text:
What stops myosin during muscle relaxation?
I understand that when the muscle is relaxed tropomyosin blocks myosin binding sites on actin filaments thereby preventing muscle contraction. What I am concerned with however, is whether myosin filaments - given that ATP is found in the muscle fiber- continue trying to bind to actin, and hydrolyzing ATP...
So how are mysoin filaments stopped from trying to bind to actin when the muscle is relaxed, to stop the hydrolysis of ATP?

Relaxation of vertebrate skeletal muscle is thought to occur in the absence of  ${Ca}^{2+}$ as a result of tropomyosin physically blocking the binding of myosin to actin. This steric blocking model of muscle relaxation predicts that myosin subfragment 1 (S-1) will not bind to actin under conditions where the acto-S-1 ATPase rate is inhibited.[1]
However, in a paper that questions this model, it is concluded that in the absence of ${Ca}^{2+}$, troponin-tropomyosin inhibits the ATPase activity by inhibiting a kinetic step in the cycle of ATP hydrolysis, perhaps $P_i$ release.[2]

That is the simple answer, but I think a little elaboration on the above paragraphs might help add some substance:[2]

Vertebrate skeletal muscle contraction is the result of a cyclic interaction of thick myosin filaments with the thin filaments, composed primarily of actin, troponin, and tropomyosin, causing these two sets of filaments to slide past each other. This cycling is driven by the hydrolysis of ATP by myosin in a reaction which is activated by actin.

When the sarcoplasmic reticulum lowers the free ${Ca}^{2+}$ concentration from $10^{-5}$ to $<10^{−7} m$, muscle contraction ceases and the associated actin-activated myosin ATPase activity is inhibited. The proteins troponin and tropomyosin are responsible for this effect of ${Ca}^{2+}$ on the interaction between myosin and actin.

At levels of ${Ca}^{2+}$ low enough to cause relaxation, tropomyosin is positioned away from the central groove of the F-actin filament where it appears that it might interfere with the binding of the myosin cross-bridge. This structural work formed the basis of the steric blocking hypothesis which suggests that relaxation occurs when tropomyosin, in the “relaxed” position, physically blocks the binding of the myosin cross-bridge to actin.

Three-dimensional reconstructions from electron micro-graphs have suggested that the myosin cross-bridge and the tropomyosin molecule may be in close contact with each other on the actin filament, a requirement for a steric blocking type model.

The steric blocking model predicts that in the absence of ${Ca}^{2+}$ the degree of association of S-11 should be much weaker with regulated actin than with unregulated actin. In fact, in the absence of ${Ca}^{2+}$, the binding of S-1·ADP to regulated actin is strongly inhibited in a cooperative manner.

At low levels of saturation of the actin filament with S-1·ADP, the binding of S-1·ADP to the regulated actin filament is about $10^3$ times  weaker than at high levels of saturation.

However, the fact that S-1·ADP binds weakly to regulated actin does not prove the steric blocking model since, in relaxed muscle, the cross-bridges normally exist with bound ATP (or ADP · Pi) and not bound ADP. Therefore, the steric blocking model predicts that troponin-tropomyosin should inhibit the binding of S-1·ADP·Pi as well as S-1·ADP to regulated actin in the absence of ${Ca}^{2+}$.

Using stopped flow turbidity measurements, we have previously measured the effect of ${Ca}^{2+}$ on the association of S-1 · ATP and S-1 · ADP · Pi with regulated actin. Surprisingly, in the absence of ${Ca}^{2+}$, the binding constant of S-1 · ATP or S-1 · ADP · Pi to regulated actin was only decreased to 56% of the value in the presence of ${Ca}^{2+}$ although the rate of ATP hydolysis under the same conditions was decreased to 6% of the rate with ${Ca}^{2+}$ present. These data suggest, in disagreement with the steric blocking model, that inhibition of the rate of ATP hydrolysis, in the absence of ${Ca}^{2+}$, is not the result of inhibition of the binding of S-1 to regulated actin.

1- https://pubmed.ncbi.nlm.nih.gov/27065174/
2- https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1266292/#FN2


text:
Are the transitions between the different brain frequencies states easy to see on an EEG?
Are the transitions between the different brain frequencies states: Gamma to Beta, Beta to Alpha, Theta to Delta, etc. easy to distinguish on an EEG? How quickly can the brain transition between any of these states?

Delta/theta/alpha/beta/gamma are not different states and so there are no changes "between" them. These are terms used to label different bands of the frequency spectrum. Every EEG has energy in all of these bands. Brain state can change/be measured by the relative changes in different bands (either relative to each other, or in absolute power change over time), but there is always some energy in every band.
Here are some example spectra from different brain states (stages of sleep and anesthesia states) across different brain regions:

(from Banks, M. I., Krause, B. M., Endemann, C. M., Campbell, D. I., Kovach, C. K., Dyken, M. E., ... & Nourski, K. V. (2020). Cortical functional connectivity indexes arousal state during sleep and anesthesia. NeuroImage, 211, 116627. Disclosure: I am an author on this paper)
WS and WA refer to "wake" in the sleep and anesthesia experiments respectively; N1, N2, and REM are stages of sleep. S refers to sedated under anesthesia - subjects can still respond to commands, and U refers to unresponsive under anesthesia. These are actually not from EEG but from electrocorticography where the electrodes are placed directly on the brain, sometimes called iEEG, but there are a lot of similarities with EEG.
You can see that in all brain states, there is energy across all the frequency bands (identified with Greek letters), but there are changes with state. For example, delta has more power during N2 sleep across the brain. A trained eye could also easily pick this up in the time-domain EEG signal, but it's much easier to convert to the frequency domain like in this figure.
You'll notice that the energy decreases with increasing frequency. This is normal, and is typical of natural frequency spectra with certain properties, see Pink Noise; it's rare to ever have less power in the delta band than any other band, for example. You will also see that for the most part the spectra are gradually changing: there are few peaks in the spectrum, and it can be a bit misleading to refer to energy in a specific band or to compare between bands when there is no peak there. Some exceptions are that there is typically a peak in the alpha band for humans, especially with eyes closed. Hippocampus tends to generate rhythms in the theta band, and rodents have very large hippocampus relative to the rest of cortex, so you'll often see a theta peak in rodents especially during locomotion.
Lastly, these EEG differences are probably not the best way to discriminate between different brain states. There are lots of other measures that seem to do better. In the rest of the paper that I've taken this figure from, my colleagues and I use a specific measure called the weighted phase lag index which does a much better job at discriminating between putative conscious and unconscious states.

source: Stack Exchange

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

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Is 'disorientation event' a common term among biologists?
On the South Carolina Department of Natural Resources web page about the marine turtle conservation program it says, "When a hatchling sea turtle is attracted away from the ocean towards a direct or indirect source of light, biologists describe this as a disorientation event."
Does something like the disorientation event describing the sea turtle behavior also occur in other species?

The source you link seems to describe the term as specific to sea turtle biology. Not every biologist studies sea turtles. Are you asking if it is used in other species? Or are you asking if it is used in scientific papers specific to sea turtles?

Presumably they are just explaining a term that has been used or coined to describe the phenomenon under a more general heading using scientific or formal language, so the reader understands its subsequent use. The idea conveyed to you that biologists mutter it to one another at coffee time is incorrect and, I imagine, unintentional.

@BagiM I am asking if it is used in other species.

@Bob516 You should edit your question to clarify. As written, there is nothing in your question that implies you are asking if it is used in other species. With that added piece of information, I am also unclear if you are asking if this term is used or whether something like "disorientation events" in sea turtles also occur in other species. It's important to be precise in your questions.

As sort of a "teach to fish" answer, let's approach how to answer a question like this:
Google Scholar is a pretty good index of scientific literature: good enough for this purpose. If you search:
"disorientation event" -turtle
you will return all results that use the specific phrase "disorientation event" except those that mention turtles.
You can also do the search:
"disorientation event" turtle
to find the turtle papers. As of today, "disorientation event" returns 57 results; 14 also include the word "turtle", 43 do not.
Among the 43, it looks like the majority of papers are discussing human disorientation, particularly in the context of human pilots but also in the context of cognitively impaired individuals or simply lost pedestrians. There is one paper that uses the term referring to rats in a maze-like task.
Overall, these results lead me to conclude that "disorientation event" is not a common general term used by biologists to refer to non-turtle species losing their way, although I would also say that I would expect a biologist to understand the meaning of the term given sufficient context.

I'm only familiar with the bird research and it is not a commonly used term in ornithology. Birds use multiple methods for navigation which include the sun, stars and the earth's magnetic field. When biologists talk about birds becoming disoriented (usually by magnetic fields or they could appear to be disoriented after a fallout event, due to a hurricane etc) they don't refer to it as a disorientation event, as far as I know, there isn't a term to describe these events in ornithology.
I feel like I should clarify, since I used a term and then said there isn't a term...
"Fallout" or migration fallout is when severe weather prevents birds from reaching it's destination (e.g. breeding grounds or wintering grounds) and instead taking refuge in an unusual place (what we could consider unusual, as it's not their normal path of migration, not their "normal" stopover site). It's not actually referring to birds becoming disoriented, which is why I would say this is not a term to describe a disorientation event.

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


text:
What retrospective analysis happens after a clinical trial fails?
After a failed pharmaceutical clinical trial, what retrospective analyses are typically performed to understand why the drug program failed the trial? For example, are further experiments done to determine whether it was due to inaccurately predicted pharmacokinetics versus whether the biological target was non-causal? Do such analyses look only at the data gathered in the clinical trial itself, or are there teams which do further experiments to understand the precise mechanism of the failure? Are there investigations to replicate and reproduce earlier data and reports that led to the green light for the clinical trial, in order to catch fraudulent data generated by company scientists?
Another way of asking this question: how do pharmaceutical and biotech companies internally implement the scientific method, given that they don't publish peer-reviewed biology papers with all their internal findings? In other words, to what extent do clinical trial failures advance our understanding of biology?
I am asking in particular about Phase 2 and Phase 3 trials, because they seek to answer whether Drug A improves Disease C. Typically, Drug A attempts to affect Drug Target B which was believed to play a causal role in Disease C, so I wonder whether there tends to exist a process for revisiting the hypothesized biology of Target B (and revisiting the process that led to hypothesis) after Drug A fails.

You mean as opposed to burying the results or falsifying them? Sorry, just being honest and cynical (it happens a lot. Remember, the majority of pharmaceutical companies are in it for the big bucks. Money spent with no profitable potential outcome is not to be followed by more, unless there are potentially REALLY BIG BUCKS!!! ahead.) This site, btw, expects you to show evidence of your research into answering your question before we do so. Strange for a Q&A site, but this is an advanced Q&A site, if you will.

I clicked the wrong close box, but I think that questions about clinical trials are not about biology. They may or may not be acceptable on SE Medical Sciences, but getting a useful answer depends on having a list member with experience in the pharma/biotech industry — not very likely.

I don't know what you mean with a trial 'failing'? I run clinical trials and to me, at least, a 'failed' trial is one where something went wrong enough such that it caused erroneous data (e.g., inappropriate test design for the specific outcome measure), no data at all (e.g., fatal technical failure that could not be resolved) or other causes (e.g., COVID regulations that restrict patient access). I bet that's not what you're after.

@AliceD -- I have reworded the question to clarify that I meant that the drug program failed in the clinical trial. This is of course the fault of the drug program, not the trial itself.

@AliceD - I suspect that the OP is asking what happens if a newly developed substance is tested and fails to have the desired effect, but I'm not sure, as a drug program isn't a term I'm familiar with.

Yes, that's exactly what I'm asking!

What phase of trial?

@BryanKrause - Phase 2 and 3. I added clarification and explanation in the original question.


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

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

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

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

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

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

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

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

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


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Can creatures that can see color in completely different visible spectrum exists?
From wikipedia - "The visible spectrum is the portion of the electromagnetic spectrum that is visible to the human eye."
So humans can see the light from 400-700 nm and this is because our eyes can interpret/sense this little portion of the electromagnetic spectrum.
I wonder - could somewhere out there exist a creature which is possible to see different part of the spectrum ? I know that on Earth a creature can have a different visual spectrum "flavour" but I do not know whether it is possible the visible spectrum to be completely different - e.g. on some other planet can creatures exist that can say to see light in lets say  1500-2000 nm ?

maybe [this] (https://biology.stackexchange.com/questions/58005/are-there-animal-species-that-sense-infrared-light-with-their-eyes) can answer your question. They show animals on Earth that uses different molecules to transduce the visual stimuli, which is the key element to sense different portions of the electromagnetic spectrum, here on Earth, and in any planet as long as I can tell.

See also https://biology.stackexchange.com/questions/57708/what-is-the-biological-potential-for-vision-of-wavelengths-outside-the-human-vis/57710 - may be considered a duplicate. Note that speculation about completely foreign biology is not on-topic here, questions have to be about real biology that can be studied.

From what I have read so far - asking this question about life vision on other planets - is an on the edge on sci-fi and assumptive. As we haven't found complex life on other worlds - we can guess. However as far as what I read - based on the conditions the life live (e.g. their star type, distance from it etc.) and their chemistry - maybe life could be completely different - their vision could theoretically be different as well - sensing their world in different spectrum of light.

Maybe this question is similar with asking - could vehicles engines be completely different from what we have now on Earth. I suppose yes.


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Are all fusion genes somatic in origin or can fusion genes be germline?
Fusion genes should have an origin.These are essentially hybrid genes that are translocated in its entirety. Eg. BCR-ABL, EML4-ALK are known to be implicated in cancer pathogenesis. Do these translocation events occur somatically or is there a possibility for it to be inherited?

What do you mean by fusion genes? Can you please add some context? At the moment it is unclear what you are trying to ask.

Hybrid genes that are translocated in its entirety. Eg. BCR-ABL,  EML4-ALK are known to be implicated in cancer pathogenesis. Do these translocation events occur somatically or is there a possibility for it to be inherited?

Hi and Welcome to Stack exchange. I think your question is not properly phrased. These hybrid genes you mention are indeed related to carcinogenesis, as in they are mutations commonly found in specific cancer types. It is unclear whether you are asking if (any) translocation events can also occur in the germline, or whether cancer-associated translocation mutations (such as the Bcr-Abl, Tpr-Met or Gag-Onc) can occur in the germline, and thus be inherited.

Thank you. Sorrry if it wasn't clear.  I'm asking if  cancer-associated translocation mutations (such as the Bcr-Abl, Tpr-Met or Gag-Onc) can occur in the germline, and thus be inherited. ?If yes, do you have papers supporting this? I haven't been able to find germline origin fusion genes.

There is at least one (possible) description of an inherited (aka germline) fusion gene:  KANSARL.  See the paper "Identification of KANSARL as the first cancer predisposition fusion gene specific to the population of European ancestry origin" by Zhou, Yang, Ning et al., Oncotarget. 2017; 8:50594-50607.

KANSARL fusion gene is familially inherited and may be ubiquitously expressed in KANSARL-bearing individuals
  The presence of KANSARL fusion transcripts in normal and adjacent tissues in CGD and VPD raised the possibility that KANSARL fusion transcripts are derived from a germline-inherited fusion gene. To investigate this possibility, we performed RNA-seq data analysis for the lymphoblastoid cell lines derived from the families in the CEU population (CEPH/Utah Pedigree 1463, Utah residents with ancestry from northern and western Europe), which includes a three-generation family with 17 individuals [47]. Supplementary Table 9 and Supplementary Figure 8 show that KANSARL fusion transcripts were detected in 15 of 17 family members, as indicated by black squares and circles in Supplementary Figure 8, except son (NA12885), which is deviated from the first Mendel law. A reasonable explanation is that the grandfather sample (NA12889) might have been mixed with the son sample (NA12885). To prove this possibility, we performed analyses of the WSG data (PRJEB3381) and RNA-seq from 1000 Genome Project, and shown that both WSG and RNA-seq of grandfather sample (NA12889) are KANSARL-negative while WGS of the son (NA12885) is KANSARL-positive (Supplementary Table 10). Supplementary Table 10 shows the genomic breakpoint 1 and 2 of the KANSARL fusion gene (Supplementary Figure 5 and 9) identified by analysis of WGS data among some members of CEPH/Utah Pedigree 1463. Therefore, Both WGS and RNA-seq data support that the father (NA12877) and the mother (NA12878) have the genotypes of KANSARL-/KANSARL- and KANSARL+/KANSARL+ respectively and all their offsprings are the genotype KANSARL+/KANSARL-


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What is the role of the pyrrolidine/piperidine moieties in fagopyrins?
Fagopyrins are phototoxic compounds that cause fagopyrism. They are chemical compounds related to hypericin and pseudohypericin. Some variations lack one or both methyl groups, which I think is to streamline the molecule so it better fits in membranes and so increase damage. The main difference from (pseudo)hypericin though is the presence of pyrrolidine or piperidine (or both) moieties, which may come from L-proline and L-piperidine-1-carboxylate (in turn from L-lysine) respectively. So, what is the function of those moieties in the fagopyrin molecules? Does it render fagopyrins more toxic than (pseudo)hypericin?

Radical generator
Looking at the molecules they are highly conjugated —must be dark red or similar!
And the disease is photosensitivity. Aromatics + UV? That is a standard UV radical reaction. It may be enough as a catalyst, but you'll get more will a cyclic amine, such as pyrrolidine or piperidine. If you want to go technical confer: Hofmann–Löffler reaction.
The radical will be passed on to other molecules, such as oxygen (generating peroxide), which will damage DNA and will raise an alarm biologically ultimately attracting neutrophils, which are expecting some attack (not poisoning), thus causing local inflammation, which manifests as skin irritation.
Demethylation
With the caveat that secondary metabolism is highly promiscuous and that some modifications are more accidental that anything else, let's look at the methylation and membrane permeability.
Promiscuity and secondary metabolism evolvability
This figure I found has the methylation patterns. A first glance I have assumed it was the usual C-methyltransferase action adding methyl groups, but instead it is a removal twice in the case of fagopyrin B and once in C and D. Specifically, fagopyrin is clearly two condensed anthraquinones molecules (emodin?) —which is a rather interesting non-standard change, I have not looked but so hope that someone has found the enzyme responsible! As you point out an anthraquinone is made by polyketide synthesis: the last acetyl-CoA results in a methyl group on the aromatic structure, which is occassionally oxidised to a carboxyl group (e.g. rhein) and in this case decarboxylated —I do not think a C-methyltransferase can remove groups even with pushed stoichiometries nor do I believe I have heard of one. But anyway. The anthraquinone condensing enzyme may not be able to tell apart the standard and the demethylated metabolites, which is otherwise meant for another pathway, i.e. it could just be promiscuous.
Membrane
Let's calculate the effect on solubility (python3 w/ RDKit).
Wikipedia has the SMILES string for the main fagopyrin and it's easy to spot the methyl groups.
from rdkit import Chem
from rdkit.Chem import AllChem
from rdkit.Chem.Draw import SimilarityMaps
# let's make the molecules
normal = Chem.MolFromSmiles('O=C1C2=C(C3=C(O)C(C4CCCCN4)=C2O)C(C5=C6C(C)=CC(O)=C15)=C7C(C3=C(O)C(C8NCCCC8)=C9O)=C9C(C%10=C7C6=C(C)C=C%10O)=O')
demeth = Chem.MolFromSmiles('O=C1C2=C(C3=C(O)C(C4CCCCN4)=C2O)C(C5=C6C=CC(O)=C15)=C7C(C3=C(O)C(C8NCCCC8)=C9O)=C9C(C%10=C7C6=CC=C%10O)=O')
# no need to orient them as the indices are the same. Whoohoo
img=Chem.Draw.MolsToGridImage([normal, demeth],
                              molsPerRow=2,
                              subImgSize=(200,200),
                              legends=['w/ methyls', 'w/o methyls'],
                              useSVG=False).save('/Users/matteoferla/Desktop/mols.png')

Now let's calculate logP (Partition coefficient).
    print('w/ methyls', Descriptors.MolLogP(normal))
    print('w/o methyls', Descriptors.MolLogP(demeth))

w/ methyls 6.71
w/o methyls 6.0

They are really soluble in octanol and insoluble in water. The unmethylated version is less hydrophobic.
Let's look at what is causing the difference by looking at the Crippen contributions to logP. Using the BluePurple colormap (suggestions welcome for best colormap for this descriptor), so that purple is hydrophobic while light blue is hydrophilic. Note that this is not partial charge (Gasteiger).
for mol, name in ((normal, 'meth'),(demeth, 'demeth')):
    AllChem.Compute2DCoords(mol)
    contribs = Chem.rdMolDescriptors._CalcCrippenContribs(mol)
    fig = SimilarityMaps.GetSimilarityMapFromWeights(mol, [x for x,y in contribs], colorMap='BuPu', contourLines=10)
    fig.savefig('/Users/matteoferla/Desktop/'+name+'_crippen.png', bbox_inches='tight')

The difference is a result of the methyl groups, being slightly more electron withdrawing than hydrogens making the carbon between it and the hydroxyl/ketone more hydrophobic. But overall does not change the polar sides, so is in effect unlikely to have an effect on its high membrane permeability.

The methylated fagopyrins are in fact the first fagopyrins, from which the unmethylated fagopyrins derive. The methyl groups are in the aromatic structure and in fact derive all the way from the first polyketide synthetized in the pathway (which leads in St John's wort to hypericin and pseudohypericin, which also have methyl groups (two in hypericin and pseudohypericin having one, the other being hydroxymethyl)). My conjecture regarding membranes is from extrapolation from how cholesterol fits better in membranes than its precursor lanosterol, which may be faulty reasoning.

I had mistakenly though they were extra added in addition. My bad. I have expanded that part of the answer —although it is a bit off topic now. The radical generator paragraph is satisfactory, though?

Yes, it's sastifactory enough.

Great. Don't forget to mark the question as solved then.


text:
Limbs in synapsids
Within synapsids, there was a change from a lizard-like sprawling posture (like in pelycosaurs) to a more erect stance. Non-eucynodont eutherapsids seem to have had a facultatively erect hindlimb and sprawling or semierect forelimbs. Eucynodonts seem to have had an obligatorily erect hindlimb and semierect forelimbs. Yet so many mammals (especially monotremes) and one tritylodontid seem to have had non-erect hindlimbs. What could have driven them to a non-erect hindlimb? Were there mammals with facultatively erect hindlimbs?

Your main question is unclear to me. Please do not ask multiple questions. I would suggest that you rephrase your question title and the background so that your main question is clear.

Monotremes do not have a sprawling posture, squat posture is not the same as sprawling.Pleas ask only one question per question.

I think you are confused about what erect limbs means, monotremes have erect hindlimbs. Erect is not the same as pillar erect (which is exceedingly rare) Just because a limb is bent or a joint can rotate does not mean it is not an erect limb. More importantly terms like semi-erect don't actually mean much, it is a weak gradation not discrete categories.  Like most things in biology nature does not respect our attempts to pigeon hole. Many animals can in fact switch between locomotive style.
To answer your second question, limb posture is often modified for specialized environments like aquatic living or burrowing. Which is why seal and mole limbs also have odd arrangements.


text:
What are names of the colon delimited fields in this FASTA header?
The human chromosome DNA data in Ensembl release 96, here is in FASTA format.
Reading the Wikipedia article on the FASTA format, I understand the first line, prefixed with >, is variously referred to as a "comment" or "sequence headers". However, looking at FASTA files from different sources, it appears this first line is quite variable in actual content.
What are the colon separated fields in this FASTA header (as found above on the Ensemble FTP site)?  Most fields are guessable, but an explanation of each field would be much appreciated.  I believe the 46709983 is the number of base-pairs in the chromosome.
>21 dna:chromosome chromosome:GRCh38:21:1:46709983:1 REF
Finally, how should I have figured out the meaning of the header notation for myself?  Is there a list of common or known header formats?

According to ensembl's website (albeit somewhat buried in a page about downloading data via FTP) it says:
"The header line in an FASTA dump files containing DNA sequence consists of the following attributes : coord_system:version:name:start:end:strand This coordinate-system string is used in the Ensembl API to retrieve slices with the SliceAdaptor."
A brief rundown of these attributes as I understand them:

coord_system- Is simply the coordinate system used to locate a particular feature within an assembly: "chromosome" and "BAC clone" are common examples as described here.
version- This is the current version of the assembly reference. And refers to an Ensembl archive as detailed here. (Yours appears to be from the human GRch38 assembly).
name- This seems pretty self explanatory. In this case we are looking at chromosome 21.
start- Again, self explanatory. Any complete chromosome or contiguous sequence is going to start at "1".
end- End of the fasta sequence. [start] - [end] + 1 = total length
strand- This refers to orientation (i.e. forward or reverse strand) 1 is forward (-1 is reverse)

Here is a link to a pdf containing this information and more about using Ensembl (see page 23)...
Unfortunately, to answer your final question, there is no easy way to come across this information and there are as many ways of labeling fasta files as there are sequence databases. Sequence repositories have come a long way in the last 10 years but there is still a lot of work to do toward standardizing data formats and making databases more user friendly.

Thanks David. I had looked at that page last week, in fact (it was helpful to know Ensembl supports rsync), but not read it closely enough, evidently. Cheers!

@RichardMichael fasta header can be anything. It is flexible because different fasta files would have different kinds of sequences. Therefore one standard will not suit them all. Moreover, fasta header is not really meant for annotation. If there is a GTF associated with the fasta then you will have the genomic co-ordinates and some other information (for e.g. the gene name) in the former.


text:
What is a deep exhalation/inhalation?
I tried to find the academic definition of deep exhalation/inhalation but found nothing special.
I speculate that the correct definition is as follows:

• Deep Exhalation: Exhaling the air with effort as much as possible,
  after a normal "inhalation".
• Deep Inhalation: Inhaling the air with effort as much as possible,
  after a normal "exhalation".

The corresponding volumes of the air which is being moved inside respiratory tracts would be:
Vdeep exhalation = Tidal Volume + Expiratory reserve volume (ERV)
Vdeep inhalation = Tidal Volume + Inspiratory reserve volume (IRV)

But, in case we define them as below, the previous conclusion regarding the volumes turns wrong and consequently should be revised.

• Deep Exhalation: Exhaling the air with effort as much as possible,
  after a normal "exhalation".
• Deep Inhalation: Inhaling the air with effort as much as possible,
  after a normal "inhalation".

Vdeep exhalation = Expiratory reserve volume (ERV)
Vdeep inhalation = Inspiratory reserve volume (IRV)

I think it's impossible to assess without any subtle definition. I'm really confused.
Any help would be highly appreciated.

You should investigate the concept of a collapsed lung. I think that may allow you to answer your question.

@TheNate Thank you. I'll give it a try. In the meantime, possible to let me know if there's a more active biology forum to ask questions? It seems Stackexchange is not too crowded by biologists as much as by developers!

Deep inhalation and deep exhalation are informal terms and cannot be defined by lung volumes, because saying deep by itself does not tell how deep.
In the first part of the question deep refers to maximal:

Deep inhalation that means inhaling the air with effort as much as possible = maximal inhalation
Deep exhalation that means exhaling the air with effort as much as possible = maximal exhalation

According to Physiology, Residual Volume (StatPerls):
The volume of air in the lungs after maximal expiration is called residual volume (RV).

Residual volume (RV) is the volume of air that remains in the lungs
  after maximum forceful expiration. In other words, it is the volume of
  air that cannot be expelled from the lungs. This volume remains
  unchanged regardless of the lung volume at which expiration was
  started.

The volume of air in the lungs after maximal inspiration is called total lung capacity (TLC).

TLC is the total volume of the lungs at maximal inspiration.

According to Merriam-Webster dictionary:
Expiratory reserve volume = the additional amount of air that can be expired from the lungs by determined effort after normal expiration.
Inspiratory reserve volume = the maximal amount of additional air that can be drawn into the lungs by determined effort after normal inspiration.
Lung volumes:

Image source: Wikipedia, Creative Commons License


text:
Rubbery Orange and Fuzzy Mould From Bread
So I share a house, and my other housemates are currently away. One of them had some "plain" bread (a popular type in Scotland), complained a piece had mould on it, and so I had assumed they'd thrown the rest away before they left.
So you can imagine my bemusement when I decided I wanted some toast, opened the bread bin and was greeted by this:

You can just about see where my housemate's bread was, in the red packet on the left under the mass of orange and fuzz. The loaf in front was unopened, but the packaging was just so covered in this stuff I had to throw it away.
Now I didn't think to take any more pictures, as my priority was getting rid of this, on which I may have gone overboard (if I'd had a flamethrower I'd have used it) so there's no trace left. I only became curious later, but looking around on articles about bread mould I haven't found anything whose description seems to match what I'm seeing; in fact most are just describing the usual blue/grey mouldy patches seen on the bread itself, and none of the pictures I've found show anything that looks like this, the worst showed a piece of bread entirely blue/grey with a few millimetres of fuzz on it. Articles on orange mould seemed focused on the type that can appear on grout and such, and wasn't immediately identifiable as being the same thing.
The fuzzy parts appeared fine like concentrated spiderwebs, while the orange stuff was somewhat rubbery, or at least the bits left stuck to the plastic bread bin after I got rid of the worst of it. Also of note is that there was a lot of something, presumably spores, when I opened the bread bin, or maybe just the spider-web like stuff disintegrating; fortunately I wasn't breathing in at the time. This stuff has grown quickly as well, though I expect the mouldy bread must have been bad when my housemates left, this orange/fuzzy stuff has exploded out over only about two or three days.
Anyway, I'm curious, is this just some normal progression of the common penicillium variety, or is it something else? Is the orange the natural colour, or has it leached colour from the wasted loaf's packaging?
Apologies for being a bit imprecise, my scientific background is in computers, and the scientist part of my degree really just means I'm a programer.

Post it to Paul Stamets else another mycologist. ID'ing that type of species is pretty difficult! https://www.emlab.com/resources/sampling-guides/pcr-mold-sampling/


text:
Why does it hurt when you take sweets, if you have cavities in your teeth?
When you have cavities in your teeth taking any sweetend drinks or food causes sensitivity or pain. What could be the reason?

I think bacterial metabolites cause the pain. At least my experience that salt water kills bacteria (except halophiles) with it's high osmotic pressure and so the pain goes away almost immediately. Hyper pure chlorine-dioxide (as an oxidizing agent) has the same effect, but it is a bit expensive compared to salt.

The outer shell of a tooth is enamel, which is hard and dense so that not much can penetrate it.  Under that is dentin (or dentine), which is bony but has microscopic channels running through it to the center of the tooth where the pulp and nerve reside.  If the enamel is breached, as with a cavity, crack, or wear, the dentin is exposed to the environment of the mouth.  When sugar comes against the dentin, it draws fluid out of the microscopic channels (because sugar attracts water strongly).  The fluid flow causes pressure changes around the nerve of the tooth, which reports the change to the brain where it registers as pain.  Dentin is highly sensitive not just to sugar, but also to hot, cold, pressure, and other stimuli.  (This sugar response is a short term one; the influence of sugar on bacteria is a longer-term effect in which the acid generated by the bacteria eats away the enamel layer.)

Well if it was the osmotic effect of sugar then salt should also elicit pain which is not the case. Can it be the acid produced by the acidogenic microorganisms? but then there would be a time lag or unless the acid production is very rapid.

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text:
What is the nature of false negatives on Covid-19 Lateral Flow Tests?
Mainly the thing I'm trying to understand is "how do repeated LFT testing and PCR testing interact with false negatives".
But I think the answer to that is a fairly direct function of what causes false -ves on LFTs.

Is it simply that whatever the testing "pallet" does has a random noise component to it, and sometime you get unlucky?
Is it that the sampling process is noisy, and thus sometimes you get unlucky with the swab and don't catch any viral particles?
Is it that sometimes the body is compromised but immune system controls the viruses presence in such a way that there isn't anything in the upper-respiratory tract?
Is it that some mutations of covid don't trigger the tests?
Something else?

Respectively for the above possibilities, they would mean that:

If you get a false -ve, you could just put new drops form the same sample in another pallet and immediately get a true +ve.
If you get a false -ve, you could take another swab and immediately get a true +ve.
Either:

If you get a false -ve, then that might indicate that LFTs are mostly worthless for you personally. (If your personal immune system fundamentally prevents them doing their job)
If you get a false -ve, you would consistently get false -ves for at least another <x days/hours>

If you get a false -ve, you will continue to get false -ves for the entire course of this infection ... but LFTs might work again on a different infection.
???

And likewise for the interaction with PCR testing:

LFT result has no interaction whatsoever with PCR.
If you had used that particular sample for the PCR test then you would have gotten another False -ve.
If you take 2 samples for LFT and PCR at the same time then you'll get False -ves on both.
LFT result has no interaction whatsoever with PCR.
???

Obviously, plenty of those guesses may not be biologically or statistically possible ... but hopefully they're useful as an indication of the sorts of distinctions I'm asking about and the effects that the mechanics of a False -ve could conceivably have.

Another way to phrase this could be ... "If I take lots of LFTs one-after-another, after a high-risk exposure, and they're all -ve ... does that change the odds of whether I'm actually covid-free?". "What if I take them over the course of a day/week?"

Or "If I tested continuously LFT -ve for 2 weeks, but consistently PCR +ve in the middle ... does that tell me anything interesting/useful about future LFTs"

Is it simply that whatever the testing "pallet" does has a random noise component to it, and sometime you get unlucky?
Is it that the sampling process is noisy, and thus sometimes you get unlucky with the swab and don't catch any viral particles?
Is it that sometimes the body is compromised but immune system controls the viruses presence in such a way that there isn't anything in the upper-respiratory tract?
Is it that some mutations of covid don't trigger the tests?
Something else?

Yes -all of the above, apart from the "immune system controls viral presence to not upper respiratory tract" point. That bit is almost entirely down to viral factors and attachment factors such as the presence of the receptor proteins/sialic acids etc.
Basically the way that lateral flow tests work is that they solubilize the sample, which is then dropped into the well. From there the liquid moves along into the flow part of the test, filtering out large junk and binding to labeled antibodies. When the sample reaches the test line, a second antibody binds to the label on the first antibody, which results in a coloured reaction between two chemical components. The control line does similar, but is designed to detect any antibody or perhaps something that is spiked (added) into the kit as a control. There's a description and video of how these work here.
If any one of these steps goes wrong, from getting a sample without enough virus, to no reaction at the control line (or at the test line), then you could have a false negative. A common problem is not sampling enough virus to work. I don't know how much virus is needed to be added, but in my tests on early versions of these with purified virus (not nasal swabs), I could get down to about 1000 viral particles per test based on qRT-PCR assays of viral concentration. The sensitivity of these tests will depend on the brand and exactly what they are testing for, and should come on an information sheet which you can either get with the test or look up on your health authorities' authorization of the tests.
However, the most common false negative I suspect will be that the test subject has been tested outside the test window, and there is not enough virus present to trigger the test as positive. Generally you need to be between about 3-days and 2-weeks post-infection for these tests to detect SARS-CoV-2 in patient samples.
On the other hand, PCR tests are much more sensitive, and can detect the virus before you are infectious, and long after the infectious window has passed.
There's a good graph of this from a paper by Dankova et al at the International Journal of Environmental Research and Public Health1:

In this case the lateral flow test is marked as "Ag" (for antigen; these tests are often called rapid antigen tests (RATs) too). As you can see the Ag section is quite short and starts well after the infectious period starts.
Now for your next bits:

Respectively for the above possibilities, they would mean that:

If you get a false -ve, you could just put new drops form the same sample in another pallet and immediately get a true +ve.

Possibly, but this would be a failure of the first test rather than a testing/sampling problem

If you get a false -ve, you could take another swab and immediately get a true +ve.

Maybe, this could be a sampling error, nothing to do with the test itself, or a test failure.

Either:
* If you get a false -ve, then that might indicate that LFTs are mostly worthless for you personally. (If your personal immune system fundamentally prevents them doing their job)

No, they shouldn't be personally worthless to you, they don't have anything to do with your immune system or any part of your body. When there is enough virus there, they should detect it.

  * If you get a false -ve, you would consistently get false -ves for at least another <x days/hours>

Maybe - this could be that you've sampled outside the window for the test to work, as you sort of hint at, or that you didn't sample properly

If you get a false -ve, you will continue to get false -ves for the entire course of this infection ... but LFTs might work again on a different infection.

No, this is very unlikely unless you have a dramatic genetic change in the virus such that the antigen is no longer picked up by the test.

And likewise for the interaction with PCR testing:
*LFT result has no interaction whatsoever with PCR.

They don't interact - they don't detect the same thing. The PCR detects the viral RNA, the LFA/RAT detects viral proteins.

If you had used that particular sample for the PCR test then you would have gotten another False -ve.

Maybe, PCR is much much more sensitive and capable of detecting the virus for longer, so a negative on a LFA/RAT doesn't mean a PCR would be negative. False negatives by the PCR tests are very rare as the tests include internal controls to ensure a correct sample has been taken.

If you take 2 samples for LFT and PCR at the same time then you'll get False -ves on both.

Unlikely. Same as immediately above. Repeat sampling of the same sites could remove the necessary material for the test to work. However, generally the PCR swab is taken in the deep nasal tissues, while the RAT/LFA is from shallow and/or throat. The PCR should also work on the RAT/LFA samples, but I believe is less reliable due to the presence of nasal mucus which interferes with the reaction. I'd have to really dig through the literature to find a reference for that, but I think I read one a couple of years ago.

LFT result has no interaction whatsoever with PCR.

Same as 3 points above.
1: Dankova, Z.; Novakova, E.; Skerenova, M.; Holubekova, V.; Lucansky, V.; Dvorska, D.; Brany, D.; Kolkova, Z.; Strnadel, J.; Mersakova, S.; Janikova, K.; Samec, M.; Pokusa, M.; Petras, M.; Sarlinova, M.; Kasubova, I.; Loderer, D.; Sadlonova, V.; Kompanikova, J.; Kotlebova, N.; Kompanikova, A.; Hrnciarova, M.; Stanclova, A.; Antosova, M.; Dzian, A.; Nosal, V.; Kocan, I.; Murgas, D.; Krkoska, D.; Calkovska, A.; Halasova, E. Comparison of SARS-CoV-2 Detection by Rapid Antigen and by Three Commercial RT-qPCR Tests: A Study from Martin University Hospital in Slovakia. Int. J. Environ. Res. Public Health 2021, 18, 7037. https://doi.org/10.3390/ijerph18137037


text:
How the brain is affected by Alzheimer's disease

What exactly happens to the neurones in the brain?
why can't they be repaired/restored?
Why is it that there are so called 'good days'? What happens to the brain on such days?

Essentially, there's a net dysregulation of a number of genes where the additive effect of each dysregulation causes neurotoxic amyloid plaque formations, and neurofibrillary tangles of hyperphosphorylated tau protein. Not only so, these mutations induce calcium and cytokine dysregulation, and increase oxidative stress.
Specific to molecular mechanisms of amyloid beta (abeta) oligomer toxicity, a good article here makes some good descriptions. For example, abeta can reduce copper and iron ions. Oxygen reacting with these reduced metals become reactive oxygen species. They also noted that abeta reacts with many receptors, like TLR's which ended up promoting JNK-mediated apoptosis. I'd give that article a read, and I'll try to get some molecular pathology mechanisms for other facets of AD on board here.
They can't generally be repaired because the issue is with genetic mutations, and some of the mutations engage in positive feedback loops with existing conditions that make a more pronounced effect. For example, tau protein is regulated in part by O-GlcNAcylation. This is like phosphorylation, but with sugar moieties, but it becomes downregulated when glucose is low, thus increasing phosphorylation on tau (Liu et al., 2004) . Mutations that affect GSK-3, insulin resistance and/or diabetes thus can play a role in AD pathogenesis.
Some data exists to show restoration of potentially AD-causing abnormalities involving HDACs. For example, abnormal HDAC2 in AD brains hypoacetylated promoter regions for some housekeeping and plasticity genes, and they rescued the AD phenotype by knocking down HDAC2 (Gräff et al., 2012) . These are of course mouse models typically.
As for question three, I really can't say except for stochasticity. I did a review for an undergraduate course that goes over some of the recent literature involving AD genetics/pathogenesis. It might not be professional quality but it gets the message across, linked https://drive.google.com/open?id=0BwKiapIJL9T2ajc4ajhTVVRvRWc

all_licenses: Creative Commons - Attribution Share-Alike - https://creativecommons.org/licenses/by-sa/3.0/


text:
Gene Circuits; experiments
First, my background - I'm a newcomer to biology.
What is a gene circuit, and how might I simulate one in a laboratory? Thank you.

What kind of laboratory? Are you looking for computer simulations?

No, I was referring to a physical laboratory. What sort of equipment would I need?

You question is likely too broad in its current format. You have, essentially, two questions in one. Why not do some research on what gene circuits are to start with? Explain briefly what you know, and then get at the question of how to model them in the lab. Learning something about gene circuits first might help you better define your question of how to simulate one.

I'm just going to give a broad idea of what a biological circuit is.  There's definitely more than one way to define them, but hopefully this will give you some idea.
Broadly, biological circuits are reminiscent of electrical circuits in that energy or information flows through the cell.  In biological pathways (a more typical terminology), genes in the cell (usually proteins) will use a signal (usually in the form of a chemical compound or a modification of a protein, but sometimes a simple ion or even electrical current (rarely)).  The signal then can be transmuted into a different chemical compound or it can even alter a protein so that it functions differently.
Here are a couple of classic examples.  The first is the Citric acid cycle (also called the Krebs cycle), discovered in the 1930s.  Here you can see that Citrate is chemically transformed into acetate and carbon dioxide and chemical energy in the form of NADH (reduced nicotinic acid dinucleotide).  Each step of the cycle has a different compound which is handled by a different protein enzyme.  While all the proteins and compounds may coexist in the same part of the cell, there is nonetheless an orderly circuit of chemical energy mediated by the genes of the cell and controlled by the cell as it adjusts the amount of enzymes available for each step of the cycle.

Another example of an entirely different sort of gene pathway works differently but has the same set of concepts.  Mitogen Activated Kinases (MAPKs) are proteins which have generally two states an activated state and an inactivated one.  As you can see below, an outside signal like high salt osmolarity or a signalling molecule is sensed by a receptor on the cell surface.  By some method a MAP Kinase is activated, perhaps by the addition of a phosphate to the surface of the protein or by dimerizing the MAPK.  Once activated, the MAPK will then phoshphorylate another kinase, which may activate yet another.  Finally a protein in the nucleus will be activated and cause transcription of some target genes.

In the latter case, a very small change to the protein costs little energy and information is being transmitted, but by biochemical signals where proteins are modified and affect other proteins.  That's a more subtle circuit than in the former case where relatively many individual molecules might be processed by enzymes together.
This hopefully gives you some idea of what a biological circuit looks like.  There are many other examples and subtle variations but that's a quick tour.
Experiments involving these pathways are too numerous to mention - individual proteins may be modified, their concentration within the cell can be altered by say mutations in the chromosome, pathway intermediate compounds like Succinate might be added to see how the citric acid cycle responds, isotopic labeled compounds can be added to see where they go in the cell.  There's nearly 100 years of experiments here.  that's a lot.
Hopefully this will just give you some idea of where to start.  Nearly any biochemistry textbook covers these topics in better detail, but then they are often over 1000 pages long!

A genetic circuit can be likened to electrical circuits, except rather than switches, resistors, wires, etc., you use promoters, ribosomal binding sites, coding sequences, repressors, etc. - This will get you well acquainted with the new jargon around bioengineering: http://parts.igem.org/Main_Page


text:
When was the purpose of bone marrow discovered?
I'm currently reading William Cheselden's book Osteographia or The Anatomy of the Bones, which was published in 1733 (for the pretty pictures, naturally; not up to date anatomy). When he addresses the topic of bone marrow, he says,

Every cylindrical bone has a large middle cavity, which contains an oily marrow, and a great number of lesser cells towards their extremities, which contain a bloody marrow. [...] The bloody marrow is also found in all spongy cells of the bones. [...] The use of the first kind of marrow I imagine is to soften, and render less brittle, the harder fibres of bones near which it is seated; and that the other marrow is of the same use to the less compact fibres, which the more oily marrow might have made to soft; and that for this reason, there is less of the oily marrow, and more of the bloody in young bones than in old ones.

Which strikes me as completely incorrect -- though correct me if I'm wrong. So, when was the purpose of marrow in hematopoiesis discovered, and by whom?

Answer: In the late 1800s, by a few different guys building on each other.
I personally had no idea, but a little searching around found this little gem, which seems up our alley: The origins of bone marrow as the seedbed of our blood: from antiquity to the time of Osler.  It's only ten pages so definitely worth a read, but a few passages of note:

Neumann and Bizzozero... are credited with making the initial observations leading to the recognition of the marrow as the seat of blood formation... In his report published in October 1868, Neumann described the presence of nucleated red blood cells in the bone marrow sap of humans and rabbits by squeezing bone. He was the first to conclude that during postembryonic life, erythropoiesis was taking place in the marrow.

However, Neumann concluded erroneously that the proliferation of marrow cells occurred inside the blood vessels of the marrow; the concept of marrow sinusoids was not coined until Minot's description in 1901.

It later says that, in the mid-1880s Osler stated

that there can be no doubt that nucleated red cells originate in the bone marrow...

It's actually a pretty interesting read, all in all, and like all of the best discoveries in science, it seems like a few people built on each others' work over the years, with a bunch sort of figuring it out around the same time.


text:
What is the animal in Nosferatu movie?
I was watching Nosferatu, and this dog-like animal appeared, with very curious stripes. I was wondering if this is clearly a specific animal, and which one it is, or if it's too mixed up and low resolution to tell. You can see in this video, at 11:43 and 12:22 (close up) to 12:33.
https://www.youtube.com/watch?v=PH7L4V-3VxA&t=703
Sorry about my lack of a more scientific research, but I couldn't be farther from being a biologist. This is all I got: from the stripes, it immediately brought to my mind a Thylacine (which is what caught my attention), but even though it would not me an anacronism (it was extinct in 1936, the movie is from 1922), the movie is European (filmed in Germany, Slovakia and Romenia) and the story happens in Europe too, so it wouldn't make sense to be a Thylacine (not to mention that in 1922, you wouldn't find them right around the corner ;) ). Further investigation confirmed the already almost obvious, the stripes are too in the front in their body to be a Thylacine. My second thought, from the apparent big head and the way it moves (hips lowered), it resembled a hyena to me. But it doesn't seem to have ears big enough, they also wouldn't make sense in context of the movie, and hyenas usually have spots instead of stripes. A quick search showed me that there are striped hyenas, and from pictures it looks kind of similar, but the snout doesn't seem to match. Also, they don't occur in Europe, according to Wikipedia.
So at this point I'm in doubt if it's a striped hyena (that doesn't seem to make sense to me), another real animal that I don't know, or if it's a fictional creature, some animal "modified" specifically for the movie (painted, extra/less fur, artificial modifications in height, body size, ear size, etc). Although that also doesn't make sense.
Any pointers appreciated, sorry if this should belong in scifi or another SE.

It looks like a natural Hyena to me. But you can look into the possibility of "Wild dogs".

definitely a hyena. MSB they could have footage from other movies or even zoos, recycling footage is a age old practice. Notice it is never seen with anything else in the same shot. likely B-roll. Just look at the second shot where it stands up in profile, very easy to identify.

@John Early vampire movies are famous for misplaced wildlife. The 1931 Dracula movie famously depicted a wild armadillo in Transylvania.

It's a striped hyena, it is relatively rare/endangered these days. Hyenas are closer to cats/felines than to dogs. They are in the suborder Feliformia.
https://en.wikipedia.org/wiki/Striped_hyena
some images here

Did they occur in Europe in the past?

The range used to be at least up to lebanon and Georgia/Armena, So there's chances that they were in western europe a few thousand years ago. Elephants used to live in egypt, north africa and turkey only until roman times too.

there was a cave hyena in europe until about 8000 years ago.


text:
Are there any open plant databases (database/library/collection), containing species information and pictures?
I would like to download a plant database containing photos and species details. Do you know if there are any openly available online?

Large online floras have the advantage of not only having details and often photographs and illustrations, but also being (more or less) definitive, that is, botanists will refer to them.
See my answer here for links to examples, and also for some of the problems with using floras (e.g. not easily downloadable).

They really need to release a database version of Mabberley's Plant Book

The United States Department of Agriculture have a plant database (http://plants.usda.gov) where you can download search results and checklists. Look at their download page. However, I think that you can only download text (no pics), and it mostly (only?) contain plants found in the US. I have not used the download functionality myself, so I do not know anything about flexibility or interface.


text:
Edible and non-edible leaves
For humans, what's the difference between an edible leaf like lettuce, and a non-edible (in the sense of null nutritional value) leaf like grass?

What would the answer to this question help you achieve?

What context are you looking for, digestibility, why one is more palitible, what selective pressures make humans not think grass tastes good. Because as it stands the answer is "one tastes good and the other does not" Please flesh out your question, also show some attempt to answer the question yourself as "homework" questions are considered off topic without it.

For grasses leaves tend to be inedible due do with the high quantity of silica deposited in the leaves to form structures known as phytoliths Wikipedia.
While this has been shown to inhibit digestion by insects (Hunt et. al., 2008, Massey et.al., 2006), I'm not aware of any studies on how this affects digestibility for humans.  There are however anecdotes about people starving to death with grass stains around their mouths during the Irish Potato famine.

I'm not convinced the ability of humans to subsist on grass is due to inhibition of digestion; I think it's more likely that we wouldn't be able to digest the carbohydrates in grass anyway. It doesn't seem likely to me that high quantities of silica would be the major limitation of us digesting something. Grazing animals manage just fine on grass, albeit with adapted digestive systems.

@Jam
I'm not aware of a significant difference in the types of carbohydrate present in grass  leaves vs. those of "edible" leaves like lettuce.
However, there is some research showing that silica inhibits both palatability and digestibility for grazing mammals (Shewmaker et. al., 1989, Hartley and DeGabriel, 2016).

Nutrient content of lettuce and grass can be similar.
According to USDA.gov, 100 g of green leaf lettuce contains:

Protein = 1,4 g
Digestible carbohydrates = 1.5 g
Calcium = 36 mg
Potassium = 194 mg
Magnesium = 13 mg
Fiber (cellulose or similar) = 1.3 g

According to Feedipedia (see Nutritional Tables), 100 g of Bahia grass contains:

Protein = 3.5 g
Digestible carbohydrates = 0.6 mg
Calcium = 160 mg
Potassium = 400 mg
Magnesium = 27 mg
Fiber (cellulose) = 7.8 g

The "leaves" (shoots) of most grasses are considered inedible, because they:

are unpalatable
are hard to chew because of high cellulose content
can probably make you sick; at least it can make dogs vomit (PNAS)
contain silica that can wear your teeth; some types of grass are also toxic (eattheweeds.com)

Would it make sense to eat grass in a survival situation? No, because 100 g of grass contains only about 20 Kilocalories, mainly from protein and a little bit from cellulose fermentation by intestinal flora in the colon (gut.bmj.com). It's also quite possible you would vomit or get diarrhea after eating grass.

I don't know if all those things are true (i.e., I'd want to see a reference for having the same amount of micronutrients, differences in chewing difficulty) but in any case that comment I think is much closer to answering the original question. I'll clean up this comment thread.

Good answer but the Daily Mail isn't a particularly academic source.

@Jam, OK, it is known that dogs and cats eat grass to make them vomit when they are sick; there are literally no studies that would even mention eating grass by humans.


text:
Why don't surfactants destroy or incorporate into cell membranes?
How do surfactants remain on the surface of pneumocytes without  (1) acting as a detergent or (2) the phospholipids getting incorporated into the membranes of pneumocytes...
I'm guessing the answer has something to with the secretions of clara cells, but I'm curious for a more biophysics-y answer... for example how do the phospholipids that compose surfactant not form miceles or are the miceles simply larger that the individual component phospholipids (I'm basing this off the answer to "how do detergents get in hydrophobic membrane interior"), but even so why wouldn't the micelle simply fuse into the membrane

Found this so far, it's from "Topology and lipid selectivity of pulmonary surfactant protein SP-B in membranes:
Answers from fluorescence"--
"The presence of the hydrophobic surfactant proteins SP-B and SP-C is strictly required to facilitate an efficient transfer of phospholipids from surfactant stores (in the form of bilayers) at the aqueous hypo-phase into the interfacial film, and to maintain the film operative along the compression–expansion breathing cycles"


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Are there any 6 limbed reptile fossils?
Were any 6 armed "tetrapod" fossils ever found? I've seen some lobe finned fish with two sets of shoulders in an evolutionary bio book... I'm curious because I'd like 4 limbed and 2 winged dragons to have existed :)

I don't know about dragons, but the fossil record does show that some fascinating, tiny vertebrates (including members of the genus homo) existed some 425 million years ago :).

as i understand it cambrian-->orovician-->silurian-->devonian... vertebrate popped up in cambrian... the attached link is talking about silurian... my question (six armed tetrapod) probably localizes to the Devonian...

Sorry, that link is a joke. It is a guy who won an IgNobel for finding what he considers to be fossils of tiny equivalent of various modern life forms,

this research was actually done?!?

Yup :). You should check out the Annals of Improbable Research and the IgNoble prizes, they're great.

I think this is a reasonable approximation. The Genus Draco

I think, you misidentified the unpaired anal fin of coelacanth as an extra pair of limbs.
I personally haven't ever heard of six-legged vertebrates, although the phenomenon of supernumerary legs is well known as an anomaly. Such anomalies can be easily induced in different vertebrates (including mice: Rutledge et al), if you treat their embrya with retinoid acid (which normally defines embryonic polarity) or fibroblast growth factor. In nature, different factors can lead to development of extra legs, and the most well-known and wide-spread cases are limb abnormalities in amphibians, induced by trematodes and pollution (including retinoid acid mimics?) (Blaustein & Johnson).
That said, I would not be surprised by a discovery of a fossil amphibian with extra limbs. But such a find then should be interpreted as an abnormality, if not proved otherwise. It's true that the fore and the hind limbs are serial homologues, but their number seems to have been fixed very early (in contrast to the number of the fingers).

this is the original poster of the question (Jasand)... you're probably right about "unpaired anal fin of coelacanth"... I'm not too knowledgeable about evolutionary biology or zoology... kind of a shame though... I was hoping for another lineage of amphibian/reptile like creatures with six limbs instead of 4... oh well, I guess I'll have to be satisfied with 6 limbed arthropods...
I recall something about retinoic acid affecting the hox genes... the hox genes being responsible for segmentation in insects, but general space planning in vertebrate...

I was looking at a picture of Eusthenopteron, but the picture specifically says "it has paired pectoral and pelic fins with internal bony structure"...  I see more fins than that... probably the extras are cloecanth and whatever... I suppose the number of fingers is variable because it began after the sarcopterygians... but I was looking at these lobe finned fish for the hopes of finding more than 2 sets of paired limbs...

Yes, the unpaired anal fin creates a very strong feeling of another pair of fins. There is great variability in morphology of the fins in "Agnatha" (jawless fishes), such that even a case of paired anal fins was discovered in one fossil. Both paired and unpaired fins seem to have similar origin in terms of being derivatives of body folds, but I don't know, whether they can be considered true serial homologues. (See also this article).

And, please, don't forget to mark the answer as accepted if you find it proper :)

Thanks, sorry I'm new to this site... The picture of the fish I was looking at was in lateral view so paired/unpaired was hard to discern... Also thanks for the follow up info...


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Why do women process oxygen faster than men?
https://www.newsweek.com/women-are-better-athletes-men-study-about-gender-fitness-says-736047 is the source that I use. Is it reliable?
Why did men and women evolve that way? What's the evolutionary advantage to women being naturally more fit?
Does childcare and gathering fruit require being athletic? I would have thought that hunting animals and fighting enemies would require being athletic.
So, how did natural selection favor women that are more naturally fit and not favor men that are naturally fit?

Beware of claims made by single tiny preliminary studies  blown out of proportion by the science ignorant media. the study only included 18 people.

Additionally, be wary of the word choices, they stand on very shaky ground. Women are clearly and demonstrably not more fit than men, nor are they more athletic. The claim is that they oxygen consumption and extraction (loosely 'oxygen processing') is faster in the 9 tested women than the 9 tested males. That could be due to lung and body size, (e.g. smaller creatures like mice in comparison to elephants probably process oxygen more quickly; and there exists a body size discrepancy between human males and females). Or it could be a host of other reasons that confound the study results.

remember that sexist and racist news headlines bypass your rational brain and aim straight for the limbic system in the brain: i.e. when you read them, your emotional state reacts faster than your concious self which then reads the headline and understands it's meaning. so, mostly those headlines are nonsense, they just illicit instinctive attention.

There doesn't seem to be anything wrong with the paper, but as pointed out in the comments (and in the press release itself), the study was small, so any conclusions should probably be tentative. Adding a little more detail from the link:

For the study, which was very small, researchers recruited nine young males and 9 females, all roughly in their mid-20s. Females and males were of similar weights within their own genders. Everyone participated in the same exercise—walking on a treadmill—and scientists compared oxygen consumption and extraction in both genders during the workout. They found that the women were consistently more efficient than men, as they processed oxygen 30 percent faster.

Beltrame, Thomas, Rodrigo Villar, and Richard L. Hughson. “Sex Differences in the Oxygen Delivery, Extraction, and Uptake during Moderate-Walking Exercise Transition.” Applied Physiology, Nutrition, and Metabolism 42, no. 9 (2017): 994–1000.
A few more details from the paper itself:

you have to be very careful about interpreting what "faster" means in this case. The paper says:

The greater maximal aerobic power [VO2max] of men compared to women is well recognized (Cureton et al. 1986).

For example, "good" VO2max for 20-29 year old males is 42.5-46.4 mL/kg/min: for 20-29 year old females it's 33.0-36.9 mL/kg/min. This means that at peak intensity, men can process oxygen faster than women.

In contrast, the focus of this study is how fast women and men ramp up their O2 metabolism as they exercise.

Here's Figure 2 from the paper:

based on the figure and on table 1, the "mean response time" is about 50 seconds for women, 60 seconds for men.

the other caution about this study (besides the small number of participants) is that the authors appear to have tested 32 different parameters of oxygen uptake metabolism, for both men and women; many researchers would recommend a multiple comparisons correction in this case, to account for the fact that it is more likely for some comparisons to appear significant by chance when making many comparisons.

Finally, it would be hard to be do much evolutionary speculation for the reasons behind these sex differences ... one might want to start by doing a comparative study, to find out if these differences are unique to humans or whether they also appear in our close relatives (chimps, gorillas, etc.)

It is incredibly hard to know for sure which evolutionary preasuress in our past led to specific taits we see today - in completly different enviroment - but my bet is on surviving childbirth in prehistoric conditions. Also note that women used to spend significant portion of their adult life pregnant, and so any form of resistance to exhaustion would be quite benefitial for them.
Some sources:

... increased aerobic fitness was associated with shorter labor in nulliparous women who started labor spontaneously.

https://obgyn.onlinelibrary.wiley.com/doi/full/10.1080/00016340903093583

... moderate-intensity exercise performed throughout pregnancy was associated with a reduction in the rate of cesarean, instrumental deliveries...

https://www.tandfonline.com/doi/abs/10.3109/14767058.2012.696165


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Mechanism to limit the exponential growth of the number of ancestors that are n-generations away from an organism?
The context is organisms with sexual reproduction, with 2 parents per organism.
Construct the family tree of one such organism, back into geologic time.
Take a(n) as being the number of ancestors that are n generations distant.
The function a(n) has an exponential character (at least in the beginning, with n sufficiently small).
For 2^n, simple math gives:

After 20 generations, you have about 10^6 ancestors.
After 30 generations, you have about 10^9 ancestors.
After 50 generations, you have about 10^15 ancestors.
After 1000 generations, you have about 10^300 ancestors.

I've read one estimate that there are about 10^80 atoms in the Universe. What does this mean?
It's important to note the the members of generation n usually aren't all alive at the same time.
As an example, for humans, the birth-dates of generation-20 are roughly between the years 1720-1520, for example.
It doesn't take very many generations for a(n) to exceed p(t), the population as a function of time.
This is accounted for (at least for sufficiently low n) by the fact that a(n) represents organisms that aren't alive simultaneously, while p(t) does.
I understand that.
But, this effect, important as it is, seems to be linear with time.
As such, it doesn't seem capable of limiting the exponential growth of a(n).
In this context, inbreeding is often raised.
But, in my opinion, inbreeding is not germane.
Here, all that matters is that each organism has 2 parents.
Period.
Whether or not inbreeding was involved doesn't change that basic fact.
All inbreeding means is that one ancestor is a member of more than 1 generation.
That's not relevant to my question.
Edit later:
No, inbreeding is germane. It means that 2 members of a(n) can have the same two parents in a(n+1). That reduces the exponential growth of a(n).
It seems that a(n) must be limited by something, for sufficiently large n. What is that something?

In addition to @mgkrebbs answer, note that "inbreeding" refers to breeding among closely related individuals. Individuals several generations removed are not closely related.

Of course a(n) is limited, and much more tightly than by the number of atoms that exist.  The analysis in the question goes off track with "inbreeding is not germane. Here, all that matters is that each organism has 2 parents. Period."
Consider a person whose parents are first cousins. Then:

a(1) = 2
a(2) = 4
a(3) = 6, not 8

While each of the two parents has four grandparents, together the two parents have only six grandparents because they share one pair of grandparents.  This is due to pedigree collapse.
This table shows the actual collapse for some people with ancestry known to nine generations and with significant inbreeding (from de.Wikipedia):

I just realized that it's germane. I have edited the question a second ago. So is inbreeding the only mechanism for limiting the exponential growth of a(n)?

I see. It's this pedigree collapse idea which is the key. Thanks!

@JohnO at a point all organisms are a product of inbreeding since we all evolved from the same LUCA.


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Are all of my ancestors from 400 million years ago fish?
Say you have your family tree for the last 400 million years or so, back to the Devonian, the age of fishes. You take the set of ancestors that are about 400 million years old (which will be across multiple generations). The question is are they all fish?
Or, is it more complex than that? Can there somehow be non-fish in that set?
Note added later: this question is not a duplicate of another question.
In the context of that other question, howewever, my question can be stated as "Is Dawkins correct in stating that my 185th million ancestor was definitely a fish, with no exceptions?"

Possible duplicate of Same 185th million grandfather?

I would say no, it's not the same question.

Yes they all were because there weren't any land vertebrates, vertebrates were all fish at 400 million years ago.
It is a close call based on fossil evidence from 395 million years ago, there are footprints of 3 meter tetrapods from littoral/seaside fossils. https://www.sciencedaily.com/releases/2010/01/100107114420.htm
The earliest land vertebrate skeleton is from 375 million years ago. https://en.wikipedia.org/wiki/Tiktaalik

It is technically still a fish, so probably yes, the ancestral species of all land vertebrates were still fish. There are various experimental early quadrupeds, some with 6 fingers, which are cool reading.
They still exist in the form of lungfish.
Here are images of the earliest land vertebrates

It is worth noting the problems with the term "fish" . Depending on how you use the term humans can also be fish.


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How far can a human see at night?
I am not talking about seeing in total darkness, which I understand is not possible. I am looking more about a question how far can a human see during starry night or with half moon/full moon. I tried googling for this, but found no useful results.
EDIT I think I need to clarify: I am thinking more in terms of immediate surroundings. I understand we can a source of light from afar, but what about a tree on a flat land - from how far would we see it in star light?

A better, more scientific way to ask this question would be to ask about visual acuity as a function of luminance... there is no meaningful way to answer your title question without specifying other key parameters.

You would need to further specify it, for example, at a certain lumination (half-moon), from how far you could recognize a tree as an oak (from the shape of its leaves). Anyway, half-moon can be quite bright...

Hmm.. I would like to build some kind of intuition about this, not exactly have a formula. Would I be able to discern a tree shape from star light only in an empty field? From what distance? How about full moon? Are there any resources I could take a look at or examples? Examples would likely work best for me.

At night you can actually see further than during the day. At night you can see stars that are many light years away, but during the day the furthest thing you can see is probably the sun, which is 8 light minutes away. There's probably no definite answer because the brighter and bigger the object (and the darker the surrounding and the clearer the air), the greater the distance from which you can see it.
According to Sky and Telescope, the most remote stars (as part of Andromeda Galaxy) you can see with a naked eye are 2.5 millions light years away.
Talking about the objects on earth, at half-moon, you could see to "the end," that is to the horizon.

Thanks a lot for the answer, I clarified my question.

With clear, dark skies (no urban light pollution), about 2.5 million light years.  That's the distance to the Andromeda galaxy, which is visible (in the northern hemisphere) with ordinary visual acuity: https://en.wikipedia.org/wiki/Andromeda_Galaxy#Amateur_observing
Vision does not depend on distance, but on the brightness of the things being viewed, and their size.  That is, we see stars as points because their diameter is too small to resolve (angular resolution) but they still put out a lot of photons.  We see Andromeda as a fuzzy patch of light, because it is composed of lots of stars spread over a large distance.
For more ordinary things, it depends on the amount of light, and the size. Flying in a small plane on a clear winter night with half moon or more, it's possible to see snowcapped mountains 50 miles (80 km) or more distant.

Thanks a lot for the answer, I clarified my question.

The clarification doesn't really help.  What do you mean by seeing the tree?  Do you need to see the light reflected from it, or is it sufficient to see the shape of the tree blocking starlight?  You could probably calculate an approximate answer to the first case from intensity of starlight * reflective index of the tree * the inverse square of the distance, and comparing it to visual acuity.

OK, to clarify further: In an empty field, with star light, from what distance could I discern a shape of a tree? How about a person? And how about with a half moon or full moon?


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What is the human energy consumption by organ?
The human brain uses about 25% of the human body's metabolic energy. How are the other 75% spent, in terms of portioning to its various systems?
I thought this could be answered by a simple search, but I can't find the answer after searching very hard. I only got dieting advices.
I am envisioning the best answer to look like

You presumably didnʼt find an easy answer because, unlike for the brain, the metabolic expenditure of other organs varies dramatically based on their need. In this context, basal rates are only so useful.

Your vision of an answer seems to me more of a nightmare. This is an example of a representation that would be totally inappropriate to the question you ask. Why do you think that the different coloured items (energy/tissue?) need to be shown leading into something (Total) and what is the equivalent of the traces moving up or down or splitting? Sorry to sound severe, but there is a general problem that people do not think what graphical representations are appropriate for a particular data set. A pie chart will do, but the danger is thinking this is absolute, as @KonradRudolph points out.

Woah, 25% of the energy is lost to distribution? That's a lot. I cannot understand the other 29.52% because the graph is really messy there.

Percent of basal metabolic rate by organ (BC Campus Open Education):

Liver and spleen : 27%
Brain: 19%
Skeletal muscle: 18%
Kidneys: 10%
Heart: 7%
Other tissues (lungs, intestine, skin, bone, fat tissue, glands...): 19%

Basal metabolic rate by 1 kg of specific organ tissue (kcal/kg of organ/day) (Table 5 from American Journal of Clinical Nutrition, 2010):

Heart: 440 kcal/kg
Kidneys: 440 kcal/kg
Brain: 240 kcal/kg
Liver: 200 kcal/kg
Skeletal muscle: 13 kcal/kg
Adipose tissue: 4.5 kcal/kg
Residual tissues (lungs, intestine, skin, bone...): 12 kcal/kg

Why are liver and spleen aggregated?

@MJD, It's them (BC Campus) that merged them, not me. "Liver and spleen" are often mentioned together because they share some functions.

Where is the stomach and intestines? They utilize so much energy in the digestion process.

@Loren, stomach and intestine are active only during digestion, while the heart, kidneys and liver work all the time...I mentioned intestine under "other tissues" - I'll see if I can find some more specific data.

Based on the per-weight list (and this paper), if we separated the liver from the spleen, the liver would represent ~17%, lower than the brain.


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What is the change in ratio of histone to protamine in men with infertility called?
I am neither a biology researcher nor a student. In a paper (written by a biology researcher) I am translating into English, there is the following statement which, according to the text, must have a name and I fail to find the English name:

It is showed that in men with infertility histone to protamine ratio changes and the change is called ...

What is the change called? I guess it's something unnatural/abnormal.

It is termed "abnormal packing".
Source: "Sperm Chromatin: Biological and Clinical Applications in Male Infertility and Assisted Reproduction" by Armand Zini & Ashok Agarwal (2011), p 172.


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Can we use cancer cells to generate blood vessels?
Is there any possibility to use cancer cells, which generate blood vessels, to generate our blood vessels when we are wounded or when we have varicose veins in our legs?
Thanks for your answer in advance.

Great question, it's hard to control cancer, this approach is harder than the elimination, so I think controlling it is a level higher than destroying it.

Using cancer cells in this manner would be far too dangerous, as there is nothing to prevent the cells from implanting and forming new tumors. Fortunately, we already know a great deal about angiogenesis, which is the process by which new blood vessels are formed or grown out of existing ones. If you want more details on how the process works, the article I linked to goes into a good amount of detail regarding the key players and how they interact.
It would be much easier (and safer) to use our knowledge of the cytokines and growth factors responsible for blood vessel formation to develop biological therapies that could potentially be used to treat varicose veins. However, current therapies can be quite successful, and there may not be a large enough market to justify the quite large expense required to develop angiogenesis-based therapies.
Unless a patient has some sort of genetic or other issue, angiogenesis is already involved in wound healing. As new tissue grows back, capillaries and perhaps slightly larger blood vessels expand out from the nearest sufficient vein/artery pair to vascularize the new cells. There may be issues with patients who are taking angiogenesis inhibitors as part of a therapy plan for cancer, for example, in which case compromises would have to be made if necessary.

It is also worth noting that although angiogenesis occurs in many cancer cells, the blood vessels formed are not as structurally sound as normal blood vessels, they are 'friable' and as such have a tendancy to bleed. In some tumours for example this can lead to major haemorrhage.

@Spinorial that is correct. This is due in large part to the inherent dysregulation of tumor signaling pathways and lack of "proper" angiogenesis as one would see in growth or wound healing, for example. To anthropomorphize, tumors are only interested in getting nutrients to support growth, not in building a proper, sustainable blood vessel scaffold that will last. A tumor is evolving as it grows, responding to its current environment, and doesn't have a genetically-set evolutionary "plan" like normal cells and whole organisms do.


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Is taking a shower unnecessary if good bacteria surround our skin?
David Whitlock, a scientist, has not taken a shower for 12 years. Instead, he sprays a bacterial mist containing live bacteria to remove odor and maintain the number of good bacteria.
It is because using soap can remove good bacteria on our skin. So he chose not to take a shower but to spray the mist.
This kind of behavior sounds strange to me. But can it be very effective to maintain good bacteria and prevent disease?
I cannot do like him but I am just curious.
Thanks.

You can read about the guy here: http://www.livescience.com/52719-do-we-need-showers.html He uses soil bacteria from the Nitrosomonas genus, which can break down ammonia and product nitric oxide (NO). According to him horses have these bacteria on their skin. Using soap can destroy these bacteria on our skin and the proper recolonization can take months. So these are really sensitive microbes.
He claims that these bacteria were once part of the human skin microbiome, but was removed when people started to use soap.
I found some circumstantial evidence only:

The groups that'd had more contact with the modern world tended to
  have less microbial diversity, the researchers found. The Yanomami in
  the study had almost double the amount of bacterial diversity as the
  people in the U.S., and about 30 to 40 percent more diversity than the
  Guahibo Amerindians and Malawian participants, said study researcher
  Jose Clemente, an assistant professor of genetic and genomic sciences
  and medicine at the Icahn School of Medicine at Mount Sinai in New
  York City.

http://www.livescience.com/50526-amazon-bacteria-microbiome-diversity.html

This just shows that the biodiversity is much greater on the skin and in the gut of tribe people living in isolation from modern society.
I read a few years ago that tribe people have even soil bacteria on their skin, so it might be true, but I did not find more information about the concrete species living on the skin of these people, so it is inconclusive whether he is right or not. Taking shower is not necessary btw. if you can bear with the odor...

the Phrase "good bacteria" doesn't mean it's not gonna be harmful to you . actually they called : normal flora . they are refer not just to bacteria they include all types of microorganisms .
http://www.ncbi.nlm.nih.gov/books/NBK7617/
I give you an example : there is some bacteria in our bowel they help our digestive system to work better . but these bacteria in case of some infectious disease or in the people with Immunodeficiency disease like AIDS turn to be pathogens .
the vision of David Whitlock is not irrelevant in fact in the field of industrial biotechnology we use micro organism to clean and digest environmental pollution like oil spills & ... just like him use bacteria too clean out his body but in fact the thing is he put non pathogens bacteria on his skin so there is no place for other bacteria .
but as a professional view  there amount of normal flora on our skin is 10 times more than our cells so you can not think our skin is a surface and you can just wipe every thing on it just by showering and ... I'm telling you these thing are odd and there is no scientific evidence that support this odd things . maybe in 100 years when we ran out of drinking water we force to make cleaning sprays base on this view . but you know such a crazy but possible thing in theory .


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Can the Donnan effect be reversed so phospholipids follow ions?
I know that there are flipases and flopases that facilitate this sort of thing, but I'm curious about other possible influences. Can the Donnan effect be reversed so that phospholipids follow ions? For example, calcium efflux from cells causes it to be more energetically favorable for phosphatidylserine (slightly more negative, and thus slightly more likely to follow a positive charge) to be ejected from inner to outer leaflet.

While moving lipids to match charge could work, I don't know about any examples. Lipids are large and flipping rates tend to be slow. My guess is that ions can react to lipid distribution faster than lipids can react to ion distribution.

Yea, i suppose, though membrane biophysics is still a mystery to me... Perhaps the flipases/flopases make it more energetically favorable for lipids to follow the ions and not just the reverse...

Flippases would increase flipping rate, but there are plenty of ion channels that would increase the rate at which ions can move back and forth across the membrane too.

I am refering to apoptosis, platelet activation, and any other scenario where phosphatidylserine moves from inner to outer layer... in these scenarios there is also a calcium influx...  I can't help but wonder if there is a connection...

I'm confused about what this question is actually asking. The title is unclear and the only actual question is can the donnan effect be reversed so phospholipids follow ions.

for example, why does phosphatidyl serine get exposed to the outer leaflet after calcium efflux from a platelet?


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negatively charged albumin as major carrier of acidic/negative charged drugs in blood
I reading that orsomucoid (alpha-1-acid glycoprotein) is the major carrier of positively charged (basic) drugs in the blood, while albumin carries negatively charged (acidic) and drugs with neutral charge.
On the other hand I've read that albumin is excluded by the basement membrane in the glomeruli, and in general by negatively charged glycosaminoglycans in the interstitial space, because albumin is negatively charged.
I did a quick search online and I couldn't find the information explaining this contradiction. Does anyone have an explaination?

Running the sequence for human albumin through expasy protparam confirms albumin is negative at neutral pH. This paper provides experimental evidence that albumin is negative because it reverses the charge on positively charged DNA-peptide particles. However, simply because albumin is overall negatively charged doesn't mean it has a uniform charge. There are probably pockets with positively charged or hydrophobic character.


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Does melatonin change the appearance of humans?
Melatonin (not to be confused with melanin) was sold as a wonder drug during the 90s. I remember images of mice, which supposedly got a more beautiful fur. I would like to know whether the effect is true and whether it also has an effect on humans skin (or appearance in general).
Obviously, googling about melatonin generates a lot of suspicious results.

Melatonin is a hormone produced by the pineal gland located in the brain, and its production is inhibited by light to the retina and permitted by darkness (reference). It has a lot of effects on the body (reference) but I will stick to just discussing its apparent effects on aging and skin.
Melatonin works as an antioxidant and helps in removing free radicals from the body (reference). Research has shown that free radicals could damage the skin (reference), so I would have to conclude that melatonin could have a part to play in maintaining the beauty of your skin.
It is a known fact that melatonin levels in the body decrease from age, and its decrease has been correlated with some of the effects of aging (reference). As you have mentioned in your question, there is research proving that melatonin could decrease the effect of aging in rats (reference). Also melatonin was found to increase the youthful rhythmic activity in a shrew (reference). In the paper titled melatonin and skin aging it has been stated that

In UV-induced solar damage, melatonin distinctly counteracts massive
generation of reactive oxygen species, mitochondrial and DNA damage.
Thus, there is considerable evidence for melatonin to be an effective
anti-skin aging compound.

Moreover in the paper titled "On the Role of Melatonin in Skin Physiology and Pathology", it has been proposed that

Melatonin (synthesized locally or delivered topically) could
counteract or buffer external (environmental) or internal stresses to
preserve the biological integrity of the skin and to maintain its
homeostasis.

So in conclusion, I would have to say that melatonin does have a lot of positive effects on the skin but, given that it is a hormone and there are side effects (reference), it should be used in moderation.