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Is retinoblastoma truly an autosomal dominant condition?
I am getting, in my opinion, very conflicting information from sources about the inheritance of retinoblastoma, a type of cancer. Hereditary retinoblastoma is associated with defects in the gene encoding the cell cycle-regulating, tumor suppressor protein RB1. Most sites claim that retinoblastoma is inherited in an autosomal dominant manner, which would suggest that the offspring only need one defective  allele to inherit the condition. At the same time, however, all online sources claim that only one working copy of a tumor suppressor gene is required to maintain its functionality and that both copies of a tumor suppressor gene must be defective for the onset of cancer. This understanding is known as the two-hit hypothesis. But to me, this idea clearly conflicts the claim that retinoblastoma is an autosomal dominant condition and suggests the opposite: that, in order to develop retinoblastoma, there can be no working copies of the RB1 (tumor-suppressing) gene (hence making retinoblastoma an autosomal recessive disorder).
I don't know if there are any flaws in my interpretation and if somehow both explanations are correct with the issue being me not understanding it clearly. How can a condition be autosomal dominant (i.e. requiring only one affected allele) while also only requiring one working allele to prevent it? It seems illogical.

Welcome to Biology.SE. Please add references and/or links for your sources. In addition, it would be helpful if you included a quote from at least one of the sources claiming autosomal dominance for retinoblastoma — there may be some context you are missing. Also note that it is possible for a gene to have both dominant and recessive alleles or even for an allele to be both depending on the phenotype under consideration ...

"Dominant" and "recessive" have a philosophical quality, and this makes them more confusing than an introductory course will suggest.
You could argue that Rb "really" has incomplete dominance in that Rb(+/+) embryos survive, Rb(-/-) embryos mouse embryos die at E13.5-E15.5, whereas Rb(+/-) embryos often die from tumors after birth.  But from a practical point of view, if you have a patient with retinoblastoma or achondroplasia, you'll be drawing a pedigree in which anyone inheriting one copy of the gene has the same issue.
Additionally, we have the issue of cell-autonomous phenotypes.  In the case of retinoblastoma, any given cell has a very low risk of losing the other copy, and you can think that at the level of the cell it is almost like it is "recessive".  The risk of forming a tumor is higher, but you won't see that in any random cell under your microscope.  So the phenotype in this case isn't cell-autonomous.  (I haven't researched whether there is any other cue you can observe that would allow you to score single cells as Rb(+/-) on sight, but I know they don't get tumors!)
Bottom line: when describing an allele as "dominant" or "recessive" at the level of the organism, think about it from a genetic counseling point of view.  Do both parents transmit the allele (or an allele that subsequently underwent mutation) to affected offspring, or just one?

Hi, I think you were hinting at this in your answer though I've found a rather lucid explanation: "If a person has inherited a[n autosomal dominant] cancer susceptibility gene, it does not mean they will automatically develop cancer. It simply means that the person has inherited a mutation in a gene that gives them a higher chance to develop cancer than someone without the mutation" from https://www.urmc.rochester.edu/encyclopedia/content.aspx?contenttypeid=85&contentid=p07104. Thanks a lot for the reply!

@ZuhairQureshi Retinoblastoma is, unfortunately, a poor example for this.  The penetrance of the tumor phenotype is over 90%, and 40% of affected children develop tumors in both eyes independently.  There are lower-penetrance variants of the condition, but whenever it takes only one allele to increase the chance of a tumor, it is still dominant.

Two-hit theory/Knudson Hypothesis is for sporadic development of retinoblastoma, once it develops it is transmitted to the offspring in an "autosomal dominant" fashion.

https://eyewiki.aao.org/Retinoblastoma#cite_ref-Shields_text_3-1 read this for more info

So the sporadic form of retinoblastoma requires both copies of the alleles to be defective, but then when transmitted to the offspring in a hereditary manner, requires only one defective allele? If not, then how are you defining " 'autosomal dominant' fashion"? I read the link you posted and it feels quite similar to what I was reading yesterday: saying the disease requires both alleles being defective to develop while still calling the disease autosomal dominant. Thanks for the help.


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Examples of passive membrane transport proteins that only transport in one direction and their mechanism
I would like to know about those transporters with alternating-access-type mechanism, that can only efficiently shuttle molecules in one direction but the other direction is severely kinetically inhibited. From this question I know that they exist, but Google searches are futile in finding examples. Wikipedia is not much help, either. I also skimmed the seventh chapter of the Campbell biology book, about the structure and function of the cell membrane, but there was no clue.
More generally, I have found examples of enzymes that is inhibited only in one direction, such as F1-ATPase (even without the inhibitory epsilon subunit) with its mechanism of ADP inhibition, which primarily affect ATP hydrolysis and not ATP synthesis. I just have not found examples of this in passive transporters specifically.
Furthermore, is the mechanism of unidirectional inhibition inherent to the transporter domain itself, or does it require a separate domain, as in the case of the voltage-gated ion channels, to sense the gradient flowing in the other direction and then inhibit the transporter domain?
Is there even an universal mechanism?
My guess for an universal mechanism would be the former, as I am aware of the basic kinetics of the active ABC transporters, in that they preferentially open to one side of the membrane.

“Google searches”? Have you tried Wikipedia, or a text book, or  a Google Scholar search for reviews or looked on NCBI Bookshelf? We welcome you to SE Biology, but suggest that you finish reading the [Tour] and then look at the Help on Asking Good Questions. A single specific question expressed clearly and precisely — independent of the title — is what is required. Please do some more research and then focus. At the moment you start by asking for a list, and end by floating ideas on the evolution of transporters. Again, focus.

id be interested to know if there is such a review.  between archaea, eubacteria and the many many branches or eukaryota i doubt if this is entirely known.

Voltage-gated proton channels are passive transmembrane transport proteins that will only transport protons in one direction. These channels will be open when there is a lower pH in the cytoplasm, allowing protons to flow out of the cell, but will close when the pH is higher in the cytoplasm, not allowing protons into the cell. [1] In this case, the protein does not sense the direction of flow, but rather opens only in conditions where one direction of flow is possible.
Most voltage-gated proton channels have a separate voltage-sensing domain from their pore domain. However, HV1 does not have separate voltage-sensing and pore domains. [2] Therefore, neither combined nor separate regulatory and transport domains is universal. I am not aware of the mechanism in either case, or whether their are other proteins with different mechanisms.

DeCoursey, T. E. (2003). Voltage-gated proton channels and other proton transfer pathways. Physical Rev, 83, 475-579. https://doi.org/10.1152/physrev.00028.2002
DeCoursey, T. E., Morgan, D., Musset, B., & Cherney, V. V. (2016). Insights into the structure and function of HV1 from a meta-analysis of mutation studies. J Gen Physiol, 148(2), 97-118. https://doi.org/10.1085%2Fjgp.201611619

I'm fascinated by such questions @symmetrickittens so i'll just post a first pass here.
There are probably too many families which are not characterized right now to make a comprehensive answer.  This review estimates that 21% of prokaryote proteins are integral membrane proteins.  A large percentage of these are of unknown function, and there are many variants of each gene which may be functionally distinct.   This last reference just talks about the human proteome.  Each new genome sequenced has a substantial proportion 20-40% of protein products predicted with no clear function [anecdotal recollection from reading genome papers].
As such there are some nice reviews taking some fat slices of sequences which are really exciting to read (if you are a nerd like me). The above reference predicts 1700 structural membrane protein families.  This review of human membrane proteins discusses 89 transporter families but leaves 41% of membrane proteins uncharacterized.  Remembering that we diverged from eubacteria the better part of a billion years ago, there are probably well more than 89 protein transporter families!
A good fraction (majority?) of research is focused on human biology. If you can get used to the idea, then starting with the human transport protein proteome is not a bad place to start.  Here is a link to the Transporter Classification Database from the Saier Lab at UCSD.  They have proposed 1708 families of transporters.  I sincerely doubt they are promising not to discover more!

Uh... perhaps I was not clear enough. I asked for list/examples of a very specific kind of membrane transporter. I edited the question to reflect this. But you are somehow very informative, nonetheless.

TOM porins are an example.  https://en.wikipedia.org/wiki/Translocase_of_the_outer_membrane

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Why is random protein selection not used more often in biotech to create proteins with desired enzymatic activity?
mRNA/cDNA display allows random libraries of up to ~ 10^13 proteins to be subject to selection for binding to arbitrary binders. In the listed studies, proteins selected for ATP binding also had ATP hydrolysis activity. This likely means that selection for transition state analogue binding can create enzymes as well, or at least functional uniform binders. More stringent selection schemes with lower diversity can then be used to improve this initial activity.
Functional proteins from a random-sequence library
ATP selection in a random peptide library consisting of prebiotic amino acids
The question is, why isn't this process used more in biotechnology to create proteins with the desired enzymatic activity? Is scouring database for appropriate natural proteins that much more better, or are there technical barriers that I'm missing here?

Used more often in biotech to do what?

To create proteins with desired activity for what purpose? "Biotech" is extremely broad, covering everything from basic research to pharmaceuticals to food to engineering problems.

I have narrowed it down to enzymatic activity.

Think about it - if you can find an existing protein with [some of] the characteristics you desire, why would you go through the bother and expense of creating something from scratch?

I'm not sure if this is the kind of tools you are asking for. "https://pubmed.ncbi.nlm.nih.gov/16919347/". They uses an evolutionary algorithm to search proteins with high enzymatic activity.

Think about it from a numbers perspective. Briefly, $10^{13}$ is a very small number in the combinatorics of protein sequence space.
There are $20^{100} = 1.267651*10^{130}$ possible peptides of 100 amino acids, a rather small protein. That's more proteins than there are atoms in the universe by 50 orders of magnitude. If you like, here's a paper I found via google that happened to pick this same example, they also have some discussion of the sequence space of naturally occurring proteins.
Do you want to do $10^{117}$ such $10^{13}$-plex random peptide experiments to on average 1X sample that 100 amino acid sequence space, or do you want to do one single $10^{13}$-plex mutagenesis experiment on a known protein that kind of does what you want already, which will let you readily sample the local sequence space around that protein?
You can undoubtedly shave a few orders of magnitude off there by encoding your random peptide generative model with non-uniform aa sampling, structural motifs, sequence Markov models, or whatever. But that isn't going to help you very much. You could also argue that you don't have to exhaustively sample the space as long as you get in the locality of something useful. But a useful protein is almost certainly longer than 100 aas, so you still need to sample astronomical numbers of random proteins.
Even if you get lucky with your random polypeptide approach, you are almost certainly only sampling an unoptimized protein, so you will have to turn around and optimize whatever random polypeptide you find.
The existing protein can admittedly probably only get you to a local optimum. But the search for the global optimum is through an incredibly massive domain of possible proteins.

I was expecting more of a technical than theoretical answer. My intuition is that every approach will have pros and cons, and random protein generation has to have pros too. It would depend on the details of the process.

@symmetrickittens certainly, I've addressed the pro already: it's possible to search for a globally (or "less locally") optimal protein. That could readily be worth the search, we have no reason to expect that existing enzymes are globally optimal! As for theory vs. technical, search through sequence space is theory, on their own the numbers are pretty daunting. Empirically, consider the ratio of de novo gene birth vs. gene duplication as ways of generating useful genic sequence in genomes (a ratio of "very few" to "almost all"). If I have a little time later, I can try to add to question.

@symmetrickittens put differently: when the numbers are this far against you, the theoretical becomes the technical. My knowledge of the breadth of the Pacific Ocean is theoretical, but it gets technically useful when considering whether I can row to Australia from the N. American west coast.

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Do the eggs of fraternal twins come from the same ovary?
With fraternal twins two matured eggs are released and fusion of the two with sperms result in formation of these fraternal twins. Then do the two matured eggs come from one ovary or both the ovaries at the same time?

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Immune system initial response
One thing i can not still comprehend about the immune system is the following:
A bacteria is first recognized by neutrophiles. But then neutrophiles have to have the ability to release chemotaxines upon the recognition (or the bacteria?)? Its not mentioned anywhere in my script how macrophages and other non abundant innate immune cells come to the source of an infection in details.

Have you looked into the role of the complement system? It generates cytokines. In fact those molecules play a role in attracting neutrophils.

On the contrary it's not neutrophils that initially recognize a threat, but rather distressed epithelium, and immune cells like DCs or macrophages that are already distributed in the tissue that recognize pathogen- or damage-associated molecular patterns (see PAMPs and DAMPs). The primary response to these patterns is the secretion of cytokines.
Among the many cytokines secreted include a subset known as chemokines, from the Greek work for movement. The combination of chemokines and cytokines induce chemotaxis of immune cells circulating in the blood, such as neutrophils, by telling these cells that the nearby tissue is inflamed. IL-1ß, IL-6 and CXCL2 are examples of neutrophil attractants secreted by macrophages and monocytes. Complement fragments like C5a are also known to induce an inflammatory response, inducing the secretion of these molecules.

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Do cows chew in a preferential chirality?
One of the enduring myths in molecular physics, when talking about chirality as pertains the existence of enantiomers and the differences between them, is that the way cows chew is also chiral, i.e. the up-and-down and the around-in-a-plane movements combine in such a way that you can distinguish a cow chewing from its mirror image. This is mentioned in e.g. Wikipedia, among other resources.
A recent question in the Physics site asked for the source of this factoid, which turns out to be

Movements of the Lower Jaw of Cattle during Mastication. P. Jordan and R. de L. Kronig. Nature 120, 809 (1927),

and this is a rather unsatisfactory source: they report on a survey that finds that 55% of cows chew in a 'right-circular' fashion and 45% chew left-circularly, but they then go on to disavow any statistical significance in the result:

The number of observations was, however, scarcely sufficient to make sure if the deviation [in the ratio of the two kinds] from unity is real.

Given that this isn't a physics question, I thought I'd bounce it over to the mammalian behaviourologists out there: have there been further studies about which way cows chew? I imagine that they're out there, but I wasn't able to find them.

I'd say as a biologist it's almost as interesting if individual cows indeed chew a constant direction (sort of analogous to 'handedness') versus whether there are population-level biases toward chewing a certain direction. If the former is true, regardless of whether the average cow has a biased direction it makes a reasonable entertaining example. Interestingly, Google Scholar notes just 6 citations of the paper you refer to; all 6 are making the chirality connection, none of them have any association with biology whatsoever.

@Bryan That's an interesting distinction I hadn't considered.

It seems there is a commentary on that original article RIEHM, H., & GUGGENHEIM, E. (1928). Movements of the Lower Jaw of Cattle during Mastication. Nature, 121(3045), 357. - they comment that they observe the same direction of chewing in an individual when taking in food and ruminating. They also point out that since the direction of food travel is opposite, the same direction of rotation makes them both left and right handed with respect to food travel. I find that argument a bit silly from a biology perspective but maybe a physicist would appreciate it. :)

Another related example from biology is hand-clasping: when you interlock your fingers together, which thumb is on top? Individuals have a strong bias. Interestingly, this is independent of left/right handedness, and also independent of arm-crossedness: when you cross arms, which hand goes under and which goes above the upper arm? There is some loose correlation with parents for these traits, but in the overall population they are not particularly biased.

This study deals with the chewing direction of cows. It splits the chewing into three phases, the first jaw movement, the middle ones and the last one. It finds out that the first one is always in the opposite direction of the middle ones, that generally the middle ones are usually in the same direction and that seemimgly cows change chewing direction from one middle jaw movement period to another.

@BrianKrause here's a partial answer to your comment, even with a small dataset and no statistics attached to it.


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Betaine HCl stomach pH
It seems betaine HCL is often recommended for those suffering from "low stomach acid" -- which, as I understand, is having too high stomach pH for proper digestion (especially for proteolysis via pepsin). However, I have a few questions then -- though I'm not sure if my reasoning is correct here:
Understandably, one wouldn't want to drink pure or highly concentrated HCl by itself to increase stomach acid! But then, what role does the betaine play?
I'm guessing betaine HCl probably does not dissolve in water to give the same pH as just straight (or concentrated) hydrochloric acid -- since then it would seem just as dangerous as drinking plain HCl!
In that case, if it doesn't decrease the pH as much, making it safe for oral consumption, what value does it bring for "lowering stomach pH" anyway? I mean, one could just drink a little vinegar or citric acid for the same effect?
Or, perhaps, is betaine-HCl just a means of some "delayed release" of HCl to lower stomach pH without hurting the mouth and esophagus during its initial consumption? Betaine may just be a useful carrier here, given it's quaternary ammonium and carboxylic acid groups (e.g., a zwitterionic carrier)
Alternatively, could the value of betaine HCl simply be in providing a source of Cl- anions, possibly for increased pepsin activity? (I'm not sure if pepsin requires merely low pH or specifically also needs Cl- anions as well) Betaine-HCl does seem to be often formulated with additional pepsin enzyme(s) as well...

Betaine HCl (trimethylglycine) was present in over the counter "stomach acidifiers" but the US FDA says there is no evidence for its efficacy and has banned its use for this indication (source: US FDA) - it may be freely available elsewhere, I am unaware of the regulatory status in other jurisdictions.
There is no biological reason to expect the "HCl" portion for most drugs to have any substantial effect on stomach acid. Lots of drugs are packaged in an acidic form as "drug HCl" - this is usually because the acidic form of the drug is more soluble. Drug doses are commonly in the microgram to milligram range (though obviously this varies for different drugs) - at those concentrations, the stomach acid is much too concentrated to be affected by the small amount of acid added from the drug.
The catch with Betaine HCl is it looks like websites are advocating for taking several grams to provide enough HCl to affect stomach acid. I suspect that supplement makers suggesting these high doses is what led the FDA to ban the drug OTC in the first place. Although betaine is produced as part of normal metabolism, there are some side effects reported, mostly mild.
Note that anhydrous betaine is prescribed (and approved by US FDA) for homocystinuria, and used as a supplement to animal feed, but neither application is related to stomach acidification (and the anhydrous form is not acidified).
One recent study supports use of Betaine HCl with patients who are being treated with acid-suppressing drugs such as proton-pump inhibitors, to be given along with other drugs that require an acidic environment to function/be absorbed. However, it is important to note that this study was in fasted patients: they consumed nothing but a little water with the betaine HCl. In this circumstance, the little bit of HCl in a moderate to large dose of betaine was sufficient to lower stomach pH. However, the results likely would have been very different if the patients had eaten a recent meal.

+1 Great answer, looks like skepticism was the right call here indeed, according to WebMD as well : ) http://www.webmd.com/vitamins-supplements/ingredientmono-312-betaine%20hydrochloride.aspx?activeingredientid=312&activeingredientname=betaine%20hydrochloride

@ManRow Yeah I actually saw the webmd note first but then went looking for some more robust sources. :)


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What is the latest estimated probability for the self assembly of a primitive cell?
Peusner (Concepts in Bioenergetics, 1974) estimated the probability of the self-assembly of a primitive cell as $10^{-254}$. Given how much more we now know about cell biology, what is the latest consensus figure? I've found lots of papers and discussions about the mechanics but I haven't seen anyone else put a figure on it.

Is a primitive cell a protocell or protobiont in this context, or more like a modern cell as we find them today? Or something else?

I hate to say it, but if you can’t find such a figure, nobody here is likely to — probably because such calculations are not testable and have no relevance to experimental biologists. And why give a link to the Wikipedia entry for “cell biology”?

@Galen The best description I've found is "partitioned units resembling modern cells."

@David Surely it can be modeled?

I imagine so. But the devil is in the assumptions. It's all so much medieval theology — angels on dancing on the head of a pin. Biology is a practical subject.

@David I can't believe no-one's even ball-parked it though, there must be someone who has run the numbers.

It is easily the case that no one has 'run the numbers'. As David points out, there are different combinations of assumptions one can make. I rate them somewhere above "medieval theology" since we can impose physical laws and established statistical trends, but  even so they are quite varied and speculative. Even if some calculations have been done, it isn't clear how a 'best' figure could be chosen.

@Galen I can't quite dismiss it as theology either. Surely it's a significant factor in the estimation of the extent of extraterrestrial life?

There might be a marginal probability of life forming in a uniformly sampled region of space, but I doubt we are close to having such a number that we can have confidence in. Assembly theory seems like a more promising approach to identifying biosignatures, but that approach is still in its infancy.

I think an explanation of why this would be almost impossible, as a 'frame challenge', would be useful. .

See What is a frame challenge? and Does Stack Exchange allow for answers which question the validity or stance of the original question?.

@user438383 It's possible to estimate badly but it's not impossible to collate all of the developments of the last 50 years and update Peusner's estimate. If he was even half right then we are alone in the universe so it's not an inconsequential question.

@Jack - Does it really matter if we are alone in the universe? Does life elsewhere out there give meaning to our existence? If a million lifeforms exist that we will never encounter (a strong possibility, that latter phrase), does it mean our lives are less meaningful? It's interesting to speculate, but that's all it is, speculation.

@anongoodnurse It matters in the sense that it ceases to be an area of worthwhile research.

@Jack - I'm not sure of its worth right now. We have war, poverty, disease, starvation, lack of potable water, etc. Many things to take care of at home on our little watery rock.

It's not a useful question, as a majority of the discussion above has been trying to point out to you.

@MattDMo Of course it’s a useful question, because it’s a proxy for how much we actually know about the associated processes.

It's not a useful question for this site. It has 3 downvotes and 5 closure votes (some may be by the same people). I'd say that's a pretty clear consensus by the established users. And, as Maximilian points out in their answer, it's not the only way life could have evolved, so I'm not sure it's that useful in general. At any rate, I'm not going to debate this any more. You asked a question in a comment, I answered it. You can agree with it or not.

@MattDMo But how would you even compare two different accounts without calculating either probability? This makes no sense.

I think that it's worth directly examining the citations of the book in question.
In doing so, I found the following quote:

The abundance of the first 31 elements in the Periodic Table on Earth and in the known universe is highly correlated: Peusner [11] estimated the self-assembly of a primitive cell occurring as a spontaneous act, where the molecules and elements were present at a specific location on the Earth in a suitable sequence, as 10−254. Conversely, even a highly improbable event can occur. This only adds to the paucity of information and the confusion we struggle with when researching the origin of life. According to Peusner [11] this suggests the origin of life and evolution occurred in an ordered manner from the simple to the more complex.

In other words, there is a counterfactual to "self-assembly of a primitive cell" for the origin of life. Peusner himself seems to have considered this a somewhat ridiculous straw man according to this reading, not that I've directly read his book- in other words, abiogenesis via spontaneous generation of cells isn't constantly happening all around us, which hopefully isn't news to anyone.
Instead, the argument goes, you could gradually add components until you ended up with a primitive cell. This would presumably involve a sequence of still-improbable-but-much-more-probable events. This would presumably involve the RNA world or other such cases as intermediate steps to a cell. I am not sure what the probability of such things is, but there does seem to be some amount of speculative literature on this out there.
NB: I infer from the comments that you are mostly interested in xenobiology and the probability of other life existing, and are only interested in the cell assembly probability as the presumed path to the existence of life elsewhere in the universe.

'gradually add components until you ended up with a primitive cell' sounds ridiculously panglossian without any math derived from established biological and physical processes. With 50 years' of additional research, we must be able to make a more educated guess, but it seems like the answer to my specific question is that there is no more current estimate.

@Jack I think the point is that it's less panglossian than "cell from nothing", which seems to be what you're asking about. The lack of additional research on "cell from nothing" might be taken as a clue of how viable a path it's considered to be, whereas origin-of-life research is alive and well on other possibilities.


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What is the physiological difference between looking at small things vs far away things?
If you look at an item that is far away, vs a smaller version of the same item up close, such that both objects take up the exact same degrees of arc in your field of view, what do your eyes do differently to focus on that item? I know that your brain may interpret the information differently, but do your eyes themselves actually do anything different?
Edit:
What I've looked at so far:
I have already learned about the basics of how the eye uses ciliary muscles to bend the lens to look at up close objects, and then relaxes in order to look at far away objects.
What I do not understand is how, or even whether, the eye behaves differently when dealing with size. For example, what is the difference between reducing the font size on your computer monitor vs simply moving your computer monitor further away? You can reduce the seconds of arc taken up by the text by either method, and decrease the angle of the light hitting your retina by the same amount.
I have read many articles and watched videos about how the eye works, but all of these materials have focused on distance of viewed objects from the observer, without regard to size. My question here has to do with how or whether changes in size of an observed object elicts a different physiological response than moving that object closer and further away.

Welcome to the site. What research have you done on your own to answer this question? The Biology.SE community has agreed that questions that show little or no prior research effort are off-topic on this site unless you have shown your attempt at an answer. Please [edit] your question and tell us where you've looked for answers, what you do know about the topic, and where exactly you still have questions. Our goal is not simply to be an answer site, but rather a site that promotes self-learning with some expert help along the way.

Please read about the lens of the human eye.

@anongoodnurse I've read a lot about the mechanisms by which the eye works including but not limited to the functioning of the lens and the muscles/tendons surrounding it. Now, I've only gone as deep as learning about ciliary muscles / zonular tension, but so far I've found nothing that moves in the direction of answering this question, which is why I'm here. What specifically regarding the lens are you referring to? Thanks. Again, I'm asking specifically about situations where the same percentage of your field of view is taken up by these different-sized versions of the same object.


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What is the best estimate of RGB color sensitivity of human eye?
Web has a lot of references for human eye color sensitivity curves. Examples are

This article:
J.J.Vos, Colorimetric and Photometric Properties of a 2° Fundamental Observer (1978) [3]
has a very different dataset that has maximum of the blue channel sensitivity at about 33 times lower compared to the maximum of the green channel sensitivity. This paper also has the red channel maximum higher than the blue channel maximum, and the second graph above has them all the way around.
What is the current best state of knowledge about spectral curves of RGB channels of human eye?
Are there numerical tables that approximate these spectral curves?

What do you mean by "sensitivity"? I think you'll find these charts are all using different measures rather than conflicting in any substantial way. And what is your ultimate goal: what do you want to do with this information?

By sensitivity I mean the amount of perceived brightness per photon of light.
The purpose is research is color perception. I have some ideas about how to improve computer cameras' color perception and would like to have an accurate information on how human vision perceives light.
Corresponding sensitivity curves for cameras are called "quantum efficiency" and are typically published in camera specifications.

If you want to know about perception, then you will want to study perception, not the sensitivity of individual cones, and you don't need to know about different receptor types at all but rather about perceptual sensitivity itself. There's also a big difference between sensitivity in terms of "can you detect a brief, dim flash" versus discrimination: can I tell this color from that color. Both are going to be complicated by conditions in ways that a physical camera is not.

My research focuses on numerical values and numerical processing.
I also don't think that this question is meaningless. One can have a blue light with a fixed intensity and a red light with a fixed intensity and it is possible to compare how bright does a human perceive it.

I'm not saying the question is meaningless, I'm saying it needs to be made precise, and that if you want to know about perception it's wrong to base your measurements on photoreceptor cells in the retina. The perceived brightness of a blue light of fixed intensity and a red light with fixed intensity will depend on a lot: how bright is the room, and what color light illuminates it, or is it completely dark? If completely dark, for how long before the stimulus? Is it a flash or constant light? etc... Perception isn't a camera.

I understand this. For flash vs. permanent light there should be two different spectral graphs. For low vs. high intensity there again should be two different spectral graphs. When the light hits the retina it creates some effect that depends on the wavelength. I am interested in the intensity of that effect depending on wavelength and type of sensing cell (RGB).

"I am interested in the intensity of that effect depending on wavelength and type of sensing cell" - again, do you want perception or retinal physiology? If the former, "type of sensing cell" doesn't make any sense.

@Bryan Krause, isn't the perception adjusted to compensate using 3 different channels which can be amplified or attenuated for accuracy?

@jenniferM.  They use spectral photometry of isolated cells to measure the responses... https://scholar.google.com/scholar?hl=en&as_sdt=0%2C5&q=photoreceptor+spectral+photometry&btnG=

The graph of same amplitudes is called a normalized view, the peak of the three graphs is multiplied to 1.0... It doesn't really matter about the individual cone/rod efficiency because there are different counts and ratios of them as necessary.
The relative spectral sensitivities of the five photoreceptors in human retina, including S-, M-, L-cones, rods, and ipRGCs (A), LED spectral distributions (B), and LED chromaticities in CIE color space. (ref 2015)

Scientists use spectral photometry of cells and measure their response, so that's the field you can study to know the spectral sensitivity.
The brain/ganglions can adjust for differences to give a balanced/optimized mix, and there can be 2 times more of a specific receptor cell type if it 0.5 times as receptive, so the perceived view is more or less psycho-normalized to see white accurately.
Current understanding is that the 6 to 7 million cones can be divided into

"red" cones (64%),
"green" cones (32%),
"blue" cones (2%)

based on measured response curves. They provide the eye's color sensitivity. The green and red cones are concentrated in the fovea centralis . The "blue" cones have the highest sensitivity and are mostly found outside the fovea, leading to some distinctions in the eye's blue perception.
The cones are less sensitive to light than the rods, as shown a typical day-night comparison. The daylight vision (cone vision) adapts much more rapidly to changing light levels, adjusting to a change like coming indoors out of sunlight in a few seconds. Like all neurons, the cones fire to produce an electrical impulse on the nerve fiber and then must reset to fire again. The light adaption is thought to occur by adjusting this reset time.
The cones are responsible for all high resolution vision. The eye moves continually to keep the light from the object of interest falling on the fovea centralis where the bulk of the cones reside.


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If we cloned an extinct animal, what would become of its gut biome?
If we cloned an extinct animal like the mammoth, what would become of its gut biome?

Seems like it would depend on the animal rather than an absolute answer that applies to everything.

Got like seven questions here. Would be easier to give a straight answer if you narrow it down a bit.

any one of these questions would be a good question, but you need to pick one.

The gut biome would be populated from whatever the environment was of the newly "cloned" animal.
Presumably the baby animal would be born by birth from a live host mother, which would be the likely source for microbiota, similar to other animals.

I think this is about as good of an answer to this question one can givd. But out of curiosity: is it really safe to assume that any microorganisms capable of populating the gut of the host species, are also able to populate that of the (extinct) cloned species? Are species separated by (say) tens of millions of years of evolution typically able to host similar microbiomes?

@gaspanic I think that we can expect there to be some dropout relative to the mother. But that's true even of mother-child pairs of the same species! For example, the fecal/gut/vaginal microbiomes of the human mother are contributors to neonatal gut microbiome. that doesn't mean that the infant gut is exactly those communities! As they say in ecology, "everything is everywhere but the environment selects", which isn't exactly true but is a good way to think about colonization.

Right, I agree that mother and child will by no means have identical microbiomes. I was more thinking in terms of whether co-evolution between host and microorganisms could have led to some of the microbiome species being directly incapable of thriving in the "cloned" species gut. But maybe it's too far-fetched to think that a "cloned" species that is similar enough (evolutionary speaking) to develop in its host, would be different enough to significantly affect the ability of some of the host's microorganisms to colonize its gut.

@gaspanic there is some work on coevolution of gut microbes and host, but I find the work somewhat unconvincing as a general rule. There are some specific hybrid lethalities in wasps driven by microbiomes, and a little evidence for human genetic variation associations, but it seems very case specific. Mice will grow transplanted human microbiomes just fine.

Thanks @MaximilianPress, will check these out! Not my field of expertise.


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Does digestion require hydrochloric acid?
Would our digestion function any differently if we secreted something else, like sulfuric or nitric acid, instead? I'd assume an acidic environment may be required, but not sure if chloride is also required as well!
Perhaps we just use it out of convenience—e.g., presumably blood serum $$\left[\ce{SO4^2-}\right] + \left[\ce{NO3-}\right] \ll \left[\ce{Cl-}\right]$$ and channeling polyatomic ions across the membrane may be significantly more difficult than doing the same for chloride as well!
*Edit: In fact, Wikipedia states

In the stomach, chief cells release pepsinogen. This zymogen is activated by hydrochloric acid (HCl), which is released from parietal cells in the stomach lining. The hormone gastrin and the vagus nerve trigger the release of both pepsinogen and HCl from the stomach lining when food is ingested. Hydrochloric acid creates an acidic environment, which allows pepsinogen to unfold and cleave itself in an autocatalytic fashion, thereby generating pepsin (the active form). Pepsin cleaves the 44 amino acids from pepsinogen to create more pepsin.

So, while maybe something like $\ce{H2SO4}$ or $\ce{HNO3}$ could work too, hydrochloric acid is just more convenient to use?

Parietal cells use ion pumps to expel protons and chlorine ions into the lumen, which create the necessary acidic environment to denature pepsinogen into pepsin.
It is the low pH environment that reconfigures or denatures pepsinogen into pepsin. The acid used does not matter. For example, one experiment in classifying properties of pepsinogen used a 3.5 pH solution of 0.5 N sulfuric acid to activate pepsin.
We evolved stomachs with parietal cells that use an energetically expensive process to maintain the acidic gradient necessary for digestion and protection from pathogens.
It may be that biochemical pathways to generate other acids did not evolve, because it is either energetically cheaper for these cells to make HCl, compared with other pathways that would generate other acids of sufficient strength; or the relevant chemical components involved are more abundant than others in what we eat and drink, and thus easier to make in quantities needed for digestion and defense. Chloride ions also serve a role in maintaining intra- and extracellular fluid pressure and thus play a larger part as electrolytes in the normal function of the body — they are available and cells use them.
But to answer your main question, an acidic environment activates pepsin, and it is not chemically necessary for this to be created by hydrochloric acid.

“Why pump chloride ions at all ?” , if our requirement is just acidic environment to denature pepsinogen to pepsin , I think hydrogen ion does a good job at that , by adding chlorine we are effectively slightly reducing acidic strength

@Chemist See https://en.wikipedia.org/wiki/Parietal_cell. Chloride is secreted as an exchange to bicarbonate.


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Can humans metabolize D-malate?
Only the L-isomer is produced naturally, while racemic mixtures are produced synthetically and used commercially as food additives and energy supplements.
So what happens when we consume D-malate? Does it just partake in the Krebs cycle, the citrate-malate/malate-aspartate shuttles, and such like the L-isomer?
Or, does it just bioaccumulate and/or inhibit these processes? Until it gets excreted out?

An interesting fact that is probably of no physiological relevance, but nonetheless interesting, it that the product of the reduction of oxaloacetate by isocitrate dehydrogenase is D-malate! (see Reduction of oxaloacetate by pig liver isocitrate dehydrogenase) OAA is a very good substrate for ICdh.

I do not have specific proof, but I strongly suspect that the answer to this question is NO on the basis of the following arguments.

The overwhelming majority of sugars, amino acids, carboxylic acids
and other metabolites with and asymmetric carbon atom have been long
known to occur in only a single enantiomeric form within living
organisms. This was established long before the nature of the enzymes that catalyse their reactions were characterized.
Since the 1950s and 1960s we have understood that the stereo-specificity of enzymic reactions reflects the weak but binding of (co-)substrates to specific chemical groups of amino acid residues in the active site, and the subsequent flow of electrons between the bound components (often including the amino acid residues). The overall three-dimensional structure of the interactions that allow such catalysis only occur with one form of the enantiomeric metabolite.
The fact that malate (e.g. in fruit such as apples) only occurs in the L-form indicates that the reactions which involve it (predominantly malate dehydrogenase and fumarase) conform to the principle just expounded.
Although racemases (enzymes that interconvert enantiomers) exist for certain compounds in certain species, malate racemases have only been reported in obscure bacteria. They are not known to be present in man.

The problem is that this is so well established that studies with D-malate of relevance to the question are hard to find. One thing to do would be to examine the three-dimensional structure of malate dehydrogenase with a suitable malate analogue bound and model the enantiomer. This requires some work — a cursory trawl shows that usually the enzyme is crystalized with the product, oxaloacetate bound.
I have not looked at the mitochondrial transport system involved in the shuttle: something else for the poster to try. Nor can I find information on whether D-malate is taken up by the gut, and what its fate is if it is.

Interesting! Just found https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1185386/ (back from 1970, found to inhibit gluconeogenesis from malate but without any effect on the TCA cycle otherwise)

@ManRow — The problem with this type of paper is that it's all "what" and little "how". That's not to criticise the work, which in the context of the time provided data to test hypotheses about the pathways. However if people sell malate as a supplement you would think someone should do experiments following the fate of radiolabelled  D-malate in, say, rats. Not the cutting edge of science, but you would think the FDA would demand something of the sort.

@ManRow — In case I did not make myself clear, the interest here was not in D-malate per se, but in what inhibitors might reveal about L-malate metabolism.

The existence of D-amino-acid oxidase (discovered by Krebs) is surely an exception to this argument

@user338907 — You need to explain more clearly which of my points it negates, and it would be of interest if you could mention what is known of the function of that enzyme. At the moment I don’t see any connection with D-malate.


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Is there such a thing as 'genetic memory'?
I have come across the concept of genetic memory in two books I recently read:

In the book 'Call of the Wild' by Jack London, a dog called Buck has memories of a primitive hairy man who presumably domesticated one of Buck's ancestors.

In the book 'Congo' by Michael Crichton, a female gorilla called Amy draws pictures of places from 'genetic memory'. The author goes on to say,

Genetic memory was first proposed by Marais in 1911, and it has been vigorously debated ever since.

To me, this sounds a bit like Lamarckism, which we know is incorrect. So is there such a thing as 'genetic memory'?

"The Call of the Wild" was written in 1903, at which time little or nothing was known of genetics. Presumably the author was extrapolating from the idea of animal instinct. "Congo" was written later (1980) but as a science fiction novel. And fiction it certainly is: the idea that memories can be passed on in one's DNA is complete nonsense.

I want to emphasize that actual memories passed on genetically are pure fiction as far as we know. However, there are genetic markers such as methylations, induced as a part of stress responses, that are thought to be inheritable, but they do not cause actual memory, just induce different cellular responses in the person inheriting them.

Certain innate animal behaviors could be rationalized as a kind of genetic memory, just not in the sense described in these passages. Domesticated dogs may instinctively fear strange people approaching their social unit, leading to aggressive displays towards strangers. Drawing pictures of specific places may seem far fetched (and was certainly fictionalized in this case), but there are some complex behaviors driven by genetic instinct. Food caching (and recovery), nest building, courtship displays, parental care, some migration patterns, and even communication behaviors.

You may want to read this

It's probably worth mentioning that genes are precisely "memory", but in a different sense to what is implied by the common usage. Genes are memory of all the past evolution.

I recommend looking into "transgenerational epigenetic inheritance", see for example here. It's possibly the closest thing to what you mean, but it isn't "memory" in the way that you mean.

There is an accepted form of "genetic memory" known as "epigenetics (wikipedia)", provided the concept is applied in accordance with scientific guidelines.
For example, from this study, we learned that

Epigenetics is the branch of genetics that studies the different
mechanisms that influence gene expression without direct modification
of the DNA sequence. An ever-increasing amount of evidence suggests
that such regulatory processes may play a pivotal role both in the
initiation of pregnancy and in the later processes of embryonic and
fetal development, thus determining long-term effects even in adult
life.

In simple words, a mother's (especially, during pregnancy) experience may  "carry on" to, and affect  her child's future (through epigenetics). But nothing so specific as a hairy man or a scene etc.
Further detailed information can be found in a vast amount of literature e.g., in this review, the author concluded

In C. elegans, the transgenerational inheritance of
temperature-induced changes in the expression of heterochromatic genes
was associated with altered trimethylation of H3K9 over fourteen
generations. In addition, H3K9me3 is critical for establishing
heterochromatin and essential for normal meiosis. Gestational
exposure to bisphenol decreased H3K9me2 and H3K9me3 in germ cells of
the neonatal testis., suggesting a possible role for these marks
during early developmental stages.

Please cite one specific molecular aspect of a mother’s “experience” that is passed on in the manner you state, describing the mechanism.

@David I found some more illustrations, but I believe the reader would benefit more from reading the original research articles (many of which were published on high profile journals like Nature and Science) listed in the review.
I've read over a few pages and concluded that the QA format on Stack Exchange is not suitable for scientific publications.


text:
does retrovirus need to manipulate cell cycle by neutralizing Rb and/or p53?
Early studies of transforming retroviruses led to discovery of oncogenes, while studies of DNA viruses (like AV40) led to discovery of p53 and Rb and tumor suppressor genes. Frank McCormick says in https://www.youtube.com/watch?v=wag9ISMeLDg&t=347s at 4:33 time: "DNA viruses have very different lifestyle than retroviruses, they need to inactivate Rb to get into S phase to replicate DNA...and then neutralize p53".
Why would retroviruses have "very different lifestyle" than DNA viruses? I assume they need to hijack same cell machinery to replicate (since its RNA is reverse transcribed to DNA firstly) as DNA viruses do. Can someone explain, please?

Welcome to SE Biology. Why do  you "assume" retroviruses need to use the machinery for DNA-dependent DNA polymerization that DNA viruses use? They have their own RNA-dependent DNA polymerase (aka as reverse transcriptase) to generate dsDNA copies which are not replicated further but integrated into the host genome. Have you researched the host cell components the two types (very much a simplification as DNA viruses differ) use?

@David thanks for your explanation, my bad I haven't realized reverse transcriptase is used for amplification as well, not only to create single DNA copy of virus' RNA to be integrated into host's genome.


text:
Is ghrelin only secreted when the stomach is empty?
Several texts indicate that ghrelin is secreted when the stomach is empty. However, some(not all) texts also indicate that ghrelin is secreted when blood sugar levels are low. Is the second statement true? If so, how does it relate to the first statement?
Consider a hypothetical situation:A person drinks water at regular intervals such that his/her stomach is sufficiently full throughout the day.During this period he doesn’t eat and his blood sugar level is low. Would ghrelin be released at any point in such a situation(excluding the night)?


text:
Are giraffes living on Calauit island an example of Island dwarfism?
When I traveled to Calauit island I was stricken by the small size of giraffes living there. The giraffes are the descendants of Africa animals imported in the 1970s.

Like Noah and the biblical ark, a boatload of animals was shipped from
Africa to remote Calauit Island in the Philippines in the 1970s
The descendants of these animals—20 giraffes, along with dozens of
zebra and antelope—are now among the most intriguing legacies of the
late dictator Ferdinand Marcos.

The following picture will give you an idea of how small they are (my wife's height is 160cm). I asked the local guides why they were so small (around 3 meters height, some even less than 3 meters), they told me because they are island born and they have become smaller compared to their ancestors.

To me this seems to be a perfect example of Island dwarfism. But when I google it I can't find any result of this. The only result I got was the dwarf giraffes found in Uganda. The science.org even used the title "World's first dwarf giraffes spotted in Uganda and Namibia", also check NYTimes article "Dwarf Giraffes Discovery Surprises Scientists" for detailed information of that finding.
So are Calauit giraffes an good example of Island dwarfism? If not, what is the explanation of their small sizes, e.g. does the NYTimes article's words "The condition, also known as skeletal dysplasia, affects bone growth, often resulting in short stature." apply here ?
PS. the original article NYTimes refers to was published at springer nature under a Creative Commons Attribution 4.0 International License, so you should be able to read it free.

Update
Updates to question and comments clarify:

3m high giraffes (small)
locals say giraffes are smaller because they are "island born".

The first data point indicates that the giraffes are in fact smaller than usual (usually >4m).
Being "island born" would be considered as an environmental perturbation. This would indicate malnutrition or something similar, covered under my 4th hypothesis below. Granted, it is not clear to me what exactly the local folks meant.
Original answer
Island dwarfism is a natural macroevolutionary process that is presumed to take a very long time due to long-term ecological pressures. The example you provide appears to be one in which humans took some giraffes to the island 50 years ago, or ~5-10 generations of giraffes (estimates differed in their generation time).
The body size evolution of distinct island varieties is measured in the millions of years. Based on Table 1 from the linked paper, I think that I interpret that the expected rate is something like a 10% size change per million years.
In other words, if those giraffes were island dwarfs, that would be an astonishingly fast natural adaptation. I can think of several possible explanations other than island dwarfism as we generally think of it:

The giraffes you observed were normal sized. Average height for a female giraffe is ~4-5m, or ~3m at the shoulder. Their shoulder height at least does seem a bit short in the picture, but it might be a weird perspective thing.
The giraffes you encountered were small, but that's because they were immature and had not reached full stature. (No dwarfism.)
The giraffes you encountered were derived from a variety with relatively small stature. (There is some variation, especially the females are not so tall, at 14 feet maximum height). Supposedly the animals were from Kenya which I believe are one of the bigger varieties, but who knows.
The giraffes you encountered were dwarfed by poor nutrition due to a suboptimal habitat (developmental loss of stature, not evolutionary).
There is genetically determined dwarfism / short stature, but it's due to genetic drift (the original giraffes had substantial dwarfism, as has been observed in natural populations, as you note).

I would probably want to exclude all of those hypotheses (and perhaps more) before I would say anything about island dwarfism. Evolution usually happens really slowly, unless it's acting on existing variation!
For a general description of the evolution of island dwarfism/giantism, see here.

When I first saw those giraffes I didn't know the term "Island dwarfism".  I asked the local guides why they were so small (around 3 meters, some even less than 3 meters), they told me because they are island born and they have become smaller compared to their ancestors.

Hi is your 4th reason, poor nutrition basically the same as the NYTimes article (I attached) words "The condition, also known as skeletal dysplasia, affects bone growth, often resulting in short stature" ?

@Qiulang Thank you for updates, I will update my answer. I don't have NYTimes access so I can't evaluate exactly what it says, but skeletal dysplasia is usually considered a genetic disorder, as noted in the freely accessible publication that I linked to regarding dwarfed giraffes. This would then be similar to my 5th point. Either poor nutrition or genetic skeletal dysplasia could lead to small stature.

Hi thanks for the update. The original article NYTimes refers to was published at springer nature under the Creative Commons Attribution 4.0 International License, so you should be able to read it free. I added this information to my question too.

@Qiulang- thanks, yes, this is the same BMC Research Note linked to in my answer. In that paper, as well as more generally, skeletal dysplasia is considered a genetic disorder. I consider it most likely that the short stature of your giraffes is environmentally rather than genetically determined, and is probably not due to such a disorder.


text:
Is palmitic acid really that dangerous?
According to Wikipedia,
"Palmitic acid is the most common saturated fatty acid found in animals, plants and microorganisms. It is also the first fatty acid produced during fatty acid synthesis and is the precursor to longer fatty acids. As a consequence, palmitic acid is a major body component of animals. In humans, one analysis found it to make up 21–30% (molar) of human depot fat, and it is a major, but highly variable, lipid component of human breast milk."
(https://en.wikipedia.org/wiki/Palmitic_acid)
Yet, specifically palmitic acid is also said to be "harmful" (that it increases LDL levels and puts people at risk for heart disease), per the World Health Organization (http://www.freezepage.com/1348239076FHWAJDADVT).
So, I am skeptical --- possibly most ubiquitous saturated fatty acid in nature and a central component of our fatty acid metabolism, is somehow "more" dangerous/unhealthy compared to other saturated (or unsaturated) fatty acids? I'd suspect the opposite should be true -- it seems to me it should be the saturated fatty acid we should be most capable of handling well!

Let's first clarify some concepts. Free fatty acids, including palmitic acid, are not present in animal tissues (or in the diet) to any large extent; they are esterified with glycerol to from triglycerides (fat), which is the storage form. This is a very important distinction, because triglycerides are chemically inert molecules that can be stored in very large amounts in cells without causing problems (adipocytes are pretty much just one big fat droplet), while free fatty acids are dangerous to organisms because they disrupt cell membranes --- fatty acids are basically soap.
When nutrition studies like the WHO report talk about dietary intake of "palmitic acid", they really mean intake of triglycerides that contain a large proportion of esterified palmitic acid as side chains. There is a large body of epidemiological studies indicating that intake of fats rich in palmitic acid correlates with cardiovascular disease and other "metabolic" disorders, although some reports show no significant effect. In clinical trials, replacing saturated with unsaturated fat seems to provide some health benefit; but there also are studies indicating that monounsaturated fat can be worse than saturated fat. So there is some evidence that too much saturated fat is problematic, although the issue is not straightforward.
The causal mechanism is to my knowledge still not clear. You are right that cells are normally perfectly capable of handling palmitic acid; it is a good substrate for beta-oxidation and a common fuel source for human cells. However, in pathological situations, free fatty acids can accumulate in cells and in the blood, probably because of excessive lipolysis. Many studies show that this can cause insulin resistance and trigger inflammatory signals, and even cell death by apoptosis. Some reports show that palmitic acid in particular causes these effects, whereas oleic acid (monounsaturated) does not, but I don't think there's any consensus on why palmitic acid is special.
My own hypothesis (if I may be so bold :) is that palmitate only appears to be special because cells have evolved to sense it as a "proxy" signal for free fatty acids in general. Since fatty acids are clearly dangerous to cells, sensing them is important, and because palmitate is the naturally most abundant fatty acid, it would be the easiest fatty acid to detect. It is known that palmitate is recognized by toll-like receptors, in particular TLR2 and TLR4, and that sensing by these receptors trigger "proinflammatory" signalling. But this alone doesn't prove my "proxy" hypothesis, of course.

Nice answer, +1! Can you add some resources which make you think "palmitate only appears to be special because cells have evolved to sense it as a "proxy" signal for free fatty acids in general"? I mean, at least a verified basis for a hypothesis is better :)

Sorry, I don't really have any reference for that last paragraph --- it's just a hypothesis, purely based on reasoning from principles. It is clear that palmitate does causes signalling responses (it's known to be sensed by TLR4), but I know of no clear rationale why palmitate would be physically more dangerous than other long chain fatty acid. This leads to my "proxy" hypothesis. As I said, it's just a hypothesis, I have no proof. (I actually hesitated to put this part in, as it is pure speculation, but I thought it could be interesting to share.)

@another'Homosapien'   Done, but that is not really the key part of the argument ...

+1. Only one thing to say - no one will disallow you to be bold; men often do that. Being too bald, however, may be arguable in science ;-)

+1 great answer indeed : ) I'm aware that fats are both generally consumed (eaten) and stored as triglycerides, not as free fatty acids (though i did not explicitly state that in my question, since i thought that was obvious/well-known). But, I was not sure why nutritional research seems to specifically single out (triglycerides with) palmitate chains with such criticism/disdain (especially for such a common and centrally important fatty acid).

@ManRow,  Yes, it is a bit strange. To some extent this could also be experimental bias: most experiments are done using palmitate only, and so any effects discovered are reported for palmitate, although they could actually be evidence of a more generalized response to fatty acids.

What is the reason for free fatty acids being detrimental? If in excess? What about the  triglyceride uptake mechanism of muscle cells/adipocytes.


text:
Dangers of excess blood protein?
Like glucose, amino acids are also insulinogenic as well. So, presumably, just like glucose, the body would also like to keep amino acids levels in the blood stream below (or within) some certain concentrations as well.
This question Why is too much glucose harmful? details some of the means by which high blood sugar levels can affect various cells and body function. But, would excess blood amino acid(s) levels have similarly adverse effects?

Your question is unclear and contains dubious assumptions. First the title refers to proteins, whereas the question refers to amino acids. Please correct that. Proteins are not insulinogenic. Second your assumption that because high blood glucose is harmful the primary purpose of insulin is to prevent this harm is at odds with the obvious accepted idea that it does it so the organism can obtain energy from or store this. Hence the supposition that insulin stimulates amino acid uptake to prevent harm, rather than to utilize them is completely unjustified.


text:
Food safety during roadtrips
I will be moving across the country in the coming weeks, and I have realised that I will likely have leftover perishable food in my apartment before I leave and I was thinking of trying to prepare some of it the night before I leave to bring with me. The trip will take me four days, and I was going to cook (extra thoroughly) hardboiled eggs, pork, bacon and sausages. I might even add some salt or something. And keep all of my packaging as sanitary as possible, eg. straight from pan/pot to sterile ziplock.
The eggs I'm unsure of because of the protective outer layer that is chemically removed during processing. The pork and bacon, I feel like they will be alright if they're eaten first. And I'm not too worried about the sausages because they've been processed and cooked.
I think a visual and olfactory test of the foods before I eat them would be wise - especially if nearing day 4. But, realistically, if I keep the food out of the sun covered up it will probably stay safe to eat, right? Or is this a bad idea?
I think that the food would definitely be safe to eat up until the end of the second day. But, what about any longer than that? How did people back in the old days travel with food?
Edit:
Just to clarify my question. I am not asking about whether or not my apartment is sterile. And I'm not asking about whether or not bacteria can multiply. I'm very well aware of these answers.
I'm looking for a realistic estimate on food longevity - not the food-standards enforced onto food manufacturers or restaurants by the FDA/Health Canada.

I'm voting to close this question as off-topic because better suited for Health.SE imo

@AliceD Is Health.SE for food science? I figured since food scientists rely heavily on microbiology this would be the ideal place for answers.

I think this is a biological science question. Food science, but still science.

The biggest factor in whether bacteria can grow in food is water bio-availability. Most non-sterile methods of preserving food (note that canning IS sterile) utilize this fact. Over salting while curing, adding lots of sugar, and dehydrating (or freeze-drying) all either remove water or remove the ability of the bacteria to utilize the water and hence grow in that medium.
This is the biggest reason that a hamburger from McDonalds can seem to petrify without devolving into an ugly mess. If the burger and bun and condiments dry out, bacteria can't grow on it. Put that same burger in a ziplock bag with a few drops of water and you will have the nastiest mess possible in a few days.
Honey and jams can remain at room temperature for months or years, even after opening despite being "watery", and this is because there is so much sugar in the solution, that all water tightly bound to the sugar molecules, leaving none for the bacteria to use (Note that some yeasts still can). Similarly, because of lack of water, crackers last for years, while bread spoils.
For your question with eggs and bacon, unless it was a hard-boiled egg that was cooked twice as long to ensure pasteurization throughout the yolk and you left the shell on, I wouldn't risk it after a couple of hours.  Bacon, once cooked, very little water activity. Fat doesn't count for bacteria propagation, they need water. I take cooked bacon on camping trips all the time. I also take sharp cheeses with me and they are good for days.
Your other option is cooking beans (with seasoning) or something and dehydrating them in the oven on a cookie sheet before you go. Then you just need to add hot water. I do this for camping as well.
Edit:
I didn't mention that high salt solutions (see pickling) function outside this paradigm somewhat, in that you are creating such an isotonic concentration in which bacteria membranes lyse.  I also didn't mention methods of pickling like kimchee and sauerkraut that use salt to positively select for species of bacteria (that aren't pathogenic to us) that can tolerate that salt concentration (mainly lactobacillus) as well as some yeasts.
Edit2: With a Source about water activity

How did people back in the old days travel with food?

Keeping said food alive until needed. Salting. Curing with smoke. Drying.Canned food. Buying it on the road.
Bacon and sausages. Have a lot of preservative in them (salt). So if you fry them, it will keep for a few days. Keep the oil on to stop exposure to air. Boiling on the other hand will remove said preservative, reducing your food shelf life.
Hard-boiled eggs.. so long as the shell remains intact..it will last the day and very likely last day 2.
The food listed would almost certainly last 2 days if kept in an air tight zip lock and kept in a cool place.
Day3 and Day4? It depends on the ambient temperature.
If it is below 10 Celsius. My guess is that the food will last till day 3. Probably till day 4.
However if it is above 20C, I don't know. My guess is that the food will be going bad.
Now... you have to realize that you are risking food poisoning (day3-day4). And this is the 2010s not the 1850s. You are not traveling the Oregon trail by wagon. Food is available everywhere.
So my recommendation, well if you want to boiled eggs and sausages. Sure, eat them on day 1 (and maybe day2, breakfast). But for day2, day 3 and 4, go out and buy some food. Moving cross country is an experience in itself. Experience the food from all the small towns that you pass through. These are parts of the country that you would rarely if ever visit.

Your apartment isn't sterile, and cooking kills many but not all bacteria - cooked food isn't sterile either, no matter how thoroughly cooked. No matter how well you pack things, they will have bacteria on them. Without refrigeration, that bacteria will multiply and may make food unsafe, or at minimum unpleasant to eat. Also, some forms of food decay aren't because of bacteria, but due to chemical changes in the food itself - protective layers won't prevent these types of spoilage.

Please note the use of the word: sanitary

Also note: protective layer removed

@Bob Sanitary isn't the same as sterile. There are bacteria floating all around the air around you all the time. Sterile devices (for example, for surgical procedures) are produced in special facilities and use chemical processes to ensure sterility. Cooking food is usually enough to kill bacteria that are present in quantities that could be harmful, but if you leave that food at room or elevated temperature, it is going to grow. You might not like this advice but please don't dismiss it.

I am aware. Please refer to my edited question.

I'm going to take issue with how you worded your response, "cooked food isn't sterile either, no matter how thoroughly cooked".  This is not true, else canned goods would not be good for years. The issue is that, absence of a sterile environment, he can't get it from a covered pot into a container and it still remain sterile.


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Possible to get Furniture carpet beetle specimen for collection?
I was wondering if anyone knows how it'd be possible to get a Anthrenus flavipes (or furniture carpet beetle) specimen for my collection?
I can't find a source anywhere online, only the dermestid beetles used to clean skulls and such. Any help would be appreciated!
Bump

You might try calling up a local exterminator (ideally not a franchise) and asking them to save you a specimen the next time they are called out to deal with such insects. Donate some beer/weed/customer referrals by way of thanks and they'll help you out with future specimen hunts.


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identification of purposeful (engineered) genetic changes vs. random mutations
Okay, first - I'm not a proponent of intelligent design. I do not think it's a valid scientific theory (it has no mechanism of change/design). Second, I could be wildly off on what I think I know, in which case, my apologies for the question.
My question is, I know that scientists manipulate the genes of organisms (both animals and crops we use as food). I think this could be considered legitimate intelligent design (right? I'm talking as opposed to looking at an organism and saying that this couldn't have evolved naturally, therefore it was intelligently designed).
So, mankind has modified organisms - outside of knowing we did this, can we tell they were intelligently created? If so, how? Can we tell when a genome has been altered?
Also, if I'm totally off base, please correct me.

to be fair we have engineered segments of their DNA, not the entire thing.

"To create" (to me) implies more than "to alter", which is what gene-splicing does. But that is just semantics. Can we tell if they were purposefully altered by man? I doubt it. Maybe if a particular, trademarked nonsense sequence was inserted into the genome as well, yes. But I doubt that is done (yet). These tactics have a way of backfiring on one. Animal husbandry is not the creation of an animal, but merely selecting for characteristics. Semantics matter here.

Honestly I thought about rephrasing just because of what you suggest - all we've done is alter genomes, but I wasn't 100%. I'm open to your question as well: Can we tell if a genome was purposely altered?
Should I edit my OP?

Yeah, I answered that in my comment. I highly doubt it, but I didn't post that because I never post an answer I'm unsure of, and I didn't want to slog through a bunch of scientific literature to find out if I am correct. If you want to edit, feel free. I changed the title because left as it was, few peple would click on it.

I did want to say that I have in mind what my friend (a CSI) has said in the past, that there is almost always evidence when a murder is committed; I grant that altering genes is not a murder, but I was thinking that the general principle might apply towards anything that mankind has messed around with. I'm probably wrong here, but that's where my head is at.

You are correct. Where man has been, there is usually evidence left behind. If man has been mucking about in a genome, maybe there is evidence, but if there is, I don't know about it. :)

One should be able to tell this from comparison of the sequence with that of the original organism in GenBank etc. The differences in an engineered organism will generally be extensive and of such a kind that a specialist in the field will be able to identify their origin and deduce that they did not arise naturally.
However there is no general and guaranteed method. If I were to engineer a single base change, there would be no way to distinguish that from a natural mutation. The only thing is that if the mutation were beneficial then it would probably have occurred naturally and I wouldn’t have needed to engineer it.

It has to be on a case by case basis. If I see a mouse or a fruitfly expressing jellyfish green fluorescent protein I know it cannot have acquired it by vertical transfer. That's why I deliberately mentioned a specialist or expert. The answer may not be the neat one the OP hoped for, but it's the way it is. It's like asking how an art expert can tell a genuine Picasso from a forgery.

Depends on the type of alteration.
If we are talking insertion/alteration/deletion of whole genes, we can easily discover the changes by genome sequencing and comparison.
If we are talking a single point mutation somewhere in the genome, it is harder to detect the change as such mutations can occur naturally (roughly 20-30 such mutations occur per human generation).

The number is higher. The 1000 genomes project estimates it around 20-30 de novo mutation per generation, see.


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In animals, birds, reptiles and fish, is a male sometimes unnecessary for a female to have/extend a male
Apparently in the human (animal realm) there are females that are female in body but their DNA is (XY) male, apparently 7500 in U.S., but apparently not able to have children ( http://abcnews.go.com/Health/MedicalMysteries/story?id=5465752&page=1)
I understand species like female hammerhead sharks can make clones with no male necessary for their female offspring (clones).  However, can a female make/extend a male, without receiving male fertilization?
If you also happen to know about the insect or plant kingdom please comment there as well.

Rephrasing your question
The question is worded in a funny way. If I am not mistaken your question is

Are there other means of reproduction than cloning that do not require mating with another individual? In particular, I am interested in such mean of reproduction that would allow an individual to create an offspring of another sex.

I will assume this is your question. I don't fully understand the point of the first paragraph though if this is your question.
Answer
Means of reproduction are much more diverse than we tend to think. So diverse that it is sometimes hard to really class each reproduction in non-arbitrary bucket.
Yes that exist! There are several modes of reproduction that may be of interest to you, the main one be selfing. Selfing is when an individual fertilizes itself. Now, by definition, such individuals need to be hermaphrodites, however it is not impossible that there are individuals that look males, others that look females and yet they (typically the females but not only) are able to self every so often.
Just to give a funny example to show how diverse system of reproduction might be. In social ants, the queen can either let the sperm of a male fertilize her eggs and produce a female worker (or a future queen depending on whether the larvae receive royal jelly) or chose to undergo normal meiosis but the gamete from the mother will directly develop into an individual without fertilization and make a male. This is not cloning because 1) only half of the genome is being transmitted and 2) recombination occur.
Related

What DNA does a self-fertile plant's seedling have?
Do males of all sexual species have Y chromosomes?

Hi Remi, thanks for trying to answer my question, sorry for the confusion (I tried to rephrase).  I'm trying to fully understand your ant example.   My question is, can a female produce male offspring with no fertilization by a male?  This would mean she is DNA complete male & female, and does not need the male in the species to procreate males.  Does that exist?

Yes, that's what queen do. If the eggs is fertilize, it becomes a female, if the egg is not fertilize, it becomes a male (males are therefore haploids). This is just one example among many others (although I would not be able to pull out plenty of example out my mind right now).

I don't know what you mean by  DNA complete male & female though. It seems like you think there is male DNA and female DNA. This is mostly wrong. You should have a look at this post, esp. the section Diversity among the species that have sexes of the accepted answer.

Oh, thanks Remi.  What I mean by "DNA complete male & female" is a human man's cells has the DNA makeup to produce, say by cloning, either a boy or girl, but a human woman's cells do not, having XX and not an XY.  Am I seeing things incorrectly?

Have you looked at the post I pointed to in the comment and in the post? Your issue is to think that all species are GSD while they're not. On top of that, your issue is to fail to recognize that in some GSD cases sexes are differentiated by copy number variants (CNV) (e.g. C. elegans) and therefore a single parent could just increase or decrease such number of variants.

Thanks I just read it.  So with social ants, if the male is involved in reproduction the offspring is always female, and if he is not involved, then the offspring is always male?

Yes, in most ant species at least.

Does Caenorhabitis elegans fit your description?

There are two C. elegans sexes: a self-fertilizing hermaphrodite (XX) and a male (XO). Males arise infrequently (0.1%) by spontaneous non-disjunction in the hermaphrodite germ line and at higher frequency (up to 50%) through mating. Self-fertilization of the hermaphrodite allows for homozygous worms to generate genetically identical progeny, and male mating facilitates the isolation and maintenance of mutant strains as well as moving mutations between strains.

Thanks for contributing.  I'm confused about this -- read the link you gave: how does the female create an XO if she only has XX?  Apparently, "Nondisjunction is the failure of homologous chromosomes or sister chromatids to separate properly during cell division. There are three forms of nondisjunction: failure of a pair of homologous chromosomes to separate in meiosis I, failure of sister chromatids to separate during meiosis II, and failure of sister chromatids to separate during mitosis"

Comment cut me off.  Anyway, how does she, XX, make an XO without him (XO)?

@Ray O is not a chromosome. O means absence of a chromosome. Hermaphrodites have two X chromosomes while males have one.


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tools and techniques for determining nutrient status in plants
I am interested in tools and techniques, both commercial and academic, developed for determining nutrient status and identifying limiting nutrients in growing plants. My specific interest is in alliums, but the question is general.
So far I've found two techniques. I present my understanding of them below. Please correct and supplement the presentation if needed.
Total tissue analysis for total micro and macro nutrients:
Young mature leaves are dried, ground, acid digested and fed to ICPMS or alternative method is used (nitrogen) to determine total content. Technique suffers from contamination of leaf surfaces caused by foliar fertilization and delay from onset of deficiency to actual measurable changes in leaves. Moreover, sufficiency ranges are dependant on soil and climate.
Sap analysis:
Instead of whole leaves, only sap is tested. How sap is extracted varies across labs. For example, leaves are frozen for a short period and then pressed. The fluid extracted supposedly offers more accurate and faster results than total tissue analysis. Sap from young and old mature leaves is compared, but I assume some knowledge of sufficiency ranges is still needed. Not sure what effects foliar fertilization has on skewing the results.
Companies that do sap analysis say sap analysis is the way to go. On the other side, total tissue analysis is preferred by other labs. An authoritative answer comparing above listed techniques is desired.
Are there any other techniques developed? For example techniques involving tissue microscopy? Thank you for your answers.


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Why do the bases in DNA not repel each other?
The bases in DNA are, well, basic. Adenine has a first pK$_b$ of 4.20 (Wikipedia), guanine 1.7 (Wikipedia), cytosine 1.8 (Wikipedia) and thymine 4.3 (Wikipedia). Under physiological pH of 7.4, all of these would be protonated, meaning each base in DNA would exhibit at least a 1+ charge. That would mean they would repel one another. As a vague order-of-magnitude approximation, I estimated the electrostatic potential energy in two elementary charges ($1.6*10^{-19} $ C) at a distance of 1 nm, which yielded an electrical potential energy of $2.3*10^{-19} $ J. (calculator) Converted to kJ/mol, this is ~136 kJ/mol. The hydrogen bonds in cells are only 6-30 kJ/mol strong, (source) so even a triple hydrogen bond remains below this value. So, I would expect interactions between nitrogenous bases to be energetically unfavorable.
Why is this not the case?

You got wrong values. For ex. adenine's 4.15 is acidity of conjugate acid, not pKb. They are weak bases and DNA binds to much more strongly basic histones. In result the bases are hardly protonated at all.

pKa is the pH at which a molecule occurs 50 % protonated and 50 % deprotonated. Protonated does not always mean positive charge as we can also look at the pair between deprotonated negatively charged molecule that gets neutral upon protonation. And it gets confusing when there are multiple protonation sites in a single molecule like in DNA bases.
Be aware that we always look at the equilibrium between two species when thinking about pKa. In this case we have 3 species in the equilibrium.
deprotonated<-neutral->protonated, i.e. two pKa values for the same molecule.
The distribution at physiological pH can be calculated over Henderson Hasselbalch equation
pH=pKa+log(base/acid)
10^(7.4-pKa)=Base/Acid
Guanines pKa is 9.65 for the N1 deprotonated (minus charge)/neutral pair and 3.20 for the N7 protonated (positive charge)/neutral pair
GHH+ <-3.2- GH -9.65-> G-
https://pubs.acs.org/doi/10.1021/jp020774x
so at pH 7.4 only 0.6 % occur in the deprotonated negatively charged state. For the protonated positively charged state it is 0.006 %. The predominant form is the neutral molecule.
For exact concentration of all three I lack motivation.
Thymine pKa 9.5 for the N1 deprotonated/neutral pair
Here about the same
Adenine pKa 4.2 for protonated/neutral and 9.8 for deprotonated/neutral form
https://pubs.rsc.org/en/content/articlelanding/2003/cp/b212779m/unauth
So the "Bases" are predominantly in their neutral uncharged state and I think their name results from some historical incorrect attributions

Thanks. Related: https://biology.stackexchange.com/questions/29925/why-does-high-ph-result-in-the-denaturation-of-dna

I would suggest reading more on the topic, considering for example also entropic contributions to the double helix.
Here is a recent review including a large amount of historical background.
Here is an experimental study characterizing charge repulsion of the helices.
We can look in these papers and find that cations in solution are crucial for ameliorating charge repulsion, (not between the nucleobases, which as rightly pointed out in the accepted answer are neutral under physiological conditions) but between the negatively charged backbones:

Cations are able to interact with negatively charged DNA via non-specific electrostatic coupling and hence universally screen the like-charge repulsion between DNA... Since continuum theories always predict DNA–DNA repulsion, the multivalent cation induced attraction (MCIA), driven by electrostatics, necessarily arises from spatial correlations between DNA charges and ions.


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How did the fusion of Chromosome 2 spawn a separate smarter species?
I’m familiar with the evidence that two primate chromosomes fused into human Chromosome 2, and I understand that primates with such a mutation could still breed with those without it.
My question is, was it just a coincidence that the primates with 23 pairs became a smarter species branch?  Or did the mutation somehow enable our ancestors to become more intelligent than their relatives in the same biome?
Early on, the 23s must have coexisted with and interbred with the 24s.  But at some point, they became too genetically distant to breed.  So they must have genetically separated when they were still capable of interbreeding.
Was that separation because the 23s were somehow better able to adapt to new habitats or lifestyles that the 24s weren’t able to follow them to?


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In the context of GWAS we have an alternate allele and a reference allele. Why do we only have one possible alternate instead of three?
I recently started analyzing a GWAS summary dataset. It has a column for the reference allele in which it mentions the base in the reference genome.
There is another column for the alternate allele (or the SNP). Each reference allele always has one alternate instead of three. I have read responses to this question on other forums and the answer usually goes like this:

The other two alternate alleles are very rare so not seen in the population that often.

I find this hard to believe.
On average every person has 3,000,000 SNPs (1 in 1000 bps). Does that mean in all the 3 million cases the individual always has that one alternate allele? Let's take a million individuals, do all those 3 million million SNPs always have that one alternate allele?
This just seems very unlikely, even if those alleles are very rare we have so many occurrences that we should be seeing them.
I am new to GWAS and have taken genetics courses during my undergrad. Could someone provide a satisfactory explanation? Sometimes I feel we are doing this as an approximation to make further statistical/computational analyses easier.
Edit: Although I am asking this in the context of GWAS, I have seen it in many other situations. It is sometimes referred to as the minor allele.

Estimates seem to be around 45-60 de novo mutations in an individual, e.g.: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9550265/
That means the other 2999950 mutations are inherited, they're shared with a parent and their parent and possibly siblings, cousins, so on. They won't have inherited just some random base pair at that location, they will have inherited exactly the same one as all those other people share with them.
Additionally, there are some SNPs that are going to be selected against. Any SNPs that are lethal will never be inherited, for example.
So, overall, I don't find it that surprising. Less common SNPs that haven't spread in the population are unlikely to be found in any sample of thousands or hundreds of thousands of humans in a population of billions. So, they may be out there but never observed. And unless they are observed they aren't very useful for the things people want to use SNPs for.


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Did some senses evolve from other senses or are they considered independent?
Are there evolutionary connections between different senses, in such a way that one sense is evolved from the other or from a common root, e.g. the possibility that hearing and touch are derived from a common root? If there are such evolutionary paths, are there any attempts to draw a map between different senses?

Hearing and touch are both examples of mechanosensation, i.e. touch receptors are activated by pressure changes and sensory hair cells (hearing) are activated by fluid motion initiated by sound waves. Therefore, I think it makes sense that they evolved from similar origins.
Vision on the other hand is due to photosensation, which has a very different physiology, so I don't think there's any evidence of a similar evolutionary link, but there may be (almost certainly are) similarities in the way our brains have evolved to respond to the different senses.


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Why is carbon dioxide produced in alcohol fermentation but not in lactic acid fermentation?
From my understanding, alcohol fermentation takes place in yeast and lactate production takes place in humans.
These two pathways take place only when there is insufficient oxygen, because the other parts of metabolism (TCA cycle, ETC) can't take place as they happen in the mitochondria, which requires O2.
For alcohol fermentation, there is production of carbon dioxide while lactic acid fermentation does not produce carbon dioxide. CO2 is produced when there is an oxidation of one carbon molecule. So my main question is: since there is a lack of O2, how does yeast produces CO2 while humans do not?
Also, how does NAD+ recycle all the time when glycolysis is happening?
Thanks!!!

Glycolysis needs a steady supply of NAD+ to happen - this is the driver for the anaerobic oxidation to lactate and ethanol, although this is energetically much less favorable than the complete oxidation. But without oxygen there is no other way to keep the glycolysis active for at least some energy supply.
The difference is located in the enzymes available for the conversion of the pyruvate. This is the Lactate dehydrogenase in humans (and other mammals) and the Pyruvate decarboxylase in yeast. The first catalyzes the reaction from Pyruvate to Lactate, the second from Pyruvate to Acetaldehyde and CO2, the Acetaldehyde is subsequently converted to Ethanol. Only the second step produces NAD+.
See the illustration (from here) for further understanding:

The CO2 produced in this reaction does not occur due to oxidation, but is released from the decarboxylation of the Pyruvate. See the illustration below (from here):

In the production of lactate no decarboxylation is happening which allows the backreaction from lactate to pyruvate once enough oxygen is present again.

Where the 2 NAD+ accepts electrons from to recycle back to NADH ?

You might want to add that since there is no decarboxylation in production of lactate, there is no CO2 evolved. Also that glucose already contains oxygen, so there is no need of O2 in producing CO2 from pyruvate (just saw that you missed these points from the question :)

@user307640 Each molecule of glucose makes two molecules of pyruvate, which allows to run the process twice.

@another'Homosapien' Good point.

@another'Homosapien' You don't need to shift around O2 in the molecule, you cleave off CO2 from the molecule by the decarboxylase.

@another'Homosapien' Then I misunderstood your comment. But I hope it is now clear, where the CO2 comes from.

Just to add, no offence, 'twas already clear to me, I just wanted you to add this point in your answer ;)

@another'Homosapien' None taken, that's ok. Something clear for yourself is not necessarily clearly explained for somebody else. Criticism helps here.


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Isoelectric point of aspartate

On the 3rd diagram (from left), the one with net charge = -1 ,
Why did it lose the H to OH- from the CH2CO2H from the neutral form ?
I was told that while moving to the right , the OH- will take H+ electrons meaning it should take H+ from NH3 .. ?
Is there any reason why they took the H from CH2CO2H ?
Any help would be appreciated!

The -CO₂H groups are carboxylic acid groups, better represented as -COOH. These, being acidic, have a lower pKₐ than the -NH₃⁺ group and so as the pH increases these -COOH groups lose their protons first.
The pKₐ values for the three are shown below the arrows: as you can see the α carboxylic acid is more acidic than that in the side chain, but they are both much more acidic than the protonated amino group.


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Get Network Out of proteins of interest
I have generated a list of Proteins using oncogeenes and suppressor genes of cancer.
I have 5827 mapping identifier for 3916 interactions using STRINGdb R package  .
How do I build a network of 200k protein?
Identifiers.csv

"","mapping_identifier"
"1","9606.ENSP00000003084"
"2","9606.ENSP00000003100"
"3","9606.ENSP00000004921"
"4","9606.ENSP00000004982"
"5","9606.ENSP00000005178"

and these are the interactions
"","from","to","neighborhood","neighborhood_transferred","fusion","cooccurence","homology","coexpression","coexpression_transferred","experiments","experiments_transferred","database","database_transferred","textmining","textmining_transferred","combined_score"
"1","9606.ENSP00000163416","9606.ENSP00000240851",0,0,0,0,0,0,0,0,0,0,0,481,0,481
"2","9606.ENSP00000163416","9606.ENSP00000263967",0,0,0,0,0,0,0,0,0,0,0,195,0,195
"3","9606.ENSP00000163416","9606.ENSP00000270202",0,0,0,0,0,0,0,0,0,0,0,163,0,163

Have you tried biostars.org? I think they are far more suited to computational questions.

Or you could try https://bioinformatics.stackexchange.com/

What form is your data in, it would be helpful if you could post the first 10 lines of data.

@emilliman5     I edited the question  and I'll try bioinformatics.stackexchange


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String-db locally downloaded
I need a ppi network of cancer and it should have 200k to 300k proteins (nodes)
As the web inteface don't allow more than 2000 proteins to be visualized . I have downloaded the protein_links of homosapiens from the download section .
It has 11353058 link which means 11353058 interaction .
The downloaded file is a .txt How do we do  to extract cancer interaction from this huge set ?
What are the different ways to manipulate this file .

I dare say it's outside of my realm to do network analyses, but I also don't believe it's possible to just say cancer and pull out a network. This is especially so since melanoma will differ widely from renal-cell carcinoma, lung cancer and so forth. Perhaps this paper will help you (ref).

Actually I don't really care about the type of cancer ,as far as I'm concerned with the data , the amount of data  I need a network of 200k of whatever type of cancer or any other disease from that file that's all I'm asking for And thank you for the paper @CMosychuk

It is more of data necessity than it is of biological , proteomics need


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Help identify black, brown bugs in Virginia
Please help identify these black, brown bugs found in the bathroom in a home in Virginia.  The bathroom has mold due to a pipe that was leaking.
They are very small and maybe 1 mm in length.  The stuff surrounding the bugs is human hair.  Notice the long antenna on the bug on the left that is as long as the body.
I thought they might be springtails but I do not see furculas, and the tail on the left bug looks strange, where it seems there are hairs or parts sticking out in a circular fashion.
U.jpg