture vessels. You can check this site for the usual volumes. If they have not indicated then probably they used the usual culture volumes. You can check out their supplementary methods for more details on different experiments.


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Stopping all intracellular activity in a reversible fashion
I have never studied biology but the following question seems meaningful to me. Suppose I take a cell, not that of a unicellular organism, but a human cell. Normally, there are some intracellular processes going on. If I understand correctly, one way a cell is going to die is that enough mistakes happen during these processes and it can't take it anymore.
Suppose I really need this cell alive and well in two hundred years and I do not really care what happens in the meanwhile. Is there a way to stop all the intracellular processes (protein synthesis, intracellular digestion, etc.), in a reversible fashion, so that I (or probably not me but a great-great-great-great-great-great-great-grandchild) could "start" this cell again after two hundred years pass? Now, two hundred years seem like too much for an experiment, but you get the idea; say, a month would be OK too.
Surely, some biologist thought about this at some point. Any references studying this question would be great.
EDIT: Wikipedia says that

Many bacteria can survive adverse conditions such as temperature, desiccation, and antibiotics by endospores, cysts, conidia or states of reduced metabolic activity lacking specialized cellular structures.

So at least some unicellular organisms can temporarily slow down the rate of metabolism.
I also think that some mammals can enter the state called hibernation, when their heart rate significantly decreases. I think this is different from above in that the amount of time mammals can spend in this state is less than the amount of time bacteria can spend in the dormant state (see here). From this I infer that the maximum metabolism slow-down factor is lower in mammals than in bacteria.
Ultimately, I am interested in learning how far we could push, via artificial means, the slow-down factor in complicated organisms like mammals. However, taking an entire organ and making all of its cells to go to sleep and then waking all of them up in an organized way seems to be much harder than achieving the same for a single cell. Thus my question: can we, in a reversible and controlled way, slow down the metabolism within a single human cell? What is the maximum slow-down factor then?

What has your own research told you so far? The Biology.SE community has agreed that questions that show little or no prior research effort are off-topic on this site unless you have shown your attempt at an answer. Please [edit] your question and tell us where you've looked for answers, what you do know about the topic, and where exactly you still have questions. Unresearched questions may be subject to down-voting and closure.

@BryanKrause I am not a biologist Sir, I did what I could. Is this acceptable now?

i think you are asking about Cryonics

@aaaaaa not necessarily. From what I know, during cryonics freezing destroys some organelles and it has not been shown to be a reversible process. It is like a fancy way to die. Could others confirm this?

While the main idea of your question is on-topic in biology, your question itself tends to be opinion based (if something is possible in future). Not only bacteria and tardigrades (as pointed out by @user1136) but also many kinds of human cells can be frozen and revived successfully (a lot of them die in this process of course). Nematode worms can also be frozen and revived successfully (Wormbase). Freezing and reviving large complex organisms has not been attempted successfully.


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N value in a GWAS?
Just like the title says. I am reading about a GWAS but I don't know much about them. I understood most of it but I couldn't figure out what the "n" value was.

Are you talking about n (as written in the title) or N (as written in the title)? The meaning of a variable like this might well vary depending on your source. Can you please indicate your source?

Same question as @Remi.b. The most common use of $n$ is to denote the total number of subjects used in the study. $N$ is also often used to denote the number of alleles.


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How are asexual species classified?
Are there multiple distinct genetic lineages of asexual species that are closely enough related to not be considered distinct or does any genetic change result in a new species?
I would assume there's tolerance for variety as much genetic material has either no phenotypical expression, or a very subtle one. It's also consistent with my understanding of differential antibiotic resistance. Normally I'd expect a large degree of acceptable differences as long as there could be reproduction that makes viable offspring, but that's obviously not applicable here.

It is a widely held misunderstanding that species are defined by reproduction. (Mayr's biological species concept.) This species concept works for ecologists and high school biology teachers because it roughly describes how species come to be. However, taxonomists, the people who actually define and describe species, almost all use some form of the evolutionary species concept, which does not define species based on reproduction https://academic.oup.com/sysbio/article-abstract/27/1/17/1626671?redirectedFrom=fulltext. , but on lineage patterns or fixed character states.


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Rationale behind Most Recent Common Ancestor (MRCA)?
My main question is this -
I heard Richard Dawkins say in a video that after 1000s of years, any given individual alive today will be either an ancestor to ALL of the humans (in that future time) or none of them. What is the rationale behind this?
I'm unable to find the link to that video. I'll keep searching and add it once I find it.
But my fundamental question is perhaps this - is it necessary that a given species must have at least one common ancestor? I understand that there are multiple common ancestors to humans, the most recent one being MCRA. But could it have been otherwise? I think there's some underlying logic that I'm missing.
I'd appreciate it if someone could answer in a non-technical manner since I know very little about genetics and how all this works.
Update:
Consider the following example. Here's there's heavy inbreeding and as you can see no matter how many generations pass, the population are never going to share a common ancestor from current generation or later. (They could still have a common ancestor from before). But this case violates Dawkins' statement.

But this is an unrealistic example with no mixing and cross breeding. Let's consider another example as shown below. I want to see how the individual A from current generation can be related to all the population in future. As shown in the diagram, although A is related to everyone in some future generation, he is not a common ancestor to all of them. The actual common ancestor belongs to some earlier generation.

For any given no. of generations, theoretically, I could conceive similar lineages by which someone from current generation need not necessarily be a common ancestor to all of the future population (or none). So I don't understand how Dawkins' statement is inevitable.

Your examples don't have sexual reproduction: everyone has just 1 parent. Why?

@BryanKrause first example does show two parents each. Avoided that in second example because the diagram was getting cluttered. The point of my examples is still conveyed correctly, I hope.

It isn't at all, because you are missing that for each prior generation, the number of ancestors approximately doubles. This is only not true in your extreme example of inbreeding.

@BryanKrause that's a good point. So the exponential increase in number of ancestors makes it extremely likely for the case of having a common ancestor. But it still doesn't prove that there has to be a common ancestor.

Actually it does. Try drawing it out.

@BryanKrause I feel like the argument is turning silly. You agree that it fails in my extreme example of inbreeding. All I have to do is retain some of the columns and cross-breed the rest. That will be another example where it fails. If the claim is that everyone after n generations MUST be related, then it must be provable. The burden of proof lies with you even if I'm unable to produce counter examples (which in this case I'm anyway able to provide). What am I missing?

The obvious assumption is that there is no complete isolation. You are missing from Dawkins claim the very very long time scale. If you go back 100 generations, you have 2^100 = 1.3 x 10^30 ancestors. Of course many will be repeats (they have to be) but the chance of anyone both a) having living ancestors, and b) not being your ancestor goes down dramatically with each subsequent generation. If you aren't willing to draw it out to test your thinking then it's not worth my time to convince you. The existing answer from Pelinore already explains this.

Let us continue this discussion in chat.

any giving individual alive today will be either an ancestor to ALL of the humans (in that future time) or none of them. What is the rationale behind this?

It's a simple mathematical observation nothing more than that.
One that doesn't actually require doing any math to understand.
Take a few billion people, let them mix & breed freely within the confines of a limited environment (the world) & eventually (after enough generations) every single one of the current population will be be related & therefore descended from every single one of the original population that have any surviving descendants.

Those whose line doesn't die out will inevitably be an ancestor of every living person at a future generation, eventually.
Those who die with no offspring or have last-descendants do it for them, have no descendants.

It's just a simple statement of something that's obvious when you think on it.

Why is it necessary that after enough generations everyone will be related? Is it an assumption based on enough cross breeding?

@yathish It's not "necessary", it is inevitable.

but why is it inevitable? For example, if two populations of humans are separated in two different islands, it won't hold true. I feel like I'm missing something very obvious.

@yathish: But the populations on those islands must have come from some common source (if you look back far enough), e.g. the populations of say Hawai'i, Tahiti, and New Zealand prior to European contact.  Or the population of North America, effectively isolated from other humans for ~10,000 years.

@yathish Your not thinking in big enough numbers when it comes to generations & years, if people got there once they can get there again so in the time scale of hundreds of thousands of years & more your islands aren't isolated, at all ~ besides that, where did these two populations come from & how are they the same specie if they didn't ever share a common ancestor?

@Pelinore: The islands could possibly remain isolated for the population to diverge enough that the inhabitants could be called a different species.  For example, Homo Floresiensis: https://en.wikipedia.org/wiki/Homo_floresiensis  But they still have common ancestors who were humans or pre-humans.

@jamesqf "besides that, where did these two populations come from?" think about it.. also (from OP) "is it necessary that a given species" so, if they're not the same species you've then gone & wandered outside the parameters of the question haven't you.

I don't mean to be pedantic, but distinguishing near certainty and absolute certainty is an important part of my question. I'm trying to think of this visually and it's still not obvious to me. I've added a couple of diagrams to elucidate my confusion in the question. Kindly check it once. The usage of terms like enough cross breeding and eventually by you suggests to me that it's extremely highly likely but need not necessarily be true with absolute certainty. I feel like my thought process is misdirected.. I appreciate your help.

@yathish That is very much the point, statistically speaking it is absolutely certain, that you can't see it is problematic for me when it comes to answering your question because to me it seems almost like being asked why 2+2=4 in at least the sense that I'm having difficulty formulating an explanation of why beyond "because it is" now, not that I'm trying to be derogatory the inability to explain may be a fault on my side.

^ Perhaps because I can (as you say) "visualize it", so to me it seems obvious.

Oh blimey! But what about the counter examples I provided in the question? I can scale them up to howsoever many generations as you like and disprove the statement.. Also, I'm not sure statistically speaking and absolute certainty go together.

Statistical certainty may have been a poor (pedantically speaking) choice of words then :) I'll come back to this & give it another go later, I'll need to set my eyes on it when I'm fresh & see if I can't come at it from a different angle, maybe not today though, bit groggy right now (fell asleep in the chair & didn't get enough sleep last night) o7

is it necessary that a given species must have at least one common ancestor?

You could imagine a species divided into groups, each group having a single common ancestor.  In that case, you might ask, do the common ancestors themselves have a common ancestor, somewhere further back? Our current hypothesis is that, if you go back far enough you can find a creature that was the common ancestor of any arbitrary group of individuals.
The alternative hypothesis is that life evolved independently several times, and there were originally more than one 'tree of life', and that these independent instances of life somehow evolved in parallel, maintaining compatibility with each other, enough so that there could be cross-breeding between the two trees at a later date.  In that way it might be possible that some species may not have a single common ancestor.  This seems so unlikely to be true though that it it not generally even considered, for current species.
The common ancestor of all humans might not necessarily look exactly like a human (Homo sapiens) though, it may have existed at a time before Homo sapiens evolved, because it is possible that branches on the tree of life can diverge a little and then cross again, as human and neanderthal branches did.
The wikipedia page on the human MRCA (https://en.wikipedia.org/wiki/Most_recent_common_ancestor) says the time since the MRCA is unknown, but has been estimated between 100,000 to 200,000 years ago.
 This is around the same time Homo sapiens first appeared in the fossil record, that we have found so far.


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is it possible for a son to inherit an allele on a Y chromosome?
Obviously, the only way for one to be male is to inherit the Y chromosome, but are there alleles on the y chromosomes? Or is it just automatically the recessive trait without an allele.

https://en.wikipedia.org/wiki/Testis-determining_factor this might be a good start for your own investication

The question are there alleles on the y chromosomes is unclear. Here are two possible things you might mean

Is there genetic variation among individuals on the y chromosomes
Is there anything functional on the Y chromosome

Is there genetic variation among individuals on the y chromosomes

Yes, of course, there is genetic variation of the Y chromosome just like there is genetic variation other chromosomes. Talking about SNPs (Single Nucleotide Polymorphism) only, we have already detected tens of thousands of SNPs on the Y chromosome (see this page).

Is there anything functional on the Y chromosome

Yes! As an example, one of the most famous gene on the Y chromosome is the Test determination factor (as already indicated in a comment by @L.Diagio).


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Hemispherectomy and brain changes
As far as i know hemispherectomy is a rare procedure when individual will going to have half brain removed in very young age. Because brain has quite remarkeble neuroplasticity patient usually will survived only with half of brain.

My questions is?
How much brain can be removed to not to negatively influence brain activity?
Does anatomy hemispherectomy alter secretion of glands for example pineal gland?

The glands are not a part of cerebral hemispheres; so they would not be removed. The wiki link also says that surgeons prefer to leave the sensorimotor cortex intact.

I didn't think functional hemispherectomy but anatomical one. I am sorry that I forget to mention that


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what kind of insect is this
It has what appears to be antennas in both front and back and legs front and back orange coloured dots ob front and rear of a blackish brown body

This isn't one insect, it's a mating pair; I'm pretty sure they're flies, but can't go further than that on the evidence at hand.

Those are two mating "love bugs". Flies (Diptera) in the family Bibionidae. https://en.wikipedia.org/wiki/Lovebug


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What does substrate mean?
I have been reading some literature on measurements related to biofilms.
In some articles the word "substrate" seems to stand for the material on which a biofilm is growing. In other articles, it seems to stand for the nutrients that are freely floating in (say water) where the biofilm is growing, and which then diffuse into the biofilm and which it uses to grow.
Have I misunderstood something or are both of these meanings in active use? Is there a disciplinary or some other difference that determines who uses which term?

The review article [1] uses substrate to mean freely floating nutrietnts. Also, searching for "substrate loading" or "substrate loading rate" or such (on Google scholar) gives examples of substrate as something that is fed to the biofilm.
For example Wikipedia uses the other meaning of substrate: https://en.wikipedia.org/wiki/Substrate . Scientific literature with this meaning can be related to how easily biofilms detach from a given material in the presence of shear forces.

[1] Harald Horn and Susanne Lackner. Modeling of biofilm systems: A review. In Kai Muffler and Roland Ulber, editors, Productive Biofilms, pages 53–76. Springer International Publishing, Cham, 2014.

Latin: sub- underneath and stratum = layer... The under-layer literally, the base layer.

A substrate is an underlying substance or layer, or less strictly, the medium within or upon which an organism grows. For instance, you can have a filamentous fungus grow on a solid medium (e.g. on an agar plate) or in liquid medium (e.g. in a shaken flask containing a solution) and its substrate would be the contents of the agar or solution. It's nothing more fancy than that.
For instance, you could design 4 growth conditions for a strain of fungus.
Case in point, a hypothetical table could look like this:
                        *Substrate*

                Wheat straw     Sugar beet pulp
                             |
          Liquid         1   |   2
                             |
*Medium*             -----------------
                             |
           Agar          3   |   4

Simple!

What is the interpretation of all the "substrate loading rate"s, then? Are they simply misusing the terminology?

@TommiBrander, no they are not misusing "substrate". Notice there are more words in the phrase "substrate loading rate".  The phrase is referring to the the rate at which nutrients are loaded into the substrate.

I edited in an explicit reference to a review article where "substrate" explicitly means diffusing nutrients, rather than the meaning mentioned here.

The nutrient can be the substrate. Leaves are a substrate for leaf-eating caterpillars. The skin of an orange is a substrate for mold. In these examples you'd use the word substrate rather than medium. As with all language, it doesn't help to be too pedantic about dictionary definition. The word 'nutrient' is also fuzzy but I would advise against opening a thread about the meaning of nutrient. Happy sciencing!


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What is the difference among biochemistry, molecular biology, molecular genetics and structural biology?
I have never heard of straigthforward definitions of these fields in my college lectures, and the Internet searches were not very helpful. However, from what I have learned at different subjects, this what I understand of the following areas.

Biochemistry:  The study of metabolic pathways, enzyme kinetics, bioenergetics and the chemical mechanisms of the reactions. It does study molecular structure, but only of small molecules such as monomers, metabolites and coenzymes.
Molecular biology: The study of information pathways, such as transcription, splicing and replication. It applies as well to techniques such as PCR.
Molecular genetics: The study of how a genotype creates a particular phenotype. For example, it would be the study of why an allele produces smooth peas while another one produces wrinkled ones.
Structural biology:  Elucidating the structure of macromolecules (proteins, nucleic acids) and their complexes. It uses X-ray crystallography, NMR and cryo-electron microscopy to study them.

So, are my definitions accurate? If not, why?

Why does it matter?

They are not accurate. Why? 1. Because they are inaccurate 2. Because the fields overlap and people call themselves what they like (or what seems trendy) — I won’t elaborate on that one. I seem to remember answering (i.e. not answering) a question of this sort before. You might try searching for it. It was very good.

@BryanKrause Because I'm curious.

@David I searched first in Biology Stack Exchange but I couldn't find this question.

@Jagoe My point is basically the same as David's: the distinctions between these labels are not important to biology. There is also no specific definition that everyone would agree on without allowing that the borders are fuzzy and not meaningful.

The question I recalled turned out to be on the term Biophysics, but the answer I gave illustrates my point.

I was aware that the different areas overlapped, but I thought that their different names reflected the scope of each of them.


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Why magnesium ion is needed for activity of G-proteins?
I was studying about G-protein coupled signaling sysytem, somewhere they have mentioned about need of Mg$^{2+}$ for acticty of G-protein and related it to increase of cyclic AMP production. On further reading I came to know that the said ion is related to GTPase activity of G-protein, but how does it relate to incresed cyclic AMP production?

Welcome to SE Biology. Please take the Tour and read about asking questions here. You will find that you are expected to do some research before posting. Search for “role of magnesium ions in enzyme reactions” to find the answer to this basic biochemistry question. (And please pay attention to capitalisation.)

You will find the basic answer in my response to a question on the role of magnesium in ATP reactions. The situation for GTP is the same. It has nothing specific to do with G proteins.

Ion can change secondary structure of an enzyme. Magnesium ion is coordinated within certain domains (for example, EF-hand motif) and makes them more ordered. Usually it happens via hydrophilic shell of residues embedded into a hydrophobic one (https://www.pnas.org/content/87/15/5648).
You can reverse it by adding a chelator (EDTA, for example) and protein is more disordered which can affect it's activity.


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Is my cell-culture contaminated with mold?
I am growing cell cultures at the moment, and I sometimes find 1-2 of these elongated, black structures in one of my 8 wells. Should I be concerned?
I have been growing these for about 5 days at this point, replacing the media every the other day. I figure that the life-cycle of mold is pretty fast, and that if it were truly mold that it would overpopulate the well pretty quickly. Perhaps it's just debris?

They could be pieces of tissue paper. Do these "things" grow after a while? Cell debris is generally smaller than the cells. Is there a picture with the cells in focus?

4-15-2021:
Same thing happened to me. Same look from picture above but way more. Even if the cells were growing well and all,I was about to throw away the flask. I wiped down with ethanol the bottom exterior and looked again under microscope and I would say 90% of them were gone. A simple thing to try.

Most of the time you can find shards of plastic, defects in the plate and other non-cellular debris in brightfield that look suspicious. Even some cellular debris can look suspicious, like when your viability is really poor. That doesn't look like anything to me. You'd know if you had contamination because it would be in more than 1 field, you'd have more than 1-2 of them, and your culture would either change in color, turbidity or smell. If it's a plate defect, you probably wont see it move if you re-suspend the well, either.

I know this thread is over a year old, but I found myself referring to this thread just this week (6.24.20) for help so I thought I'd post my experience in case anyone else is looking at this these days! I'm growing rabbit corneal epithelial cells and the original passage looked great the whole way through, I passaged about a week after plating, and 3 days into passage 1 contaminants EXACTLY like the ones in OP's photos began popping up. At first it was just a couple in one plate, but after a couple more days all 3 of my plates were covered. I knew it wasn't a live contaminant because the cells remained healthy and it didn't move, grow, or change; but still more and more showed up. After 5 days of this, I finally noticed that the contamination was worst around the ledge/rim on the bottom of the plate; which didn't make sense because why would a rim on the outside of the plate affect debris on the inside... and that's when I finally wiped down the entire outside/bottom of the plates with ethanol and sure enough all contamination was instantly gone.
So, if you've come here because you're seeing weird things in your plate, do yourself a favor and start by wiping down the outside/bottoms of your plate first. Might save you a lot of grief!

It would be best if you could show us some pictures of your own observations. As of now, there is nothing in your post that the community can use to validate your answer. Ideally, every answer should contain scientific references, or at least some sources or links to credible web pages. In this case, I understand personal experience can be valuable to share, but then the minimal thing to add are some images. Cheers.


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Is there natural occurrence of induced pluripotency / expression of Yamanaka factors and what is the evolutionary explanation of that?
Is there natural biological processes in which the full (full reprogramming into pluripotent state) or partial (partial reprogramming, stopped before point-of-no-return, preserving the functional distinctiveness of the cell) induced pluripotency (https://en.wikipedia.org/wiki/Induced_pluripotent_stem_cell) and expression of Yamanaka factors occurrs? What is the evolutionary explanation of such rejuvenation factors? I would like to see the natural explanation otherwise it begs for the idea that the Universe is created with the human as the goal of it (anthropocentric hypothesis) and it is quite uneasy for me.
I guess, that natural reproduction processes can involve some kind of rejuvenation/induced pluripotency and they determined the existence of Yamanaka factors.

What is a pluripotent stem cell?
A pluripotent stem cell is a cell that can differentiate into any of the major tissue categories. Every animal exists as a collection of pluripotent stem cells at an early stage of development: if you are looking for an evolutionary purpose, that's where you should start, and the purpose is pretty obvious: you start as a single fertilized egg and end up as a complex collection of tissues, so at some point that one cell has to become a collection of tissues, and there is an intermediate step which is a pluripotent cell.
None of this has anything to do with induced pluripotency, however.
What makes a cell pluripotent?
The answer to this question isn't really all that unique to stem cells: all cell types are differentiated from others based on their expression of transcription factors. Transcription factors determine what proteins get produced (including other transcription factors), which in turn determines how a cell functions and what role it plays.
Pluripotent stem cells express pluripotent stem cell transcription factors. Yamanaka started with embryonic stem cells, and looked for transcription factors that were special to those cells.
What does it mean to make a pluripotent stem cell?
Given that the identity of a cell is based on the transcription factors it expresses, the way to make one cell type act like another cell type is to change those transcription factors. A cell is a pretty complicated environment: there are lots of different transcription factors and lots of other types of proteins, so it's possible that it wouldn't be feasible to reprogram a cell this way.
However, Yamanaka and colleagues tried to artificially make an adult cell produce those transcription factors observed in embryonic stem cells. Indeed, they found that if they used the right combination of transcription factors in the right environment, the cells started to behave like embryonic cells, and they could further make those cells differentiate into different tissue types. These transcription factors are the so-called Yamanaka factors.
Summary
An induced pluripotent stem cell is a cell that has been transformed to produce transcription factors that are found in embryonic cells. Transcription factors are what make different cell types different from each other, by controlling everything else that the cell produces. All of this machinery is ubiquitous in development, the only intervention that the humans are doing is to make a cell express genes it would normally only express if it was an embryonic cell.
All of this information is already present in the Wikipedia article you linked.

Takahashi K, Yamanaka S (2006). "Induction of pluripotent stem cells from mouse embryonic and adult fibroblast cultures by defined factors". Cell. 126 (4): 663–76.
Takahashi K, Tanabe K, Ohnuki M, Narita M, Ichisaka T, Tomoda K, Yamanaka S (2007). "Induction of pluripotent stem cells from adult human fibroblasts by defined factors". Cell. 131 (5): 861–72.
Yu J, Vodyanik MA, Smuga-Otto K, Antosiewicz-Bourget J, Frane JL, Tian S, Nie J, Jonsdottir GA, Ruotti V, Stewart R, Slukvin II, Thomson JA (2007). "Induced pluripotent stem cell lines derived from human somatic cells". Science. 318 (5858): 1917–20.

Regeneration of complex tissues like limbs is known in many animals. Salamander has been used as a model for limb regeneration. During regeneration, the cells at the amputation site de-differentiate to form what is known as a blastema which in turn differentiates to form different kinds of cells.
Christen et al. (2010) have found that de-differentiation in zebrafish involves upregulation of some of the Yamanaka factors.

We found that some of the pluripotency associated factors (oct4/pou5f1, sox2, c-myc, klf4, tert, sall4, zic3, dppa2/4 and fut1, a homologue of ssea1) were expressed before and during regeneration and that at least two of these factors (oct4, sox2) were also required for normal fin regeneration in the zebrafish. However these factors were not upregulated during regeneration as would be expected if blastema cells acquired pluripotency

There is evidence for the expression of the homologs of Sox-2, Klf4 and c-Myc in regenerating newt tissues as well (Maki et al., 2009)
Having said that, I would reiterate what Bryan Krause said in his answer: these factors are essential for the renewal and maintenance of embryonic stem cells. Some of these factors (especially Sox2) are also expressed in non-embryonic multipotent cells like neural stem cells (Seo et al., 2011; Sarkar and Hochedlinger, 2013; Zhang and Cui, 2014).
c-Myc is a proto-oncogene and is normally involved in cell proliferation in all actively dividing cells.


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Can Females Songbirds Have Male Plumage?
Male birds are colorful for courtship displays, females are dull for camouflage. But, is written in a website somewhere that sometimes, when females birds are sterile, they grow male plumage due to male's feathers being a dormant gene (or something like that, sorry, I'm no professional). Is true? Can it happen? If so, how came? (and I lost the website's link, so I can't post it here, sorry again)

Please would you add a link to the website that you mentioned? That would be useful.

I don't have a link to a reference, but I was told by an ornithologist last week that in the UK, female blackbirds (usually brown plumage and brown beak) can sometimes change to more resemble males later in their lives (black plumage and orange beak).

Unfortunately, anecdotal references are not acceptable even if they come from an expert. Unless there is good statistical evidence, we cannot be sure. It would be super good if you can contact the ornithologist and ask them for a reference.


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Can monoclonal antibodies work only if the target of it is located in the cell's surface?
Can monoclonal antibodies work only if the target of it is located in the cell's surface?
or it can be used to targeting a protein located inside the cell?

You have been in this site for some time so probably you are aware of our site policy of expecting research effort from the user. Your question is very basic. Did you try to find out anything at all?

Your comment is probably related to your other question.

Monoclonal antibodies (or antibodies in general) are large proteins (around 150 kiloDaltons according to Wikipedia), so cannot cross the plasma membrane. So monoclonal antibodies target extracellular molecules or cell surface molecules. However, there are techniques to target proteins inside a cell, like lysing the cell, or using gene modifications, or otherwise a technique covered in this paper: https://www.tandfonline.com/doi/abs/10.1517/14712598.5.2.237


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Does the lack of "mirror life" tell us anything about abiogenesis?
My (extremely rudimentary) understanding of Biology is that many of the building blocks of life are chiral and that life on earth is entirely made up molecules with the same chirality.
Does this have any interesting repercussions for our understanding of abiogenesis?
EDIT:
Just to be clear I am interested in understanding how life developed from non-life (on Earth in particular and, more speculatively, in the universe broadly). For instance, the article linked in Matt's answer that it may be due to the polarization of light in our area of the galaxy is very interesting.
I see several (not necessarily exclusive) hypotheses (and probably am certainly missing some) about the asymmetry of the chirality of existing lifeforms of and was wondering if there was any sort of consensus (or at least informed speculation) on which was more likely or less.

Abiogenesis is an incredibly rare phenomena and so the opposite chiral life never developed.
Which every chiral form of life appeared first and this prevented the formation of the other chiral form of life.
There is some sort of selection principle that selects for the chirality we appear.
If simple versions of life and mirror life occur simultaneously it precludes or retards the development of complex lifeforms (A sort of anthropic principle).
``Mirror life" is not actually possible--there is some subtle phenomena that requires the chirality we have on Earth.
Something else...

Is there no documented evidence of any life using the "other" chirality at all? Across all taxonomic rankings? We are always finding new species such as extremophiles that live in ways we never anticipated. If it could be more strongly stated that it's never been documented in any species that would be an interesting point to add to the question.

Don’t look for consensus, that road leads to phlogiston, look for evidence. So you want to know how life formed from non-life and somehow you can’t find any idea that is supported by convincing evidence on searching the internet. If there was any, wouldn’t you think it would be widely known? Oh, and this is a question and answer site, not a site for speculative discussion.

@Karl — No. Genome sequencing would have indicated a kingdom completely unrelated to those known. Metabolomic analysis would have detected abnormal amounts of D-amino acids or L-sugars.

As far as I know, there isn't too much we know about why life is "left-handed". So far the prevailing hypothesis is that in space there may be a tendency for amino-acids to favor one chiral-state over another, and there's some very smart people who are testing this, as opposed to the 50:50 shot here on Earth.
To answer your question, however, the general consensus is that life came from non-living
material. Pan-spermia, intelligent design, and the rest are more fringe ideas, so the question is how life formed from non-life. One of the ideas is that the basic building blocks came from space (likely a comet or meteor), and if the idea that amino acids favor one chiral direction over another in space can help support that hypothesis.

Abiogenesis refers to both the actual way life emerged and fringe ideas, so no need to "call the OP out". I have always imagined that the single chirality was the result of enzymes being usually able to bond to only one chiral izomer substrate. If there was a single ancestor to all current life, it might very well be the reason. It would have been a 50/50 chance for either chirality to take over

@FrancisL. I realized I should probably have been clearer (and less open ended) in my question.  One thing I was wondering was whether the fact that there is only one chirality means that the odds of generating life given the right preconditions was actually very rare (as otherwise we would expect things to be symmetric) or if there was some sort of symmetry breaking phenomena.

There is no reason to expect to find opposing chiral life today even if it did exist during the early stages of life's evolution. Everything not incorporated into more recent organisms has been lost, selective process will destroy early life as better adapted life evolves. Remember the earliest forms of life will be very flimsy compared to what comes later as it has no competition.
Which ever form evolves first will quickly deplete the oceans of available material for other forms to emerge. In addition even if both emerge whichever one emerges sooner has a massive advantage as opposing nucleotides has a tendency to mutually inhibit each other. Once nucleotides are synthesized by early organsms opposing chirality will be completely eliminated until only whichever evolved first remains. Building RNA out of both chirality does work but it is severely limited so it will not persist in the face of much more flexible single chirality.
It is the same reason we don't see codon diversity in life, each may work equally well, but once one evolves it quickly outcompetes and prevents others from evolving.


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What triggers the switch between aerobic and anaerobic respiration?
I understand that when there is a shortage of oxygen cells convert the pyruvic acid from glycolysis to lactic acid to regenerate NAD+. What I don’t understand is how they switch to anaerobic metabolism occurs. Is there a certain chemical message that triggers this?

Are you referring to human cells?

Yes, the respiration in human being cells.

The simplest method of control of metabolism is by substrate concentration. So if the concentration of NADH and pyruvate is low, lactate dehydrogenase cannot function. When they build up it can and will.

The situation is more complicated than this, because pyruvate will only build up if it is not converted to acetyl CoA by the pyruvate dehydrogenase complex (see Berg et al. section 17.1.1):

Although the overall reaction is oxidative, and ultimately requires NAD+, the latter is not directly involved in the initial irreversible reaction. It is presumably for this reason that the reaction is also controlled, either allosterically (in bacteria) or by phosphorylation (in mammals). In either case the regulators are the small molecules the concentration of which is altered by the lack of oxygen: NAD+/NADH and ATP/ADP. The figure below and its legend is also from Berg et al. (section 17.2.1) — available through NCBI Bookshelf.

[The complex is inhibited by its immediate products, NADH and acetyl CoA. The pyruvate dehydrogenase component is also regulated by covalent modification. A specific kinase phosphorylates and inactivates pyruvate dehydrogenase, and a phosphatase actives the dehydrogenase by removing the phosphoryl (group). The kinase and the phosphatase also are highly regulated enzymes.]
The actual situation is quite complex and this is something of a simplification.

Thanks, can you give me the link so i could read more about the over all change that will make lactate dehydrogenase function?

@kgemp Done. You can only search (not browse) books on the NCBI bookshelf, but the two links I have given should provide a reasonable starting point.


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How to create a phylogenetic tree (using Maximum Likelihood method) in newick format for a Multiple Sequence Alignment file in FASTA format?
The file size is really big (26.7 MB). So, I am unable to use the online web tools, as they cannot handle such large input data.

Look into IQ-TREE. If you can work with R, I'd recommend phangorn to do the maximum likelihood analysis, and use write.tree() from ape to write the Newick tree(s).

RAxML (Stamatakis, 2014) would be a good place to start.


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How to define ammonites?
I miss the definition of ammonite. In my opinion, many authors confuse the term "Ammonite" and "Ammonoid". Ammonoids (Ammonoidea) are large group of cephalopods including for example goniatites (Goniatitida), ceratites (Ceratitida) and ammonites (Ammonitida?).
But what do we call "true ammonite"? Is it an ammonoid with ammonitic suture? This way, many triassic, jurassic, creataceous and possibly paleogenic (danian) ammonoids could be called true ammonites, because they have complex (ammonitic) sutures.
Can you show me where ammonites are on phylogenetic tree? Can we call phylloceratina, psiloceratina, lytoceratina, ammonitina, haploceratina, perisphinctina and ancyloceratina ammonites? Can we call phylloceratina, psiloceratina, lytoceratina ammonoids, but not ammonites?

Ammonites are not strictly defined. One can reffer to ammonites as to the whole group of ammonoids (Ammonoidea, ammonites sensu latto). This is common, but not supported by most researchers. Researchers use the term "ammonoid" for paleozoic ammonoidea and "ammonite" for Jurassic and Cretaceous Ammonoidea (ammonites sensu stricto). Ammonites sensu stricto reffer to ammonoids with complex (ammonitic) sutures, which are typical for Jurassic and Cretaceous ages. However, complex ammonitic sutures are not exclusive for Jurassic and Cretaceous ammonoids. Ceratitic sutures are not exclusive for Triassic either and occur in Jurassic ammonoids, too.

So caution must be exercised when using suture lines as a means of
  classification. To obviate some of the problems posed by this
  simplistic classification, Wedekind, in 1918, introduced the terms
  palaeo-, meso- and neoammo-noids to classify ammonoids better.

(PDF) Goniatites. Available from: https://www.researchgate.net/publication/262048294_Goniatites [accessed May 12 2019].


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What is meant by Remote Diuretics & Remote Vomiting?
I have encountered the terms Remote Diuretics & Remote Vomiting separately or sometimes in association in various articles related to medicine.
But I am unable to find any reference to what they actually mean.
Can you help me understand these terms please?
Update
Examples:

Urine sodium less than 10 mmol/L indicates extrarenal loss of urine
  (remote diuretic use and remote vomiting).

link: https://www.ncbi.nlm.nih.gov/books/NBK470386/

Go to google and search for "remote diuretic" to get more references, some are:

It would be helpful if you provided some context such as a citation.

@BryanKrause i have updated the post

"Remote" can mean distant/far away, often in space but also in time (as in, the "remote past"). In just the search results you included in your question it is fairly clear that these sources are using the word "remote" to mean (relatively)"far away in time" or simply "not recent."
For example:

associated with remote diuretic use, therefore, diuretic effects were already washed off

Referring to diuretic use in the past, so there is not current diuretic effect but the secondary consequences are still present.
Note that these terms are quite uncommon in the literature, I get 21 results in Google Scholar for "remote diuretic" and 16 for "remote vomiting" and nearly all seem to be related to the specific context of hypokalemia.


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How does shortage of oxygen halt the NADH dehydrogenase complex?
I understand that in the absence of oxygen the functioning of cytochrome c oxidase stops because it is its substrate. However I don’t understand how stopping cytochrome c oxidase also stops the previous complex (the NADH dehydrogenase complex).

At a basic level this is quite straightforward if you look at an old-fashioned simplified diagram of the electron transport chain, such as the one below that I filched from the web.

If oxygen is absent then there will be a build up of the reduced forms of each cytochrome. Starting from the bottom, in the absence of oxygen cytochrome a is not reoxidized; if there is no oxidized cytochrome a then reduced cytochrome c cannot be reoxidized, and if there is no oxidized cytochrome c then cytochrome b cannot be reoxidized. The latter is the substrate of the NADH dehydrogenase complex — NADH-Coenzyme Q reductase in the figure — so this reaction stops for want of oxidised cytochrome b.
(Years ago I demonstrated on a standard undergraduate laboratory class using rat liver (or perhaps beef liver) mitochondria, where you inhibited different stages and detected the reduced forms by their colours in the visible spectrum.)


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Cardiac cycle and atrial contraction

During atrial contraction ("a" in the figure), why does the ventricular pressure match the atrial pressure? The ventricular pressure generally stays the same throughout passive filling until it reaches the point where atrial contraction occurs. Why is there a sudden change in the ventricle pressure during atrial contraction? I can understand the atrial pressure would increase when the atria contract, but the ventricles have not contracted yet so the ventricle pressure shouldn't increase. The ventricle pressure can increase greatly when the volume exceeds a certain value and the elastic tissue of the heart cannot stretch anymore. However, the volume here is only about 110ml, so it has not reached that point. I can only think of one explanation:

The pressure is equilibrated between two sides of an open valve.

However, this doesn't explain why the atrial pressure is slightly greater than ventricle pressure during filling; it also doesn't explain why the aortic pressure is slightly greater than the ventricle pressure near the end of ejection.

Two things to think about: 1) Does the pressure in a balloon increase only when it is full and cannot stretch anymore, or does it increase while it is stretching? 2) If A and B are connected, under what conditions will there be flow from A to B? Pressure_A == Pressure_B? Pressure_A>Pressure_B? Pressure_A<Pressure_B?

Well I've mentioned that ventricular pressure generally stays the same throughout passive filling. So stretching, based on your question, still doesn't explain why there is a sudden change during atrial contraction. Are you saying stretching of the ventricles only occurs during atrial contraction? However, your final point does rule out my hypothesis or attempt at explaining it.

Maybe one more thing to think about: 3) While there is flow from A to B, is there any circumstance where B could have greater pressure than A?

Well if we are talking about systole, the ventricles relax (A) near the end, as blood flows into the output blood vessels (B). As they relax, the pressure of A decreases and becomes less than B. Also, if we are talking about the atria (A) and ventricles (B), the same situation would occur. I'm not sure how your question explains my main query though. If you would like to clarify?

Mostly just wanted to make sure you were putting some thought into answering the question yourself because I think that's the best way to learn about these things. I think you've done sufficient thought that I can provide an answer explaining things - let me know if anything remains unclear.

While blood is flowing into the ventricle, it can never be at a higher pressure than where blood is flowing from: if it was, the flow would be going in the other direction. Flow is always from higher to lower pressure, if there is no pressure difference there is no flow.
Before atrial contraction, the ventricle can have no more pressure than the uncontracted atrium, which in turn can have no more pressure than the veins (vena cava or pulmonary depending on which side of the heart we are talking about). When the atrium contracts, it increases the pressure in the atrium, which causes a flow of blood into the ventricle. Whenever a fluid flows, there is a pressure drop that depends on the resistance (very much like voltage in an electrical circuit). However, the AV valve is fairly big and open, so there is little pressure drop from the atrium to ventricle.

The pressure is equilibrated between two sides of an open valve.

...is mostly true if the valve is large enough. There is still some pressure drop, though: if there wasn't, there wouldn't be flow.
There is no need for the ventricle to be at maximum capacity for pressure to increase. Imagine if you squeeze one side of a balloon: the pressure in the balloon increases, which you can tell because the balloon stretches and expands in the areas you are not squeezing; it need not be at the maximum capacity of the balloon for this to happen. Same for the heart.
As far as the higher pressure in the aorta, I this diagram is slightly exaggerating where the pressure difference starts, but as the ventricle relaxes there is a brief time where you get a small backward flow because the relaxing ventricle ends up having less pressure than the proximal aorta. This pressure drop is what closes the aortic valve (or the pulmonary valve, same process).

Thanks for you answer. I agree with most of what you have said but there are a few points that I am not entirely convinced with. Firstly, the figure was from the Guyton and Hall textbook and corroborated by others (e.g. https://www.aafp.org/afp/2004/0601/p2609.html). I do agree that flow is from higher to lower pressure but I don't agree that "if there is no pressure difference there is no flow". For one, the figure shows that ventricle volume continues to fall even when aortic P is higher than ventricular P, likely do to kinetic energy propelling it forward.

"if there is no pressure difference there is no flow" is physics (or at least no net/bulk flow...you will still have diffusion equally in both directions) and there is no controversy. The figure is a cartoon for demonstration. There could be some inertial effect but you wouldn't expect it to be a major contributor for the overall flow.

Secondly, I didn't mean that the ventricle had to be at a maximum capacity. What I wanted to understand is why there is a "sudden" increase in pressure when there was only a slight increase during passive filling. The main idea I was putting forward was that once the heart reaches a certain volume there is "sudden" rise in pressure for given volume b/c elastic tissue can't stretch as well after this point. I now realise that I may have underestimated what that pivot point is for the "sudden", also I didn't account that the ventricles are still contracting for some time.

https://physics.stackexchange.com/questions/157038/do-particles-always-flow-from-high-to-low-pressure and Bernoulli's equation

There isn't enough velocity or constriction for it to matter on the filling side. On the outflow side you might get a little effect of velocity but not much. I'd suggest starting with understanding how fluid moves without momentum before thinking about the exceptions, that's the level I based my answer on.


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Does the difference in the height of artificial lighting affects the height of the plants?
I have some plants living on artificial lighting. I've noticed the following in the following two plants of the same species:
This one was grown with lamps very close to it (~10cm).

This one was grown with lamps far away from it (~1m).

The first one got smaller while the second one is much taller. It seems that at least for some plants, the difference of height in lighting affects the height of the plants/speed of growth/etc. As soon as I changed the first plant to a place with higher light, it seemed to grow (vertically) much faster. If that is true, I guess someone already noticed it. I'd like to read more about it, could you point me to references on this?

Don't forget that you have a sample size of 1. You therefore can conclude much from this "experiment". The difference can be due to soil differences or aeration. Also, the two plants are of the same species but they are not clones. There might well be genetic predisposition.

@Remi.b Yes, I did not conclude anything. It wouldn't make sense to conclude by asking if it is true.


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How do organophosphates actually work?
The common explanation as to what the primary mechanism of action for organophosphates (and carbamates) is is the inhibition of the enzyme acetylcholinesterase and resulting buildup of acetylcholine at neuromuscular junctions, which ultimately results in respiratory failure. However, there is evidence that this may not be the case.
Firstly, a study reported that the nerve agent VX has been found to attack at least 132 different proteins, some of which were associated with metabolism.
Source: https://www.ncbi.nlm.nih.gov/pubmed/28267914
Also, another study showed that, even when the enzyme was protected against the action of organophosphates, nerve agents still exhibited toxicity.
Source: (http://www.rand.org/publications/MR/MR1018.5/MR1018.5.chap5.html) (Found in the Chapter 5 PDF, under "Non-AchE Effects")
Also also, another study was conducted on the matter. The test subjects were mice genetically engineered to lack acetylcholinesterase. The study found that the mice that totally lacked the enzyme not only lived (For over 34 days, no less), but were also twice as susceptible to OP poisoning as mice with the enzyme and exhibited the same symptoms.
Source:https://www.ncbi.nlm.nih.gov/pubmed/11602663
So, how do organophoshates actually act to cause the symptoms associated with OP poisoning? What proteins do they affect? There seems to be a great abundance of evidence that the effects of poisoning are not due to AchE inhibition.

Organophosphates (OPs) are cholinesterase inhibitors that lead to a characteristic toxidrome of hypersecretion, miosis, dyspnea, respiratory insufficiency, convulsions and, without proper and early antidotal treatment, death.
Most OP compounds are highly lipophilic. Sulfur mustard is a toxic lipophilic alkylating agent, exerting its damage through alkylation of cellular macromolecules (e.g., DNA, proteins) and intense activation of pro-inflammatory pathways

@com.prehensible If cholinesterase is a vital enzyme, then how come test mice that were engineered to lack it entirely could survive for over 34 days?

there are multiple genes for cholinesterase enzymes, for acétylcholine, butyrylcholine, This document states that they found that BchE was equally important as AchE. The knokout mice did die faster from VX. If you look on the reference it gives many, many different targets for OP's did you see it? it's very well written. http://www.scielo.br/img/revistas/jbchs/v27n5//0103-5053-jbchs-27-05-0809-gf04.jpg OP's are very volatile and they can put lots of chlorine and sulphur esthers inside the body, which react with 100ds of metabolites even DNA, the known list is given in the above pic

Hundreds of OP's have been made since the 1930's. Phosphoric acid is used in Coca-Cola and organophosphates are esters of H3PO4, you can study ester lipid/aqueous drug chemistry. They have many different targets: http://www.scielo.br/img/revistas/jbchs/v27n5//0103-5053-jbchs-27-05-0809-gf04.jpg
OP's are lipophilic. Lipophilic substances can dissolve into cell walls which are lipid bi-layers, straight into the DNA of cells and also into the nervous system.
They can travel through cellular membrane, alveolar and dermal membranes, through dermal glands, cell walls and from one organ to another. The degree of lipophilicity of drugs cause them to either stay inside the cell membrane or go through. Prozac also being lipophilic. The body is made of a mostly aqueous phase and also a lipid phase.
Many OP's contain Sulphur and they are bioactivated through desulfurative oxidation and turned into the corresponding oxon form by the liver so the organic chemistry inside the body is very complex: dealkylation, dearylation, phosphyrylation, carboxylation, hydrolysis and they are very reactive with metabolic compounds in different phases. They can be combined with absorption facilitators to pass the skin barrier and paired with radicals which are activated by the liver.
A recommended text on the toxicity: http://www.scielo.br/scielo.php?script=sci_arttext&pid=S0103-50532016000500809
OP and acetylcholine are both esters.
Here's a good chemistry animation of AChE enzyme inhibitor process: https://youtu.be/fIvF1rhp1nA
And this one, about non-competetive inhibition of AChE:
https://youtu.be/_jfGKbbZStw
general AChE info:
https://www.youtube.com/watch?v=-gIqZ8IxctE
AChE inhibitors that affect lots of organs such as peripheral and central nervous systems, muscles, liver, pancreas, and brain.
They lead to a characteristic toxidrome of hypersecretion, miosis, dyspnea, respiratory insufficiency, convulsions and without an antidote, death.
They can bind to fatty elements inside the body, like the central nervous system. They can exert damage through phosphorous-alkylation of cellular macromolecules (e.g., DNA, proteins) and intense activation of pro-inflammatory pathways.

Actions: (1) Phosphoryliodide can combine with phosphatidylcholinesterase to form a complex of phosphatidylcholinesterase and phosphatidylcholine iodide. The latter can be further cleaved into phosphatidylcholine iodide to free the cholinesterase and restore its activity.
2) Phosphodium iodide can also bind with free organic phosphate esters in vivo, and become a non-toxic phosphatidyl iodide phosphate, which is excreted from urine.
The mechanism of action is to inhibit cholinesterase and indirectly activate M-receptor, and the organic ester poisoning is also due to the inhibition of cholinesterase, which is equivalent to the original organic ester poisoning, atropine rescue overdose, and organic ester treatment.


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What is this snake?

What kind of snake is this? It was sighted in Singapore (South-Eastern-Asia) and was ca. 40cm (~ 16 inches) long.

Could be a Temple Viper (Tropidolaemus wagleri). Hard to tell from the picture, but the head looks spaded like a Temple Viper's and I think they come in the green morph you show