text:
What does genetically tractable strain mean?
I want to study the properties of Pyrococcus Furiosus in surving to gamma irradiation by exploiting the analysis of DNA sequencing data as a bioinformatics study. Before learning how to analyse this kind of data, I wanted to have a look at some work that was already done. I found this interesting article: Genome Sequencing of a Genetically Tractable Pyrococcus furiosus Strain Reveals a Highly Dynamic Genome.
I think that it could be a good starting point. However, it is not easy to understand the whole article for me and I suspect
that the source of this difficulty is mainly due to the fact that I do not know what "Genetically Tractable Pyrococcus Furiosus Strain" means.
Searching in Google I found this article: Systematic evasion of the restriction-modification
barrier in bacteria, that explains:

Bacteria that are recalcitrant to genetic manipulation using modern
in vitro techniques are termed genetically intractable. Genetic intractability is a fundamental barrier to progress that hinders basic, synthetic, and translational microbiology research and development beyond a few model organisms. The most common underlying causes of genetic intractability are restriction modification (RM) systems, ubiquitous defense mechanisms against xenogeneic DNA that hinder the use of genetic approaches in the vast majority of bacteria and exhibit strain-level variation. Here, we describe a systematic approach to overcome RM systems.

Then it tells also that:

A strain that is not amenable to alterations of its genome or to the introduction of new genetic information during genetic engineering is termed genetically intractable.

Therefore, from this short explanations, I have an idea of what genetically intractable means. But, I still wonder why in the first article that I mentioned, the scientists should have been interested in sequencing such a genome (genetically tractable) and in comparing it with the one that was firstly sequenced (the so called reference strain) ? Moreover, what does genetically tractable mean?
Indeed, in the case of the first article, the following description is reported:

The best characterized of the Pyrococcus species is P. furiosus, the first to be isolated (19) and the first to have its genome sequenced (49). This organism has been studied by numerous “-omics”-based approaches, including transcriptomics by tiling (59) and DNA microarrays (14, 35, 51, 54, 57), comparative genomics (8, 33, 60), proteomics (32, 42), metallomics (11), and structural genomics (25). In many ways, it has become one of the model hyperthermophiles, a status recently sustained by the development of a genetic system for the organism (37). This was based on isolation of a variant in a lab strain population, designated COM1, which was highly efficient in taking up and recombining exogenous DNA in both circular and linear forms. The COM1 strain was obtained by targeted gene disruption of the pyrF. locus (PF1114) using a plasmid designed for double-crossover recombination (37).

Then what they do is:

The genome sequence of COM1 has now been determined, and comparison with the published sequence of the P. furiosus reference strain (49) (NC_003413) revealed a surprisingly large number of changes.

Thus, I do not understand (both in the case of this article and also in general case) what genetically tractable means (the description given by the article is not sufficient for me to understand) and why are we interested in doing the alignment between the reference genome sequence and the genome of genetically tractable strain ?
Sorry if my question could be trivial but my biological backgrounds are really poor. I reported the extracts of the articles because they give me an idea of the answer but, to be honest, I do not have fully understood them. Therefore, if you can explain me also those extracts, it would be great. Thank you in advance.

You've already basically got the idea of "genetically tractable": if we can readily modify an organism's genome using known techniques, then it's genetically tractable.
That's a moving target, of course, because the set of available techniques is constantly expanding, so this is more of a pragmatic definition than a taxonomic definition. It's a notion that's quite important, however, because it's far harder to study an organism or to develop applications if you can't manipulate its genome.  If you can manipulate genetics, then you can make knock-out strains, introduce new functionality, and apply many, many other powerful and useful biological techniques.
So now to the last part of the question: assuming you've now got a tractable strain, why compare it with the reference strain? Well, if you're working on engineered applications, you probably really don't need to (other than from curiosity).  If you want to use the tractable strain to study things about the original, reference form of the organism, however, then you need to know their differences in detail, in order to have some idea of how much your results obtained by manipulation of the tractable strain are likely to inform your understanding of the reference form.

Thank you @jakebeal . I have a last question: so, for example, if they destroy a gene (PF1114) and then they compare the "modified" genome with the reference and they see (by DNA sequencing) that the tractable genome has two large chromosomal segments that have inverted order with respect to the reference order and that, despite this, there are no apparent consequence for proper metabolic function, is this a sort of assessment of the fact that they are resistant to distruptions (that maybe caused by gamma irradiation) ?

@Manuela I think this is really a separate question about how to interpret the relationships between genomes. Destroying a gene and rearranging chromosomal segments are quite different types of activities, and I'm not really sure how you're trying to put the pieces together here.

Ok thank you again .

I was thinking about this discussion again... What I still can't digest is why it is correct to compare the genetically tractable strain genome DNA sequence (that is a variant of the Pyrococcus Furiosus species) which has undergone targeted gene disruption with the reference ? I mean... I would compare the Pyrococcus Furiosus genetically tractable variant strain after targeted gene disruption with the genome DNA sequence of the  Pyrococcus Furiosus genetically tractable variant strain before the modification (so before the targeted gene disruption)...

Could the reason be that a variant can be considered the same as the "original" or "main" strain? I think it is not a separate question but if you do not know and you think I should do an other post about this, I will do it.

@Manuela I think it would be good to ask your more focused question, specifically about comparability, as a separate follow-up, linking to this question.


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Neuroimaging-Genetic studies: is postmortem gene expression equal to invivo gene expression?
I am going to study methods to combine genetic data with neuroimaging data. I have a big perplexity in the methodology. Let us take this research article: Unveiling the Neuroimaging-Genetic Intersections in the Human Brain (Ibai Diez and Jorge Sepulcre).
After figure 1:

Main methods applied to study the spatial association of Image Derived Phenotypes and genetic information. Transcriptome data is
obtained from postmortem brain tissue from different brain regions
across the cortex [...].

Considering that I am not a biologist, how can we assume that postmortem gene expression is equivalent to invivo gene expression ?

We can't, but these studies don't have another source of tissue. Even so, it seems reasonable to assume that differences by group are meaningful.

@BryanKrause do you mean that if I have expression of gene A that is nearly equal among all samples (i.e. post-mortem brains), we can assume that its expression Is that and we can Say that It is higher or lower than gene B expression ?

I mean if there is more expression of gene A in postmortem tissue from Alzheimer's brains than postmortem tissue from other causes of death, that has to represent some difference in those brains and isn't attributable to at least any common postmortem changes. It's rarely meaningful anyways to compare raw expression levels between two different genes.

@BryanKrause however, I think that in Allen brain atlas they did something like mapping the expression of brain genes in order to understand neuronal functions... https://portal.brain-map.org/explore/transcriptome

That would be another example of utilizing differences.

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What is sigma factor PvdS?
I am using MEME suite tool for de novo motif discovery and when I use TomTom to compare my motifs with known motif database, I find that my genes could potentially be upregulated or downregulated by sigma factor PvdS. I would like to understand what sigma factor PvdS exactly means.
I am not really able to interpret the UniProt page. It indicates the protein: sigma factor PvdS and gene: PvdS. Then it is difficult for me to put together the GO-Molecular Function and the GO-Biological Function in order to understand what sigma factor PvdS means.
From the paper by Miyazaki et al., I find:

In response to iron limitation Pseudomonas aeruginosa PAO induces production of pyoverdin, a low-molecular-weight siderophore able to capture ferric ion with a very high affinity. The pvd genes involved in the pyoverdin biosynthesis are organized in a chromosomal region termed the pvd region, and expression of some pvd genes is regulated at the transcriptional level. Two sets of promoter regions for the pvd genes were defined that were transcriptionally derepressed under iron-limiting conditions. Analysis of transcription from such promoters in Escherichia coli led to isolation and identification of a positive regulatory gene, pvdS, for expression of the pvd genes, and pvdS was localized in the pvd region.

From this extract, I can understand that PvdS is a positive regulatory gene that is, from Wikipedia:

A regulator gene, regulator, or regulatory gene is a gene involved in controlling the expression of one or more other genes. Regulatory sequences, which encode regulatory genes, are often at the five prime end (5') to the start site of transcription of the gene they regulate.

And so PvdS regulates the expression of the pvd gene involved in the pyoverdin biosynthesis.
Then in the paper by Tracey et al I find that:

PvdS is an alternative sigma factor regulated by the global iron regulator Fur

So putting all the pieces together, can I say that my genes could be upregulated or downregulated by this PvdS sigma factor, that is a sigma factor that means a protein needed for initiation of transcription in bacteria and this protein, in this particular case, is encoded by the regulatory gene PvdS that regulates the expression of the pvd gene involved in the pyoverdin biosynthesis?  And thus the PvdS sigma factor is a protein for initiation of transcription of the pvd genes?
Thank you in advance.

This is a site for specific problems about biology that can be regarded as of general interest. It is not a site for discussing the research data of particular individuals. As for the function of the actual pad gene, you have found out more than anyone here is likely to know. I assume that you know what sigma factors are, or can read about them.

Clarification of the Question
It appears to me that the question posed in the title of this question, “What is sigma factor PvdS?” is answered by the poster — it is a sigma factor that is specific for, and allows transcription of, genes involved in pyoverdin synthesis in Pseudomonas aeruginosa. I assume that the poster knows that a sigma factor is a subunit of bacterial RNA polymerase that must associate with it before it is capable of initiating transcription. (The information is readily available on Wikipedia or in Berg et al.)
The bulk of the actual question is devoted to describing the results of computer analysis of the genome of an unspecified archaeon. Towards the end the poster poses a question:

…can I say that my genes could be upregulated or downregulated by this PvdS sigma factor…

[The sentence continues for several lines. The emphasis is mine.]
I therefore interpret the question as asking

What conclusions can be drawn from computer analysis of the type
performed, with particular reference to the biological system
described?

Answer
It is necessary to emphasize at the outset that the conclusions that can be derived from studies performed in silico are severely constrained.
Sequence similarity allows you to suggest that an experimentally uncharacterised gene might encode a protein with a similar function to a related gene. No more. Only experimental analysis of the protein allows you to state what its function actually is.
The usual type of annotation of such proteins (and by extension their genes) is one of:

hypothetical xxxxxx protein
putative xxxxxx protein
possible xxxxxx protein
xxxxxx-like protein
xxxxxx-domain protein

Likewise, the occurrence of a motif that allows pyoverdin genes to be recognized by a transcription factor in P. aeruginosa can only suggest that a functionally uncharacterized gene from a different organism might be similarly recognized and its transcription regulated in a similar manner.
In the example in question the most it is possible to say is that a system of gene regulation similar to that in P. aeruginosa may exist in the archaeon. To go any further one would need to identify (the gene for) for the putative sigma factor, show that it allowed the RNA polymerase to bind to the genes, and either show this affected transcription directly or perform genetic experiments that would allow the same conclusion.
Furthermore, I would be wary of describing the putative sigma factor as ‘PvdS’ unless the proteins predicted to be encoded by genes on which this motif is found bear a similarity to the genes for synthesis of pyoverdin, from which its gene name, pvdS, is derived. (A BLAST search should, of course, be done on the genes to determine this — probably blastx.)

I think the OP is not a native English speaker and so some of the question phrasing is cumbersome as a result. I interpreted "could" as similar in meaning to your "suggest".

Since the objection about the fact that I was discussing my research data and the different votes to close the question for the same reason (I think), I removed the last part (I already imagined that it could be source of troubles). So just knowing what sigma factor PvdS means would be great ! @David

Anyway, I was asking if my genes could be regulated by the same factor indicated by the software (sigma factor PvdS) . I did not ask if they might encode a certain protein...

@Manuela The principle for genes is the same, but I have now spelled it out. It is of little use asking what "could" be on a site which is concerned with objective answers to precise questions in biology. Many things are possible, but how probable is an objective judgement. The key point of my answer is that you can only go far in silico — to draw any real conclusions (certainly publishable ones) you need to do experiments or convince an experimental scientist that they are worth doing.

@Armand I am aware that the poster is not a native speaker as I have helped her previously. My impression is that she wants to go further than "suggest" — modal verbs in English and romance or germanic languages do tend to differ in usage, but they are one of the things that are emphasized and one learns early on in a language. Even if this were so she is asking a question that is impossible to answer without seeing all of her data, and is even then off-topic as it does not constitute a general biological problem.

Thank you @David for the answer ! As regards the first part of my question, I still have a doubt: is PvdS the gene that encodes the sigma factor that allows transcription of genes involved in pyoverdin synthesis in Pseudomonas aeruginosa ?

For the second part (interpretation of the motif), thank you! I wanted only to know if this motif could have any relevant meaning (=if this suggests a meaning for the motif, as @Armand said). I think that when you do de novo motif discovery using MEME or other softwares, the results are always suggestions.

So, finally, the very last suggestion: did you mean that I should compare the proteins encoded by my genes and the proteins encoded by the genes for synthesis of pyoverdin to say if they are recognized for transcription by the same factor (PvdS) ? Is this a little replacement of the experiment? Or did I completely misunderstand your last suggestion?

@Manuela —My guess is that you are at some advanced level of education with a training in the numeric sciences but no real knowledge of molecular biology trying to use bioinformatics tools on a problem. It would helpt to know if it is one of your own devising, one given you in a Bioinformatics course or in a lab where you are doing a project is relevant in terms of advice. To answer your question, you should do a BLAST search on each of the genes (or probably better protein translations) that have the motif associated with PvdS to see what they are related to. Surely you know BLAST?

@David no there is no bioinformatics course or lab. It is just for an exam project and I took data from ncbi after reading a paper. I have a physics background and I wanted to go towards biophysics, so yes no real knowledge of molecular biology, unfortunately, thus interpreting some results is difficult for me ... Anyway, yes I know BLAST, so thank you for the suggestion ! The fact was simply that I was surprised to find this common motif in two genes which encode proteins with similar biological function but of two different organisms which belong to two different domains.

As your archaea genome must have been published and, I imagine, the genes annotated, BLAST may not be necessary, at least in the first instance. Just assemble the annotations and see if they indicate genes that encode proteins similar to those in the pyoverdin synthetic pathway or perhaps some other pathway. If there is no useful annotation, then you would need BLAST.  If the putative proteins do not hang together (obviously there may be exceptions), your argument probably doesn't either.

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Why do fruits have to ripen?
It seems like most fruits that we consume undergo some sort of ripening process either before or after they are picked from the vine, tree, etc. I understand that sugars are released during the ripening process and this is why ripe fruits are sweeter and more palatable than non-ripe fruits.
Why, though, do fruits have to undergo this process of ripening?
Wouldn't it be simpler to just grow and already be "ripe"? Does the ripening process confer some sort of advantage to the plant?

@DavidBlomstrom that would make a lot of sense - I don't know much about botany, but if the seeds aren't developed before the fruit is ripe that would be a reason that you wouldn't want to grow a "ripened" fruit. I guess I was thinking about it from a fruit consumer perspective, not a plant development one - thanks for your comment!

Some of the main reasons for delayed fruit ripening are to protect immature seeds, to save energy, and incompatibility between fruit and flower morphologies.
Fruits that are sweet have generally evolved that way in order to attract animals that disperse the seeds. But, this attraction is only useful once the seeds have been fertilized and fully matured. If a plant were to develop a fruit that was immediately sweet this would attract the animals too soon and they would remove or damage the seeds before they were capable of producing a new plant.
Sweet fruits are very energetically costly. Many plants produce many more flowers than actually get successfully pollinated. It would be a great waste of energy to fill the ovaries of those flowers with sugar when the ovules might not ever get fertilized. In fact, one of the main theories for the success of flowering plants is the ability to abort fruit development in unsuccessful flowers.
Finally, in most cases having fully-formed fruits would get in the way of flower pollination. One of the most common arrangements of floral parts is to have the ovary sit between the petals and the stigma (superior ovary, hypogynous). If the ovary were very large that would render the petals useless. For plants with inferior (epigynous) ovaries, large fruits would probably ruin the arrangement of the floral display. A large fruit would also increase the distance between the stigma and the ovules, forcing pollen tubes to grow much longer, possibly reducing or delaying fertilization.

Mature, viable seeds have to form in most fruits, which involves the maturation of embryonic tissue. That can take a little time, from just a few days in some weed species to months and perhaps longer in some fruits like pineapple.

All fruits, fleshy or not, have a dual purpose: First, they protect and safeguard the developing seeds as they grow, then once the seeds are mature, the fruit then aids in the dispersal of said seeds into the world.
A seed is equivalent to a fetus in mammals; if either are separated from the parent too early, they will not be able to survive independently, so a fleshy fruit prevents this by several methods - unripe fruit are typically green and easy-to-miss, and lack strong attention-grabbing odors, and if something does try to eat a fruit too early it will usually be too hard to easily consume, and many plants go a step further by adding unpleasant flavors or harmful toxins to punish anything that tries it on for size.
Once the seeds can survive on their own, the fruit changes - the flesh becomes soft enough to eat, the skin changes color, standing out from the rest of the plant, it emits an enticing smell, and any chemical deterrents are broken down, replaced by sugars and other flavorful compounds to reward animals that eat the fruit.

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How much energy would it cost to synthesize all cholesterol requirements de novo?
Imagine a scenario in which some person is unable to absorb any dietary cholesterol because of some intestinal mutation (for example). Thus, they have no cholesterol available from their diet for steroid hormone synthesis, bile acid synthesis, or any other process that requires cholesterol.
If that person had to synthesize all of their cholesterol requirements de novo (i.e. from acetyl-CoA), how much energy would that require on a daily basis? In biochemistry we talk about de novo cholesterol synthesis, but a lot of the time it is glanced over because it would be so energetically unfavorable to synthesize it when you can get it from your diet.
I'm curious to know... if we could somehow inhibit all cholesterol absorption and forced the body to make all its own cholesterol, then how much excess energy could we burn? Could we use that as a weight loss therapy?

You can easily figure this out by (1) counting up the stoichiometry of the cholesterol synthesis pathway and (2) multiplying by the amount of cholesterol lost each day by an average person.

@Roland how much cholesterol is lost each day by an "average person"? Are you sure that's fairly constant across adults?

@Roland I think the problem is trying to estimate the daily losses of cholesterol from conversion to "other substances" within the body - i.e. bile acids, steroid hormones, etc. I'm not sure how or what those estimates would be and if they would differ significantly between adults.

It's gonna be a ballpark estimate of course, as always with whole-body metabolism. This paper http://www.ncbi.nlm.nih.gov/pmc/articles/PMC297311 puts the loss of cholesterol at about 1g / day. Since cholesterol is not catabolized in the body, it should be a pretty good estimate of total cholesterol turnover. I think modifications like bile acid conjugation etc are minor in comparison to loss of the entire sterol backbone. Of course, you will see some variation between individuals, diets, etc.

@Roland that's a nice paper - the biggest sink for cholesterol is bile acid synthesis - of which the bile acid pool loses ~5% everyday - I will try to crunch some numbers and figure out an answer - thanks!

https://en.wikipedia.org/wiki/Mevalonate_pathway. Then it is Farnesyl pyrophosphate → squalene → oxidosqualene → lanosterol (http://www.genome.jp/kegg-bin/show_pathway?map00100)

Great, let us know what you come up with! Also, consider that the acetyl-CoA generated by sterol syntheis is a metabolic cost as well, as it could otherwise have been used to generate ATP.

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How to convert cell units (c.u.) to mole?
If one has values in terms of cell units (c.u.) how may it be converted to $\mu$M? Should I think a "cell unit" as
$1\;c.u.= \frac{1}{\text{cell volume}}$
and
$1\;c.u.=\frac{1}{\text{cell volume}}*(\text{volume of 1 mole of in 1 atm)} \; Mole$?
an example of c.u. units, belongs to this article
Thank you.

Where does this "cell units" thing come from (source)? I have never used such a unit.

I’m voting to close this question because it is the second posting of this question. It is also unclear.

@tyersome Yes it is the second posting. If you can read the last comment on the prior question which is "I will post two questions, as David suggested, and will not erase this one to be sure that you can read my comments. Please post a comment such that I can erase this question, thank you."  I am waiting for David to read my comments, I don't want to be rude to him. I will erase my prior question.

@Chris I edited my question, hope it is clear now.

You can delete a question you have posted if it hasn’t been answered. Then post again in a revised form.

Ok, i will, thank you.

Please read a definition of molarity. A molar solution contains 1 mole per litre. A mole is Avagadro's Number (approx 6x10^23) of molecules of a particular substance. So you can only talk about the molarity of a single substance and to calculate this you need to know its molecular mass. A cell is not a molecule, but is a structure made up of many different molecules and macromolecules. So cell units (which don't even come up in a Google search but seem to be some way of quantitating cells) can have no relation to moles.

The paper references c.u. to their "ODE model construction & simulation" which is referenced back to a 2016 paper that uses the term in reference to a simulation in MATLAB.
c.u. is abbreviation for CONCENTRATION UNIT not CELL UNIT.

Given the absence of experimental measurements of protein concentrations, we use concentration units (c.u.) as  unit to represent the relative concentrations of proteins in the model

quoting https://royalsocietypublishing.org/doi/10.1098/rsta.2006.1761

I'm having trouble finding that quote or any instance of "concentration units" / "c.u." in the referenced paper

@user338907 thanks!


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Can deterministic and stochastic models be used to models different parts of the same phenomenon?
A biological phenomenon including two different causally dependent phenomenon occurs in the cell. (Phenomenon2 initiates as a result of phenomenon1). Phenomenon1 and phenomenon2 are linked with feedback loops.
The entire phenomenon is wished to be mathematically modeled. Phenomenon2 is already modeled with a deterministic model including 3 PDEs. Since phenomenon1 and phenomenon2 are linked with feedback loops, they will be connected to mathematically model the phenomenon in its entirety.
Can phenomenon1 be modeled with a stochastic model? If not please explain why.

Please edit the question to limit it to a specific problem with enough detail to identify an adequate answer.

I think that the question requires more clarity, sinc eteh answer depends on which stochastic and deterministic models one talks about. The first thing that comes to mind is that deterministic models are often just the averages of stochastic equations.

I would suggest that the physics StackExchange community (https://physics.stackexchange.com/) might be a better place to get a good answer to this question. It seems that you are interested in the problem of modeling generally rather than a specific biological application, and they have more expertise in that domain.

I’m voting to close this question because it does not appear to be about biology as defined in the [help]. Please take the [tour] and carefully read through the [help] to learn more about the site, including what is on-topic and what is not, and [ask] a good question.

@RogerVadim I see, thanks.

@MaximilianPress I think you are right, but sometimes different fields might have different perspectives/tools for the same method or for their analysis. I was curious about the approach of an expert in biological modelling on this question. If there was a biological modelling SE I would put it there. Sorry for inconvenience.

@tyersome I can also delete it, if you prefer. Thanks.

If you also can't see any way to make your question fit here, then yes I think it would be best to delete it. Thanks!


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Transcription of two different factors from the same transcription factor - seeking a relation between concentrations
Let's assume that:
Factor $X$ enters nucleus and results in the transcription of two different factors, $A$, and  $B$.
$X$ $\to$ $A$
$X$ $\to$ $B$
Can it be expressed as
$[A]=\alpha [X]$ or  $[A]=\frac{\theta (\alpha [X])^n}{1+(\alpha [X])^n}$ and
$[B]=\beta [X]$ or  $[B]=\frac{\theta (\beta [X])^n}{1+(\beta [X])^n}$
where $\theta$ is the Hill coefficient, such that concentrations of A and B have a relation between?
Note: I don't have an education on molecular biology, or biology - terminology might be wrong.

This question definitely needs more details and clarity, especially regarding the Hill coefficient, what $\alpha$, $\beta$, and $n$ are, and what specifically your question is. However, from what I do understand, from a biological perspective the answer is "not necessarily". It is entirely possible that one or both of the factors $A$ or $B$ has an inhibitory effect on the activity of $X$, causing it to be produced more slowly (and eventually turned off) as its concentration increases. This is actually a very common occurrence, and doesn't seem to be accounted for in your equations.

@MattDMo thank you for writing a comment, X, A and B are known factors, X is the nucleus triggering factor of a long molecular cascade. A and B effects the upper factors on the cascade and after $\delta t$ they effect X too but I am focused on the immediate time step between X and transcripted factors. $\alpha$, $\beta$, and $n$ are hypothetical. I hope it clarified things a bit.


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Do bigger animals have more testosterone?
I was wondering the other day outside, thinking about varieties of species and their aggression levels, etc.
I had a theory that since these highly aggressive, powerful, and viciously advantageous animals in fights with humans, such as lions, tigers, rhinos, elephants, etc. are so strong and aggressive in the wild compared to us humans and smaller animals, do they have more testosterone?
Like, in animals, does testosterone correlate with size, possibly explaining why a lion is heaps more slender, muscular, fit, agile, aggressive, and vicious than a typical human?
Basically, does the bigger size and aggression in wild animals correlate to their higher testosterone, such as larger size equal to larger testosterone in comparison to other smalelr or less aggressive animals, or is it different?

It is a good question. If I may ask, what instilled your curiosity?

Lions are more vicious than humans? What makes you think that? We are far more aggressive and violent than lions. Also, you may be surprised at how vicious and aggressive certain snakes and many insects are. Not to mention viruses which are little packets of aggression and little else. Finally,consider some extremes, the blue whale is the largest living animal and it is far far less aggressive than, say the praying mantis.

It is not that easy. Off the top of my hat I can try to pinpoint a few fallacies in your theory:

Scaling of the body happens in three dimensions and thus to a power law. As such allometric equations have to be applied when dealing with the total amount of substance in the body. Different species have different correlation factors of body mass to total substance amounts.
Angiogenesis (the formation of blood vessels) is affected by Allometry (the relationship of body size to the 'biology')
Diffusion factors are similar in closely related species. This means in order for messenger molecules with a short acting range/half-life (e.g. nitric oxide), the total amount in the animal may indeed be likely higher and the messenger in question may be produced on-site (e.g. endothelium). Testosterone as the name indicates, is however produced in the testes and released in the blood stream.
The sensitivity and regulation of the receptors themselves (which react to a substance) can be different in different species. It may also be weakly responsive to begin with at the genetic and ultimately the folded protein level. A good example of that is the melanocortin receptor MC1R in a gross section of the white human population. Even if you were to produce the same level of melanotonin, the melanocytes wouldn't respond to the same degree as in Humans with darker skin.
Messenger molecules can be re-purposed and take over or be given additional roles and functions over evolutionary-time. Again, Melatonin may serve here as an example.
After all a given messenger is already evolutionary tested, especially in regard to cross-talk, Haptens, and other adverse molecular interactions in the animal species and comes with the full set of molecular machinery adapted to it, - a "luxury" a new messenger doesn't have. As such pressure usually exists to re-use given messengers.

Like, in animals, does testosterone correlate with size, possibly
  explaining why a lion is heaps more slender, muscular, fit, agile,
  aggressive, and vicious than a typical human?

I doubt you will find typical humans or typical human populations from a biological perspective. Your view may be skewed by economic factors.

Basically, does the bigger size and aggression in wild animals
  correlate to their higher testosterone, such as larger size equal to
  larger testosterone in comparison to other smalelr or less aggressive
  animals, or is it different?

To a large degree the behavior is determined by the niche the animal is in. As to which concerted molecular messengers make the "evolutionary cut", by best influencing an animals behavior in its given "time-domain" is another question. As the question is complex much is still researched.
Take this counter-example: A mouse and an elephant have very different masses resulting in different inertial forces. Fleeing from an enemy will take different strategies in regard to the central nervous system as well as the body, and demand different levels of messenger molecules at different places, at different times for both animals. Yet the substances in question will likely be similar.


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Why is water flavorless?
I read recently that humans have an innate preference for sweet-tasting foods. That seems feasible since carbohydrates are necessary for cells to undergo cellular respiration, but why then is water not similarly good-tasting? The thirst mechanism is a very long, multi-step process that ensures that humans intake a sufficient amount of water, and it can be really satisfying to drink water when you're really thirsty, but why is it flavorless if it's so vital to life?

because water is ubiquitous. Every living object is made up of water. So it would not make sense to have a sensory perception for water. Imagine you always feeling the taste of your own saliva.

Is it flavorless or is it just something we consume so often that we just learn it to be the neutral flavor?

Try tasting distilled water : ) It stings.

Water is a compound and like many other compounds it has its own properties. Some compounds have smell while others do not, some have characteristic taste while others don't and the same happen with colour.

Because there are no taste buds or olfactory nerves that associate a taste with water (distilled). With that said, regular non-distilled water will have slight taste in it due to minerals, treatment chemicals (example: weak chlorination), and microbes.

Consumer water is not flavorless. Sources of flavor include (1) the chemical and microbial content, which is most influenced by geology and ecology; (2) chemicals added or removed during water treatment, and (3) inputs and reactions that occur during distribution and storage (Dietrich, 2006).
Two examples of ecology-related flavors are geosmin and 2-methylisoborneol, which are respectively responsible for earthy and musty odors, produced by cyanobacteria and actinomycetes (Izaguirre et al, 1982). Humans detect these earthy and musty odors at concentrations of only a few ng/l. The ability to smell geosmin and 2-methylisoborneol is affected by other factors, such as the presence of chlorine, which masks odors (Dietrich, 2006).
The capability of organisms to detect microorganisms like cyanobacteria is not trivial, as cyanobacteria produce toxic microcystins with hepatotoxic and neurotoxic properties that can cause illness and even death (Blaha et al, 2009).
In my opinion, from an evolutionary perspective, it would be more important for survival to taste pollutants in the water than to mask these components by generating a taste to water that could potentially make the detection of toxins less effective.
References
- Blaha et al., Interdiscip Toxicol (2009); 2(2): 36–41
- Dietrich, J Water and Health (2006); 4(Suppl 1): 11-6
- Izaguirre et al., Appl Environ Microbiol (1982); 43(3): 708–14

To add to the water is not flavorless point - generally speaking water you drink in cities and water you drink in rural areas tastes notably different.

Food & drink that are very cold are characteristically less flavorful than anything at room temperature or hot, it's definitely something to consider. You can also control the solutes in the water to obtain a desired taste. Reverse osmosis plants remove all solutes in water, and they'll add calcium, magnesium, etc. after the process. In my hometown, the water from the fountain in the reverse osmosis plant lobby was the best-tasting I've personally had, as it hadn't traveled through the city water lines, yet (this adds some flavor).

@DavidGrinberg you do not taste the water when you say water from two sources taste different. You are actually tasting the dissolved solutes.

Then why are all other foods (fruit, meat, vegetables) full of flavor? Wouldn't it better than to have, say, apples flavorless so that we could taste any rotting? Or I could ask the reverse question - wouldn't it better for the human body to assign a good taste to water so as to make it a nutritional "award", like most other natural good foods?

Because thirst is quenched by a liquid and in nature there are almost no liquids that are not mostly water, and none of them taste even mildly pleasant. Water doesn't need to taste good becasue water is all you have. But there are lots and lots of solids out there so certain ones have to taste good. You also can detect water more easily by its ability to wet then trying to design a chemical sensor that works to detect water in water laden mucus.


text:
What are the absolute facial features which features sexual dimorphism in humans?
Apart from beard and moustache, is there any facial feature that would help to distinguish between men and women?
It is said that men have square, rectangular or oblong face and women have oval,diamond or heart shaped face.
Also men are said to have thicker eyebrows, widely spaced eyes and prominent eyebrow ridges while women have longer eyelashes.
Again, men have wider mouth and women have fuller lips.And men have sharp jawline while women have rounder jawline.
This list can be extended further. However, there are several exceptions to the above mentioned generalization.
So,how can we instinctively determine biological sex(male or female) of someone just by looking at the face?

If you want to know how the brain 'instinctively' decides male or female you can go to https://cogsci.stackexchange.com/

@Roni Saiba How can I transfer this question to other StackExchange category? I want to know both about psychological aspect of recognizer and physiological characters of a person whose sex is to be recognized just by looking at facial features.

You can join the other stackexchange. I think moderators can transfer questions around so you can contact them in chat.


text:
Do person with strong immune system have less chance of surviving SARS-COV-2 attack?
In most of the cases dealing with SARS-COV-2 disease, the major mortality cause is due to cytokine storm in response to Corona-virus that also attack healthy organs causing multiple organ failure.

leading to inflammation and fluid buildup in the lungs.(7) Certain kinds of cytokines trigger cell death. When you have many cells doing this at the same time, a lot of tissue can die. In COVID-19, that tissue is mostly in the lung.(5)

Among the many mysteries of Covid-19 is why relatively healthy young people suddenly become critically ill — or die.Many otherwise robust patients were experiencing cytokine storms. One key sign of that was the body’s levels of ferritin, a protein in the body that binds to iron. This massive over-reaction, known as a cytokine storm, is believed to be a major reason that a growing number of exceedingly fit people find themselves fighting for their lives.(7)

Assuming healthy people having a strong immune system have greater cytokine storm against SARS-COV-2, isn't coronavirus naturally selecting people with "weaker" immune response?
However an interesting case has been observed within Haemodialytic patient(not-healthy):

HD patients with COVID-19 even displayed more remarkable reduction of serum inflammatory cytokines than other COVID-19 patients. Epidemiological, clinical, and immunological features of a cluster of COVID-19 contracted hemodialysis patients

References:

https://scroll.in/article/962574/what-is-a-cytokine-storm-and-why-is-its-prevention-key-to-treating-covid-19
https://www.sciencedaily.com/releases/2020/05/200521165706.htm
https://www.sciencedirect.com/science/article/pii/S1359610120300927
The cytokine storm in COVID-19: An overview of the involvement of the chemokine/chemokine-receptor system
Cytokine Storms May Be Fueling Some COVID Deaths
Why Some COVID-19 Patients Crash: The Body's Immune System Might Be To Blame
He ran marathons and was fit. So why did Covid-19 almost kill him?

Is this a question or a blog post? The answer (if it is really meant as a question) may be yes (or no) but before anyone can attempt to answer it they would need to know what “a strong immune system” is (as well as its relationship to athleticism etc.). Is this something that can and has been measured, or is it something purveyed by the media and other charlatans? Perhaps you could provide references to this, or ask a separate question on this specific point (preferably to SE Medical Sciences).

@David By Strong immune system, I meant adequate immune response generated by the patient to quench the effects of pathogenic diseases. Although I didn't find any journal paper that would answer the question given in the title, I welcome any comment that would provide some key insights


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Why is this the equation for the fitness of cooperators?
This paper gives the equations as:

The fitness of cooperators and defectors is respectively given by fC = b(i − 1)/(N − 1) − c and fD = bi/(N − 1).

c - cost
b - benefit
i - number of cooperators
N - population size
For the equation fC, does this mean
(b(i − 1)/(N − 1)) − c, i.e.:
$$
\frac{b (i-1)}{N-1}-c
$$
or b(i − 1)/((N − 1) − c), i.e.:
$$
\frac{b (i-1)}{{N-1}-c}
$$
Guessing the former but I just want to check.
While we're at it, could someone explain why this is how fitness is modeled?

Think about the units involved - only one of those options makes sense.

Bryan Krause and user438383 are correct in pointing out that the second equation makes no sense since it would involve subtracting c, a cost, from N, a population.
As to why cooperation and defection is modeled this way, $f_C$ is just a linear equation where the fitness accrued to this cooperator is the benefit $b$ from every other cooperator $i$ except for themselves, thus $i - 1$, minus the cost of cooperating $c$:
$$
f_C = b \frac{(i-1)}{N-1}-c
$$
Meanwhile, $f_D$ is the fitness accrued by each defector. Since there is no cost to defecting there is no $c$ost to subtract, plus the defector also gets a slightly larger benefit because they get the cooperation $b$enefit from all the cooperators in the group (whereas each cooperator only gets the benefit from all other cooperators except themselves).
$$
f_D = b \frac{i}{N-1}
$$

As Bryan Krause points out in the comments, looking at the units gives you the answer. The correct form of the equation is $f_{c}=\frac{b(i-1)}{N-1}-c$, where $f_{c}$ is the fitness of cooperators, $N$ is the total population size, $i$ cooperators, $b$ is the fitness benefit of cooperating and $c$ is the fitness cost of cooperating. It doesn't make sense to subtract $c$, which is a kind of relative cost in terms of offpsring production, from $N$, which is population size. It would be like subtracting the cost of a car from the speed of an aeroplane. It also makes sense from the viewpoint that we expect the the fitness of cooperators, $f_{c}$, to reduce as the cost of cooperating increases, but independently from the number of defectors in a population.
Also, in the paper, it gives the equation with square brackets:

then the fitness of cooperators and defectors, respectively,is given
by fC=[b(i−1)/(N−1)]−c


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How does extra chromosome 21 in Down's syndrome cause all the characteristic developmental errors?
How does the presence of an extra chromosome 21 result in the characteristic craniofacial findings, developmental errors and other health issues?
I'd like to have an exact answer, because I can't seem to find a precise answer anywhere online, it seems all they mention is the fact that nondisjunction occurred during meiosis I. But I would like to know is why this extra chromosome creating so much complications?
It wouldn't make sense to talk about the position effect, so then I'd hypothesize that all the genes on chromosome 21 are over-expressed. How does this cause all the symptoms of Down's syndrome?
Thank you very much!

wikipedia has 4-5 in depth references about the over expression of genes generating extra quantities of molecules and hormones, causing growth difference and symptoms similar to Alzheimer. https://en.wikipedia.org/wiki/Down_syndrome#Mechanism there's a lot of research about down's syndrome and genes on google scholar.


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Evolutionary advantage of F plasmid in bacterial conjugation
Hi I would like to ask a question on bacterial DNA exchange, namely conjugation via F plasmid. It seems to me that all the F plasmid codes for is the sex pilus. What is the evolutionary advantage of the F plasmid? Does it code for anti-biotic resistance as well? Or enhances binary fission for reproductive success? Also, if conjugation transfers duplicated F plasmid from a F+ cell to an F- cell, why aren't all bacteria cells (that are capable of being F+/-) already F+? Is there a mechanism that somehow degrades your F plasmid?
Thank you in advance! I couldn't find the answers anywhere online.

F plasmids allow for the genetic exchange of material between cells, it's the closest thing to sex for most bacteria. Parts of the F plasmid are homologous to the chromosome of E. coli (mainly the transposons present on the plasmid) and through homologous recombination they can pick up bits of the chromosome. A lot of studies have been done where bacteria acquire traits such as galactose or lactose utilisation through these genetic exchange. They therefore allow fitness enhancing DNA to spread quickly through a population or species barriers [Ref].
Antibiotic resistance is not carried on F plasmids but there are many conjugative plasmids that do carry resistance genes (R plasmids). The F plasmid does carry a toxin/antitoxin system (ccdB/ccdA) [Ref]. If the cell loses the plasmid it will not be able to replicate its DNA because the toxin protein is very stable while the anti-toxin is rapidly degraded. So besides the evolutionary advantage there is also the possibility that it is simply 'selfish DNA' (see Richard Dawkins the Selfish Gene for details on this).
There are certain circumstances under which the F plasmid does not transfer such as low temperature so it is possible for a bacterium to lose the F plasmid and not get it back by conjugation. Maintaining a relatively 'useless' piece of DNA does have its metabolic cost so loss might confer a growth advantage.

Seems like the F plasmid would be more of a burden than anything.  Perhaps its just a selfish epitope.  Seems comparable to a parasite.  Maybe its a disadvantage to the individual, but an advantage to the bacterial strain due to recombinants generated through transfer of chromosome in Hfr cells.


text:
What makes some viruses more infectious than others?
This week a new strain of the SARS-CoV-2 virus was discovered in the UK, and reports are saying that it's more infectious than the strains we've been dealing with for the past year. Which made me wonder: what is it about different strains (or different viruses in general) that makes them more of less infectious than others?
They've been saying that they don't think the new strain will be any more resistant to the vaccines. Does that mean they're no more able to evade the immune system? Or is it just the immune system that hasn't been primed by a vaccine?

To name a few parameters that can determine the infectiousness of a pathogen:

Transmission pathways used (aerosols, surfaces, vector organisms, feces etc.)
Molecular affinity to bind to host cell (how well does it penetrate the cell)
Strategy within host cell (lysogeny, lysis)
Interaction with the host’s immune system


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Why unripe, very young coconut fruits spoil in days, but the ones picked medium mature can keep months?
Coconut fruits can be collected at various stages of maturity.
Coconuts which are collected just when the flesh starts forming (about 5-6 months on-palm age), so they have very thin or almost no flesh, mostly just coconut water, they will spoil within just a few days in ambient temperature 30°C (86°F). Coconut water from such a fruit which stayed (in a n intact coconut) just a few days will start to taste off, and give stomach cramps.
As coconut mature on the palm, about 7-8 months of on-palm age, they grow more flesh and the flesh is becoming more firm, but not completely firm yet, while the outside of the coconut still remains more or less the same as the very young ones. Such coconuts will keep without spoiling much longer at the same temperature 30°C (86°F), provided the shell is intact, no cracks. Such coconuts are still considered young. I am not talking about fully mature coconuts, when the meat is completely hard and the outer shell starts to turn brown - this happens after about 10 months of on-palm age.
What biochemical difference is in the coconut water that prevent the medium-young (7-8 month) coconuts from spoiling as fast as the very young-picked ones?


text:
How does a turtle develop inside its egg?
This is related to Cause of premature death in turtle eggs, for those interested.
I have noticed that Kinosternon spp. eggs have three layers:

hard outer shell
white opaque membrane (like the one you see in hard-boiled eggs)
transparent memebrane that completely wraps the baby turtle

Since I am forced to manually open this species' eggs (see the linked question for details), but doing so too early will likely result in the death of the developing turtle, I would like to know more about how turtles develop inside the egg (from a physical/chemical point of view).
I am assuming turtle eggs are permeable to oxygen.

assuming lack of oxygen is the root cause of these deaths, which, out of the three membranes, is more or less permeable to oxygen (in other terms: would breaking just one or two of the egg's layers be enough to let the turtle breathe?)
when do turtles start to breathe with their lungs?
Would it be harmful for the egg to get oxygen too early?
why would a turtle possibly die in the egg if it is opened too early? Could it be because of bacterial infections of some sort? I know for a fact that some breeders hatch turtles with shell-less incubation, the same tecnique used for chickens.

Biology is not really my area of expertise, I am just a passionate turtle breeder and I have not been able to find anything relevant that could shed some light on this issue.
My idea is to get some scientific insights that could possibly lead to a change in the incubation's parameters.
So any help would be greatly appreciated.


text:
Cause of premature death in turtle eggs
Context
I am a hobbyist turtle breeder and I have been keeping and breeding turtles for 15 years (I have hatched turtles in the high hundredths).
Long story short, few years back, my friend and I acquired a group of possible heterozygous for albinism Kinosternon sp.; here you can find a simplified but representative family tree. Squares represent adult animals (blue background for males, red background for females), while hexagons are individuals whose gender is unknown. Moreover, each shape gets a color based on the genetics of the specimen: grey for possible heterozygous (50% or 67%), black and yellow for heterozygous (100%) and yellow for albino. Everything started because of M1 carrying the genes for albinism and it is a wild caught specimen from many years ago.
The problem
Unfortunately, we are having issues hatching babies from this group. Many of them die at a very late stage of development, that is, turtle completely formed, small yolk sac (that would have been absorbed within one week tops). This is not always the case, however, as I have been able to hatch some without any intervention on my part. These were hatched from different females: a clutch from a female may hatch fine, while the next ones from the very same female might not, so the problem is not related to one or more individuals, but apparently every one.
This happens to me, but also to my friend, who is also an experienced turtle breeder and we live in two different locations. This happens with inbreeding, but also when mating unrelated pairs: e.g.: M1 or M2 with a female from a totally different genetic line. The only reliable method to increase hatching success is to frequently check the eggs by candling and crack them open when they are ready to hatch. Unfortunately, this is still a risky operation and it is sometimes difficult to estimate development stage, especially with albinos.
Incubation
We incubate our eggs in an artificial incubator. We put the eggs in moist vermiculite (1:1 ratio, which is pretty standard) inside small plastic boxes with holes on each side and lid. The eggs are buried halfway. Temperature is controlled by a proportional thermostat that ensures precise temperature control. We tried constant temperature incubation at 28 °C, but also varying temperatures between 23 °C and 27 °C to emulate daily fluctuations that would occur in nature. The incubator is "big" compared to the number of eggs it contains. Talking with one breeder and owner of one of the biggest turtle farm in North America, he suggested lack of oxygen might be the cause. Hence, I moved a dozen eggs with turtles almost due (within a month or two) in a heated room (ambient temperature around 26/27 °C) and placed each lid on top of the plastic container, by allowing plenty of air to flow through, but the same problem occurs. So, lack of oxygen is not the cause, or, at least it is not caused by the incubator itself. I will try and incubate eggs once laid in that room, but I fear I will most likely end up with the same result.
Husbandry
I keep my animals in an indoor facility separated (each specimen gets its own tank) and I periodically introduce a female in the male's tank. I do not provide UVA/UVB, but just LED lighting. I provide top quality food to my animals, for instance:

commercial pellets
offal (heart, liver, lungs etc.)
live preys: mealworms and earthworms
fresh fish
cuttlebone

Causes? Solutions?
What could be the cause of embryonic death at a so late stage in the incubation process? Is there anything I can do besides what I have already tried? Would a veterinarian be able to perform an autopsy on such small animals and provide valuable insights? I think I will possibly try shellless incubation like it is done with chickens to exclude lack of oxygen as the cause.
I have tried to be as detailed as possible, but please, feel free to ask for any clarification or missing information.
Update 2022/05/28
The issue is still there, but I am pretty confident the cause is not genetic (this also happens with other Kinosternon spp.. The interesting thing is that I have had some hatchlings able to break the egg shell on their own, only to die a few hours later, while I have been able to rescue a handful of hatchlings by opening their eggs 2/3 days before the complete yolk sac absoprtion. My guess is that these turtles are diying because they do not have enough oxygen during the very last incubation days. Those who succeed in cracking the egg, carry irreparable damage and die because of this shortly after.

Welcome to the site. Excellent question. Are these true albino or are they leucistic?

Hi, thanks, but excellent questions need... Well excellent answers :) Albino, t-.

I found a couple of paper suggesting that conversely increased CO2 might help developmental rate, lowering (i.e. increase O2) could put a pause on development. At least in Australian freshwater turtles. see the three para after fig 3 here. Whoops, may be paywalled.

Thanks, unsure whether this could help solving this issue, but interesting reading, I will check it out!

Well, a real chance this is a genetic problem.
How to test.
For the next hatching, have some “normal” unrelated eggs nearby under the exact same conditions. If they also have higher mortality then your conditions will be the problem, otherwise genetics is to blame.
For an extra check, have a friendly breeder do the same experiment - give them some of your eggs to raise alongside their own.
In any case, along with the pedigree keep track of hatching rates. Then it may become possible to determine which ancestor to blame; and breed accordingly.
Quite possibly, a deadly recessive gene has been selected for.

Good idea - it's pretty common in inbred lab animals that you select for a lethal or even conditional lethal phenotype with KO lines, often with embryonic lethality at some stage prior to birth. Partial penetration of traits can be tricky to work out though.

Thank you for your answer. I would not be so hasty on blaming genetics, though. We already tried both your suggestions and they did not work. But different species or even different localities of the same species could bear different challenges. Take Acanthochelys spp., for instance: their eggs are notoriously difficult to incubate and AFAIK very few people reproduce them in captivity. This does not mean there is a genetic thing going on. As for the hatching rates, I keep a very detailed database of each egg laid, but no pattern stands out, yet.

Unfortunately, the group is only based on two males (M1 and M2 from the family tree I posted). But M1 is wild caught, so there should not be any inbreeding involved and this issue is there even if crossing M1 with whatever F. Moreover, inbreeding is pretty common with turtles in captivity: there are quite a few double recessive morphs out there...imagine the level of inbreeding to achieve that! I am not saying this is not genetic, I am just saying: let's not jump to conclusions. And, if it really is genetic, there could be a fix for this in captivity. At least, that is what I hope.


text:
How can Clostridium tetani proliferate in relatively minor wounds?
It is often reported (NIH) that some of the most common infections by Clostridium tetani are in minor wounds where, in theory, blood (hence oxygen) supply should not be completely disrupted.
How can this obligate anaerobic bacillus proliferate in such conditions? Are concomitant necrotizing infections (such as, for example, Staphylococcus aureus) to blame?

SE Medical Sciences might be a better fit for this kin of question. In addition, it would improve your question if you cited a reference for your “often reported”.  (Also the number agreement in your question is ungrammatical, but I’ll fix it for you.)

Also, please note that there's a big difference between minor wounds and tetanus-prone wounds. Differentiating between the two will help your question.

Another piece of background information: Even for organisms classified as obligate anaerobes, there can a spectrum of oxygen sensitivity. Some strains of C. difficile can grow in up to 3% oxygen, and this trait may be associated with increased virulence. I don't know of any C. tetani research in this area, but I imagine a similar spectrum of oxygen tolerance exists, enabling some isolates to grow in microaerobic conditions.

Nondisruption of blood supply seems to be a heuristic/rule of thumb/approximation of the survival of oxygen supply to tissue in and around a "minor" wound. What I mean is, it's not a 100% confirmation of persistent oxygenation, especially if we consider every relevant locus at the wound site. Remember we're talking of microbes here and at that scale, anerobic pockets can exist even in the presence of macroscopically visible redness/bleeding/oozing (signs of good circulation) and that's all clostridium tetani needs to proliferate, synthesize and release its deadly toxin.


text:
Why does the sympathetic nervous system constrict in heart failure?
As I learn about heart failure in medical school, we are consistently taught that one of the compensatory responses to heart failure (and the accompanying reduction in cardiac output) is for the sympathetic nervous system (SNS) to activate. While this has myriad effects, one that is described in most cardiac pathophysiology textbooks (eg, Lilly) is that the activation of the SNS causes peripheral vasoconstriction, raising the systemic vascular resistance (SVR).
However, I don't understand why the body would do this.  The underlying problem in HF is a reduction in cardiac output (either due to diastolic or systolic failure). Raising SVR (using the cardiac equivalent of Ohm's Law: Pressure = CO x SVR) would either a) cause cardiac output to drop, holding pressure constant or b) force the heart to generate more pressure to generate to maintain a constant CO. Both seem like poor responses to a failing heart. So why does the body do this?
Put otherwise, if I had independent control over every hemodynamic parameter in the body and I was confronted by a failing heart, my solution would be to increase HR and contractility (which the SNS does), but to vasodilate the systemic arterioles to lower resistance and thus (by Ohm;s Law once again) reduce the pressure the heart would need to generate in order to drive the same amount of flow as prior to the heart failure. Why is this a bad idea?
I think there are some preliminary questions that might help clear up my confusion. They are probably very basic, but I think they will help clear up the confusion I face.
A. Why is blood pressure (specifically mean arterial pressure, measured at the aorta) important to maintain? The goal of the heart is to maintain tissue perfusion, which seems to me to be function of the volume of blood which gets to a certain organ.
B. Does the body regulate blood pressure or cardiac output? If both, which takes priority?
I think if I understand these two questions, I might be able to better understand why the body reacts the way it does to heart failure.

Please edit the question to limit it to a specific problem with enough detail to identify an adequate answer.

This is basic physiology. The human body doesn't "think" or know/reason; it reacts to stimuli. If the CO is low, it basically reacts the same way in an attempt to normalize BP regardless of the cause (e.g. hemorrhage vs. CHF). This is also why ACE-inhibitors are used in CHF, because the body doesn't "know" why BP is lower than normal.

Perhaps it's related to the physiological results of drowning, which also causes cardiac arrest, which appear to be of the same type. In that case, you can research the reasons for the physiology of conservation of oxygen in response to drowning, which is an ancient nervous pathway that exists in nearly all terrestrial vertebrates. Perhaps there is some research to do on the specifics of that.

Best try a medical forum, this is generalist so a lot of genetics/ecology/microbiology folk here.

@LifeInTheTrees - Nit-picky, but there are also a lot of medical people here, including physicians and people who teach medical students (I've been both). This kind of question is very basic and will likely not be answered by a medical professional. A medical forum might be better, but a medical student forum might be best.


text:
Is there always a leaf(s) attatched to an auxillary bud?
I'm trying to create a 3D functional-structural plant model and I need to establish some axioms.
Is it guaranteed or extremely likely that where auxiliary bud forms there's a leaf(s) attached? That's what it appears to be from most of the images I saw. If so, what usually comes first, the leaf or the bud?
More generally, is there a rule about where a leaf is guaranteed to naturally grow? Perhaps suggest some literature on this. Thank you!


text:
How does the female body sense its own pregnancy?
I understand that after the fertilized ovum attached in the uterus the female body will not produce the required hormone surge for ovulation the next month. Therefore no new ovum will be sent down the fallopian tubes during pregnancy. My question is how does the body sense that there is a fertilized ovum in the uterus? Are there some kind of sensors for this? Is the ovum it self producing hormones which can be detected by the body? Does the brain combine a lot of "hints" to infer that there is pregnancy?
Originally the question came about in the context of chickens and how their body detects if new eggs should be produced based on if they are already sitting on an egg.

Just a nit-picky bit of info: it’s different in chickens. Chickens don’t go broody on one egg. They wait for a clutch of eggs. Women don’t wait for several zygotes to start gestation. Also, some research on your part must be attempted and shown in your post, otherwise it will probably be closed. Seems odd for a Q&A site, but it’s still the norm. Thanks.

Interesting! Thanks for the pointer. The research about how this works in chickens turned out to be difficult as most of the internet is apparently just concerned with preventing chickens from going broody. I will try to add some more info about my research anyway. Thanks!


text:
Mitochodria's Role For Neuron Regrowth
Recently an interesting study has reported.  Zhou et al., 2016. J. Cell Biol. http://dx.doi.org/10...3/jcb.201605101
According to this study, enhancing anterograde axon transport of mitochondria is essential for regeneration of injured axons.
Neurons need a large amount of energy provided by ATP to extend their axons when they are injured. Mitochondria transported to axons produces
ATP which is necessary for that.
This study shows that in mature neurons, the motility of mitochondria is reduced and the reduced mitochondrial motility might
be the cause of the deficit in regrowth capacity of mature neurons. Moreover, this study found that enhancing mitochondria transport enables mature neurons to recover their regrowth capacity.
It is said that mature neurons typically arrest their cell cycle and fail to proliferate and regrow. However, considering the fact that
only enhancing mitochondria transport enables mature neuron to recover their regrowth capacity, I can't help but doubt the commonly accepted theory.
Do mature neurons actually not arrest their cell cycle？
What do you think of this finding ？

Why do you think this contradicts the fact that neurons are cell cycle arrested? There is no DNA replication or cell division, and mitochondria can proliferate independent of cell cycle as well.

Sorry that I couldn't convey to you what I wanted to tell.

Sorry that I couldn't convey to you what I wanted to tell. What proliferates isn't mitochondria but axons are. Moreover, only enhancing mitochondria transport to axons enables even the mature neurons to regrow. So, I doubt if the mature neurons actually don't arrest their cell cycle.

Axons grow but that is not same as cell is proceeding through cell cycle. Cell grows in size but there is no cell division. It is still arrested. However during this process some growth related genes are upregulated which are also upregulated in actively dividing cells.

I got it !! This report doesn't  observe whether some growth related genes are upregulated  or not. Thanks!!

Okay. Does this answer your question? I shall post this as answer, in that case.

ok, please post this as answer

Axons grow but that is not same as cell is proceeding through cell cycle. Cell grows in size but there is no cell division. It is still arrested. However during this process some growth related genes are upregulated which are also upregulated in actively dividing cells.


text:
How does carcinoma enter into blood or lymphatic vessels？
When carcinoma begins to metastasize, it enters into blood vessel or lymphatic vessel to migrate to the site of metastasis. In that case, although I think breaking down the basement membrane is necessary for epithelium such as carcinoma to enter into them, I can't find out the reports.
Are the basement membrane actually broken down in the first step of metastasis？What are the molecular mechanisms in which carcinoma enters into blood or lymphatic vessels？

You can read about epithelial to mesenchymal transition. It is one of the processes that usually precedes metastasis of carcinomas.

Thanks for answering my question, I have already known that the EMT system is one of ways of metastasis. However what i want to know is whether carcinoma actually breaks down the basement membrane when it stats to metastasize. Do you know some reports showing histochemically the broken down basement membrane？

@ironKUMA The linked Wikipedia article has many citations to the primary literature, I would suggest starting there. You should also perform some appropriately-worded Google Scholar and PubMed searches for more information.


text:
What is the mechanisms responsible for downregulation or loss of MHC-1 expression on the surface of cancer cells？
Downregulation or loss of MHC-1 expression on the surface of cancer cells generally have been thought to be involved in the mechanism of immune escape.
It seems to be very attractive but I don't know the mechanisms of downregulation or loss of MHC-1 at cancer cells. Would you tell me the molecular mechanism,

There is no single mechanism (as you'd expect, since there is no evolutionary relationship between different individuals' cancers).  The most common mechanisms are various forms of mutations, ranging from point mutations in single MHC molecules to large deletions of the MHC locus. Mutations in genes involved in antigen processing, that are not themselves part of the the MHC locus (e.g. TAP, b2-microglobulin), are also fairly common.  Epigenetic changes are also not uncommon.  There are several reasonably recent reviews, including

MHC Class I Antigen Processing and Presenting Machinery: Organization, Function, and Defects in Tumor Cells
Different regulation of MHC Class I antigen processing components in human tumors
The escape of cancer from T lymphocytes: immunoselection of MHC class I loss variants harboring structural-irreversible “hard” lesions

thanks for some reviews concerned with the topic.I will read them.


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Proof of shape of epithelia cells
In this article, the mentioned in the introduction that the  the optimal shape of epithelia cells in drosophila tissue is hexagonal (packing is approximately 6).
Is there an article that proves experimentally this shape? Or we just depend on mathematics and calculating the average neighbours?

Welcome to Biology StackExchange! I would suggest you add some references (or explain what you mean exactly) to your claim that the optimal shape is hexagonal. Firstly, there are several biophysical models for the shape of epithelia with varying levels of complexity. Secondly, the tiling is of course not hexagonal, it has to deviate to account for topology and cell division.

@Domen, I did. Actually I am coming from more physics background. Anyway, you said "several biophysical models". All these models are mentioning that the cells are taking a hexagonal shape (of course before rounding in cell division process). I didn't find something experimental I can fed from.

You might be missing the second part of the statement in the article: "The optimal cell shape on a flat surface is typically hexagonal as this minimizes surface tension". Therefore, the optimality in the simplest biophysical model is defined as the minimization of surface tension. Under the additional constraint that the cells be the same size, the resulting optimal tiling is the hexagonal one (compare with honeycomb). However, experimentally, we generally see that the tiling is not completely hexagonal, and thus this simple model does not adequateley describe the reality.


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Biomechanics of cells (stress, strain, tension..)
I am confused about the difference between stress, strain, tension, pre-strain and prestress in cells (especially in in-vitro experiments, like cell spreading on a substrate, cell doublets, cell rearrangements in epithelial tissues).

How are these 5 physical terms different or related?
Is there a reference or a book that can explain them in a good way, I got lost usually when they use in an article the terms ("they transmit tension" or "they impose stress")

@RogerVadim already mentioned an excellent book on biophysics (Phillips, Kondev, Theriot). Furthermore, since you are interested mostly on the mechanical aspects, I can recommend David Boal: Mechanics of the Cell.

Strain and stress are two essential quantities in elasticity theory, corresponding to the deformation and the forces appearing in response to this deformation. Tension or tensile stress is a particular kind of stress appearing in elongated objects, such as ropes, filaments, etc.
One could recommend any of the existing books on the elasticity theory, but these may turn out to be a bit of too "hardcore" in terms of the level of the math and the background physics knowledge required. I therefore suggest the reading more adapted to biologists (although not necessarily easy):

Physical biology of the cell
Mathematical biology I: An introduction

or similar books on mathematical biology and biophysics.

Thanks, you have a quick idea about the difference between stress and pre-stress in cells and how is that related to the cytoskeleton and actomyosin cortex?

@ALi Pre-stress is the inherent stress that exists in the material even before you load it. Prestressed concrete  is a good example - it seems far from biology, but most of the ideas is directly transferable to cytoskeleton. Unfortunately I cannot say more - the best I can do is google, which you also can do yourself (see, e.g., this one).


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How does a neuron change its function, without changing its synaptic connections?
How does a neuron change its characteristics in order to change its function, without changing its connections with the neural networks? Basically, do any organelles change their properties and are there any major chemical modifications that could cause it and explain it?
I tried looking everywhere on the internet but I couldn't find any, perhaps neuroscientists still don't know yet.
My initial idea was that some changes of some organelles inside the neuron caused the change in function of the entire neuron. Or that there were some chemical changes that could cause the presence of a molecule that controls the global function of the neuron more than some other.
Thanks a lot for your help and answers.

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Hello. I have spent some couple hours searching for answers. I tried looking for the list of the organelles of neurons to see their functions and if they have any relationship with brain plasticity, but couldn't find any that actually participate in the manifestation of structural plasticity directly. But I didn't find anything useful. My other theory was that there were some major chemical modifications, and because the function of a neuron was based off the chemical properties of it, then its function would change if the chemistry in the cytosol for example changed. I'm no biologist, sorry.

Also, I think the two other questions are just extensions of the first one. It's just to clarify my question.

If you mean what other functional changes at the level of neurons exist, excluding synaptic plasticity, what is left is called homeostatic plasticity. That is a vast subject that includes alterations in intrinsic excitability, resource allocation (e.g. mRNA), and even hetero-synaptic plasticity, depending on how you define synaptic plasticity. Unfortunately, this subject is too broad for me to put the effort required to write an answer for this site.

The keywords are Synaptic plasticity, LTP, LTD, and STDP, among others. The organelles includes release pools, receptors, scaffold proteins, etc.
Actually there is a huge body of literature around this topic. It will take years just too roughly understand what's already done.

Thank you. But for LTP, LTD, and STDP, don't they only cause functional changes, that means between the neurons and not actually in the neurons? Just asking for a clarification thank you.

@eengeeneer a small part is indeed carried out "between the neurons", i.e. synaptic-clefts, even astrocytes could be involved. But the majority of events, including pools, vesicles, receptors, scaffolds and signaling cascades, happens inside the pre- or post-synaptic neuron.


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Darwinism and the idea of being too successful
Is there an example of any animals or insects that have evolved too efficiently and went extinct due to upsetting the homeostasis of their environment? Outside humans.
I was thinking about venomous snakes when a fruit fly landed on me while having a libation in my garden. Then I got to wondering about why, for instance, a fly that eats rotting flesh wouldn't develop a potent neurotoxin on its feet? What a terrifying creature! Then I considered that perhaps a fly could have existed like that but it may have quickly killed all of it's food sources, and, as a result, gone extinct. Are there any known examples like this in animals or insects?

For neurotoxin on the feet, consider that after killing the creature it lands on, the fly would have to wait around for a significant portion of its lifespan for the flesh to rot before it could eat it.

@jamesqf Or it could just be immune to its own toxin. Perhaps more importantly is that its a waste of energy to produce toxin that just gets smeared everywhere you go.

@DKNguyen: I meant that since flies typically live only a matter of weeks, and it takes at least days for flesh to rot, a fly that eats rotten flesh would have to wait around a long time for something it killed to become edible.  It'd be like a lion killing an antelope, but not being able to eat it until a year later.

@jamesqf Flies don't need to eat rotten flesh. They just do because they are scavengers. They eat plant matter too.

Photosynthesis.
early photosynthesizers, which would have been adapted for a reducing atmosphere, drove themselves extinct as they dumped oxygen into the atmosphere as a waste product. They were incredibly successful because they could live off of little more than the three of the most common materials on the planet. Eventually the oxygen built up to the point mostly only oxygen tolerant or later oxygen using organisms survived.
https://pubmed.ncbi.nlm.nih.gov/20731852/

I think this is a good canonical example, though the answer would be improved with a reference.

Going exinct hardly counts for being successful. Let us, take, e.g., Ebola - a virus that is  efficiently transmitted and quickly replocates, but ends up killing most of the hosts. It quickly goes extinct, because there are no hosts lefts for its replication. If Ebola still survives, it is because it infects animals other than humans, for whom it is elss lethal.
A similar example is small pox, which was less lethal than ebola and therefore continued to circulate in human populatiosn for thousands of years... but became extinct once vaccinces were developed.
On the other hand, flu and cold keep circulating in human populatiosn since time immemorial, and it is not likely that they will be going extinct any time soon, becaus ethey have developed a way of co-existing with their hosts.


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Colorado insect identification
Found this bug in my backyard, but was unable to identify it. Thanks for any hint!
Edit : I live in the south east suburbs of Denver, Centennial.
So this is quite an urban area. I found this bug on my deck, and it escaped going under my deck. The board in the pictures are from my deck (composite, not real wood). My backyard is quite small, mostly grass and not a lot of flowers. The bug's body is around 3/4".

a better location and a descripion of the area you found it will help in identifying the insect,please edit more information into your question.

Thank you, done.

How big is this bug approximately?

Around 3/4" - Edited my description as well. Thank you.


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Hepatic lobules and hepatocytes

"The hepatic lobules are the structural and functional units of the liver containing hepatic cells arranged in the form of cords. "

My textbook says that the hepatic lobule is the structural and functional unit of the liver. I'm confused as to why don't call hepatocytes the structural and functional unit of the liver instead, as they are the actual units secreting phospholipids, bilirubin and other components of the bile juice.
I framed this answer based on my understanding, please verify if I'm right or not and do suggest improvements-
"Properties of the hepatic lobule are not present in hepatocytes, they arise due to the interaction of hepatocytes. Therefore, hepatocytes on their own, cannot be termed as a functional and structural unit of the liver"

Who is "it"? What are the functions of the liver? There is more than one.

"It" refers to my books and teachers. They say that a single hepatic lobule is capable of performing all the designated functions of a liver. But that doesn't make sense to me, aren't hepatocytes capable of doing all of them in the first place??

My question about "It" was meant to prod you into citing your source. A bit of research on your part is expected. No, a hepatocyte can't perform all the functions of the liver. Why would I ask that question if you were correct?

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If you didn't have an utricule or saccule would you still know if you are accelerating and going up or down?
In the vestibular system the utricule and saccule makes you that you know whether you are going up or down (saccule) or backwards/forwards (urticule).
But imagine you don't have them anymore or they are damaged, would you still be able to know if you are accelerating or in an elevator? I thought it still would be possible because you would feel the pressure in you back when accelerating or on your feet when going up. But is it true that you still know what is going on by registrating the pressures in you body, or is it not possible any more? If it is still possible what would the surplus value of the urticule and saccule?

Your semicircular canals are concerned with balance (or spatial orientation). Proprioception, on the other hand, deals with where the body parts are with respect to each other and the physical world. (Some people lump the two; it's easier to think of them independently, because they really do quite different things.)
Proprioception (and closely associated kinesthetics) is possible because of nerve signals from skin, tendons, muscles, and joints. This gives us the senses of limb position and movement, the sense of tension or force, the sense of effort, the sense of gravity.[1] Propioception alone cannot compensate for serious balance problems.
The vestibular system exists through input from three semicircular canals located in the inner ear on each side. The canals are oriented at (basically) 90° angles to each other so that we can maintain our balance no matter which position our head is in. These are also connected to one's ocular reflexes. Together they're called the vestibolo-occular system, which functions as a reflex (VOR).

Three sensory systems, vestibular, visual, and somatosensory/proprioceptive, serve our sense of balance. Each of these systems provides unique sensory information to the brain where it is integrated (often in complex ways) to produce a final motor output to muscle groups for maintaining gaze, head and body posture, and controlling static and dynamic balance.[3]

Without these systems, we would be completely unable to get or stay in a standing position. We certainly could not walk.
An analogy would be to get strapped into one of those spinning seats, in this case, one that rapidly spins inverting you, alternating between forwards and backwards (which would kind of include up and down) but not sideways. You would be unable to focus your eyes on anything. You would see your world spinning, and you would have lost your sense of balance. You would immediately go to the ground, even though your proprioceptors were working perfectly.
However, once you did "go to ground", say, in an elevator, you probably could tell if you were accelerating upwards or downwards. Closing your eyes would help to drown out the more unpleasant 'noise' (input).
So, long story short, the answer is yes. Likewise, you would probably still be able to touch your nose, etc. But it would not be possible to do more complex things, like walk, or even sit unless your back and sides were supported.
[1] Proprioception From a Spinocerebellar Perspective
[2] mpairments of reaching movements in patients without proprioception. I. Spatial errors
[3] Anatomical and Physiological Considerations in Vestibular Dysfunction and Compensation


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How many various types of Memory B cells does an average person has in his body?
Memory B cells are a B cell sub-type that are formed within germinal centers following primary infection and are important in generating an accelerated and more robust antibody-mediated immune response in the case of re-infection.
Now there is an accumulation of cells of a single clone population which expresses many of the one same type of antibody and that these memory B cells survive for long periods of time in a body.
Disregarding the number of different cells applying for one and the same antibody, how many Memory B cells are there in average humans which relate to different antibodies?


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Why do parasites involved with malaria going into red blood cells?
When someone is infected with the mosquito bug which has the parasite, this parasite will go into the liver to grow. Afterwards he goes in the red blood cells and blocking the vains of the brains. But why do they leave the liver and go into the red blood cells?


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Where does the first oxaloacetate comes form in the citric acid cycle?
Oxaloacetate forms together with acetyl-CoA citric acid. Now oxaloacetate is used but also re-used again in this cycle. But where does the first oxaloacetate comes from? Is that from the mother or produced by DNA or....?

There's not just one molecule of acetyl-CoA that's going through the TCA cycle. Every intermediate compound is present at a certain concentration, so there will be many oxaloacetate molecules per cell.
When the cell divides, it's split in two and the contents are also divided. So a new cell will also have many oxaloacetate molecules in it. This way the daughter cell can just keep running.
For the "first" oxaloacetate molecule we have to go back billions of years, and this would be a very complex question to answer. My guess would be that the first oxaloacetate molecule was produced by a non-TCA pathway, and the TCA cycle evolved later.

Great answer. I can't think this question being answered in any better way.

So each daughter cell would have less oxaloacetate? Less cycle input power?


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How many citric cycles are (can) working at the same time in one mitochondria?
Does one mitochondria has a limit of how many acetyl-CoA it allowes within his inner membrane to produce NADHs? And if, lets say 100 acetyl-CoA are in a mitochondria are they simultaniously running through their citric acid cycle or has the mitochondria also a limit for the amount of running citric cycles at the same time?


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Are there examples of human genes using meiotic drive?
Meiotic drive is a type of intragenomic conflict, whereby one or more loci within a genome will affect a manipulation of the meiotic process in such a way as to favor the transmission of one or more alleles over another, regardless of its phenotypic expression. More simply, meiotic drive is when one copy of a gene is passed on to offspring more than the expected 50% of the time.
But do humans have such genes?

Yes! Jeffrey and Neumann 2002 report evidence of meiotic drive at a recombination hot spot in the MHC.
Note that mtDNA could arguably be considered as an extreme case of sex-dependent meiotic drive. Mothers transmit mtDNA at rate of almost 1, while fathers transmit mtDNA at a rate of almost 0.


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Does our heart have to work harder in hot or cold weather?
In hot weather our perspiration is higher and often old people get tired faster when it is hot. But is there a relation between hot weather (sweating) and our heart if so what makes it have to work harder?
And does our heart have to work less (compared to hot) in cold weather where capillaries and vessels constrict, making it harder for the heart to pump blood.


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Setup of terrarium for an early life experiment
I'm building a terrarium in which an early life environment will be simulated. Over multiple years a few experiments with different starting molecules/atoms will be held in it. The selected materials will be manipulated through grinding against each other, being mixed, slow temperature change and radical temperature change. Different starting materials with different manipulations will lead to different new molecules being formed. The more diverse and complex the molecules I end up with are, the liklier it is I'm getting closer to simulating the start of life on a planet. I expect to find ways of recognizing certain molecules through how they 'behave'. The thing I'm most interested in, would be to map out what types of changes in environment are required to get over hurdles in which diversity or complexity start to stagnate.
The way I imagine I could set it up:

Get a very big, cleaned transparent plastic bag that's flexible enough for hands to be able to grip objects through it.

Put the bag around the terrarium, the selected prepackaged molecules, gas bottles, a bottle of alcohol and some tools.

Close the bag and install a small pump on its surface.

Pump as much air out of the bag as possible.

Release some gas from the bottles inside the bag to make working easier. (Else the bag sticks to the open terrarium-box)

Cover everything inside the bag with alcohol.

Pump all the gas out again and release new gas from the bottles.

Clean the insides and the lid of the terrarium with towels.

Open each bag of molecules (salts, carbon, water, etc.) and drop the contents into the terrarium.

Seal the terrarium very well.

Are there any better ways of sterilizing an environment to a point where no molecules formed through evolution on earth are inside of it?
E.G. heating it for a long time, drenching it in a base/acid...

I don't want to discourage you from at-home experimentation, but this isn't going to work. Everything that goes into the chamber needs to be sterile, not just clean. Bacterial spores, for example, can be extremely resistant to many forms of cleaning and sterilization - some can survive high doses of radiation, others the vacuum of space. Creating clean rooms is a whole industry in and of itself, and involves everything from the air circulation systems to the water to gasses to the materials of each surface, plus a ton of experience and lots of validation to make sure it actually is clean.

Aside from the extremely difficult mechanics of setting everything up and keeping it sterile, what are your endpoints going to be? You say you're working with "molecules" - how are you going to tell if your experiment is successful? What exactly are you looking for?

Please clarify your specific problem or provide additional details to highlight exactly what you need. As it's currently written, it's hard to tell exactly what you're asking.

See a somewhat related question on Space.SE involving the difficulty in ensuring spacecraft do not accidentally bring organisms to other places: https://space.stackexchange.com/questions/54293/is-there-any-demonstrated-or-even-proposed-technology-that-can-sterilize-a-space

@MattDMo thanks for taking the time. I'll elaborate at the top of the post and make the question at the end of the post more specific.

@Bryan Very interesting. Thanks you!

I suggest you investigate chemical means of cleaning - strong acids (3-5 M nitric, 5 M HCl) neutralized with strong base (NaOH) should work. Note that we don't actually know the conditions in the early earth, but a number of "biological"-like molecules are found in the spectra of stars and in lunar dirt, meteorites etc.

this may save you a lot of trouble, this is not an easy experiment to duplicate in a small school lab but it is doable. https://www.youtube.com/watch?v=Mp9l3LhPLgE