text:
Controlling for phylogenetic signal - what is statistically appropriate?
I am currently collaborating with a fellow PhD student. We are both in the same Biology department, but my collaborator is more of a natural historian, so I am handling the statistical side of things.
He has published a few papers using only Brownian models and Pagel's $\lambda$ (with a different collaborator). However there seems to be a plurality of different methods available - Grafen, Blomberg, and Martin, to name a few. OU models seem inappropriate for our data since we have relatively small phylogenies (Cooper 2016). The literature seems to indicate that Pagel's $\lambda$ is more robust than Blomberg's $\kappa$, and in general an okay method to check for phylogenetic signal. I've also found that some people throw everything and the kitchen sink at their data, and then compare log-likelihoods, AIC, BIC, with log-likelihood ratios for any nested comparisons.
My first question is then, should you have any a priori assumptions of which method will be appropriate for your data?
I am still new to PCM so I used old R scripts and an AmNat paper (from 2019) as my reference. I am also using the same phylogenies as that AmNat paper. From that paper, and from those scripts, only two models were used, a Brownian model (which is essentially $\lambda$ = 1, anyways) and an estimate of $\lambda$. They compared the two models, chose the more appropriate model by log-likelihood ratio and that was it.
My second question is, shouldn't you always compare your models to a model with fixed $\lambda$=0?
For example, I have the following output in R,
#Brownian Model

pglsModel_BM <- gls(sum_dep ~ ContGroup, correlation = corPagel(1, phy = UltTree, fixed = TRUE), data = temp, method = "ML")

#Estimated Lambda Model

pglsModel_E <- gls(sum_dep ~ ContGroup, correlation = corPagel(0.50, phy = UltTree, fixed = FALSE), data = temp, method = "ML")

###Output of comparison is...

             Model df      AIC      BIC    logLik   Test  L.Ratio p-value
pglsModel_BM     1  3 528.4584 534.5344 -261.2292
pglsModel_E      2  4 528.0454 536.1468 -260.0227 1 vs 2 2.412992  0.1203

###ANOVA output of preferred model

Denom. DF: 54
            numDF  F-value p-value
(Intercept)     1 7.039370  0.0104
ContGroup       1 6.480427  0.0138

And the Brownian model got the go ahead. It seems that Brownian is treated as a null model, but I can't wrap my head around why $\lambda =0$ isn't also a null model or the null model. Moving forward with my assumption,
###Adding in a lambda=0 model

pglsModel_0<- gls(sum_dep ~ ContGroup, correlation = corPagel(0, phy = UltTree, fixed = TRUE), data = temp, method = "ML")

###Using anova for model comparison

             Model df      AIC      BIC    logLik
pglsModel_0      1  3 524.0962 530.1723 -259.0481
pglsModel_BM     2  3 528.4584 534.5344 -261.2292

###checking out the 0 model...

Denom. DF: 54
            numDF   F-value p-value
(Intercept)     1 289.67228  <.0001
ContGroup       1   0.21234  0.6468

I realize the differences are rather small, but all methods point to $\lambda  =0$ as the 'more likely' model.
My third question is -- although, possibly answered by the second question -- do we assume that there must be some amount of phylogenetic signal due to shared history, such that it is suffiecient to only test for $\hat{\lambda}$ and compare to $\lambda = 1$?
Note: Just to be sure, I compared all Brownian models with corBrownian to their $\lambda = 1$equivalents, and got the exact same outputs.

I have a tentative answer to my question.
In the publication for the R package phylosignal (Keck, 2016), they state:

To test the presence of phylogenetic signal, the null hypothesis is that trait values are randomly distributed in the phylogeny. Another null hypothesis might be that trait values follow a Brownian motion model but it is less often used and implemented.

So it would seem there are indeed two null hypotheses, however it seems disingenuous to not test for both, especially since it is relatively simple to do. And of the two, should you for some reason be limited to one, testing for $\lambda = 0$ (or the log-likelihood of a general linear model) should be your first choice.
Another issue was with corPagel from the package ape. It requires an initial value to estimate Pagel's $\lambda$ (Unless you fix the value, of course). Convergence is not guaranteed, and sometimes requires some fine-tuning of the initial value. This set off a bit of a red-flag, so I collected the median lambda from 5000 subsets of my data (I am using a different family/phylogeny/dataset, where the $\hat{\lambda}$ model is preferred over a Brownian, but not $\lambda = 0$).

I think this is stronger argumentation for a phylogenetic signal, albeit a weak signal.
#output of comparing lambda=0, lambda=1, and median lambda

                 Model df      AIC      BIC    logLik
pglsModel_0          1  3 636.9876 643.6899 -315.4938
pglsModel_1          2  3 681.9784 688.6807 -337.9892
pglsModel_MEDIAN     3  3 636.4812 643.1836 -315.2406

#output of comparing median lambda to the estimated lambda from the full dataset

                 Model df      AIC      BIC    logLik   Test   L.Ratio p-value
pglsModel_MEDIAN     1  3 636.4812 643.1836 -315.2406
pglsModel_FULL       2  4 637.7024 646.6388 -314.8512 1 vs 2 0.7788265  0.3775

By the evidence of the distribution of lambdas, and the median model's AIC, BIC, and log-likelihood, we can argue in favor of the median model. Residuals also look normal and random. Confidence intervals should also be obtained. But, in reality, here, the difference here between a weak phylogenetic signal and none at all are vanishingly small.


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Book request: biology of sensation and perception
I’m interested in learning about the biological and chemical basis of human sensation and perception (on both a microscopic and macroscopic level). This includes

The mechanisms underlying our “five senses,” i.e. the eye, inner ear, tongue, nose, and nervous system, and how (chemically/physically) they are triggered
How our brain makes inferences from the raw sensory data we receive, e.g. using our depth perception to infer distance from a two-dimensional projection onto each of our eyes
Comparison with other species of animals
Experimental results relating to the three points above
An evolutionary perspective hypothesizing about why these sense-detecting organs were important for human survival

There is plenty of information about these ideas scattered throughout Wikipedia, but I was wondering if anyone knows of a single book (or perhaps another online resource) that covers most/all of the points above in an accessible and interesting way.
Any suggestions?

"An evolutionary perspective hypothesizing about why these sense-detecting organs were important for human survival" is going to be pretty tough since as far as we can tell human sense are identical to a chimps senses. the exception appears to be in proprioception which is not among the classic five senses.

This is a very broad range of topics. I doubt you'll be able to find a single reference on all of it. I'm providing below some references with a focus on more introductory approaches.

The mechanisms underlying our “five senses,” i.e. the eye, inner ear, tongue, nose, and nervous system, and how (chemically/physically) they are triggered

Bear, Connors & Paradiso "Neuroscience: Exploring the Brain" is pretty extensive. It covers chemical senses, vision, audition, the vestibular system and touch. It is not cheap, but that's the only reference that will cover most of the topics you are interested in. However it focuses mostly on the physiology of the senses, and not really about perception
Otherwise I'm afraid you'll immediately have to read specialized books such as Palmer's "Vision Science", Moore's "introduction to the psychology of hearing", Goldberg et al. "The vestibular system". Those are fairly readable introductory books. I don't know much about chemical senses.

How our brain makes inferences from the raw sensory data we receive, e.g. using our depth perception to infer distance from a two-dimensional projection onto each of our eyes

For the topic of inference specifically a classical reference is Richard Gregory's "Eye and Brain: The Psychology of Seeing". It is dated (60s) but still very relevant. This is somewhat contradictory with your first point because inference is a behavior while you asked for more physiological references. Stereopsis specifically is a classical field of vision science so any descent book will cover it.

Comparison with other species of animals

I cannot recommend enough Sarah Shettleworth's "Cognition, evolution, and behavior". Though focusing only on behavior, it is a very extensive and interesting book.

Experimental results relating to the three points above

Any good book would include data and plots from classical experiments.

An evolutionary perspective hypothesizing about why these sense-detecting organs were important for human survival

Again, Shettelworth's book.

Foundations of Perception from George Mather covers three of your 5 requested bullet points, namely:

The mechanisms underlying our senses;
How our brain makes inferences from the raw sensory data we receive, including depth perception;
Experimental results.

I can highly recommend the book; it's clearly written, richly illustrated and complete, yet it is concise, interesting and highly readable.

source: Stack Exchange

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

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Can DNA rings, i.e. plasmids, form as Möbius strips?
I know that plasmids can be present in a coiled form, which keeps the DNA strands together when they degenerate, by forming catenases.
I was wondering, however, whether it has been documented to naturally happen or if anybody has ever successfully created a Möbius-strip plasmid. Technically, such a structure could readily form from a single circular strand of DNA, but the literature, as far as I have searched, has remained silent.

Wouldn’t any covalently closer circular DNA with an odd twist be a Mobius strip?

Related to your question, this paper reports Möbius strips created from multiple strands of DNA.

@canadianer you can make this into an answer, since it answers my question.

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


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Understand and reproduce withdrawn publication method - Blastp - covid19
I try to reproduce the method of this withdrawn paper. I know this paper has been debunked and withdrawn. I am curious to understand the details of the method used on it. I am a programmer and I don't work on the field of Biology.
I have some questions about "The identified amino acid and nucleotide sequence" with
MultAlign software:
I have trouble to understand how those supposed "inserts" were selected:

"Insert 1": The selection is where there are dashes and dots on the second and third lines because the sequence is not present in SARS-GZ02
"Insert 2": The beginning of the "insert" start with these dash and dots but why is it stopped at 155 ?
"Insert 3": The end at 261 is at a dash for the second line but why does it starts at 256?
"Insert 4": why these start and end of selection?

Later on the paper they used these selected regions with Blast and on the "motif alignement" column these letters are used which are a little different:

"Insert 1": TNGTKR (first letter "G" removed)
"Insert 2": HKNNKS ("YY" removed)
"Insert 3": RSYL-TPGDSSSG (4 letters at 250 added)
"Insert 4": QTNS-PRRA

Why are some different from the selection ?
Even for the first "insert", I can't find those alignement with Blast using for example GTNGTKR or TNGTKR. If someone could indicate me the good parameters in Blast to find these alignements it would be awesome.
Sorry if it sounds too ingenuous, thank you for your time reading all this.


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Synapses of inhibitory neurons
I sometimes read of "inhibitory synapses". But I understand that when the neuron is inhibitory, all of its synapses will be inhibitory (so it is a property of the neuron, not only the synapse) - is that correct?
How is this experimentally tested? I did not find an estimate of how many outgoing synapses inhibitory neurons typically have, but I assume that it might be thousands. So how do we know for all of its synapses that they are inhibitory?

I think the definitions of inhibitory and excitatory neurons are currently defined as a matter of convenience based on observations made by synaptic staining, electrical feature and its morphology.
In other words, neurons with more inhibitory synapses are inhibitory neurons, and neurons with more excitatory synapses are excitatory neurons, and so on.
By detecting inhibitory and excitatory synaptic-specific staining in different colors on the same section, we may be able to determine whether all synapses in a single neuron are inhibitory or excitatory.
Also, I think there are events happening in the process of neural differentiation that distinguish excitability/inhibition, but we don't seem to know how they are happening.
It may be determined by signals from neighboring neurons, Ca++ concentration, etc.
If, at the neuronal precursor stage, the differentiation mechanism that determines excitability/inhibition could be confirmed at the level of gene expression, it might explain why inhibitory neurons only make inhibitory synapses.
22th June 2020 added;
I find a good example of Excitatory synaptogenesis on dendrites of hippocampal-mediated (inhibitory) neurons, here;
https://www.nature.com/articles/ncomms1736
In short, this article shows what will occur after generating spine on inhibitory neuron.
(A)The synapses move along the microtubule from the tip of the process to the shaft. (B) Morphological changes in parallel fibers of cerebellar granule cells during synapse formation. When the parallel fibers come into contact with Purkinje cells, the neurexin-Cbln1-δ2 glutamate receptors A complex of synaptic vesicles is formed and synaptic vesicle accumulation occurs. Synapse matures after microprojections extend from the parallel fibers and encircle the spine to form an annular structure. (C) In early postnatal hippocampal pyramidal cells, DCLK1 accumulates at the tip of the process to promote process elongation and Inhibition of synaptic maturation.

Thank you! So the classification of a neuron as inhibitor or excitatory is based on its neurotransmitter - say a neuron is GABAergic - how could it then have an excitatory synapse?

I find a good example about your question, here;
https://www.nature.com/articles/ncomms1736
This article shows the process of generating excitatory synapse on inhibitory neuron.
I Added the brief to my answer.


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When purifying plasmid DNA after cloning, do you get endogenous plasmid in addition to your vector of interest?
Since bacteria naturally contain plasmids, when you do a cloning experiment and purify the plasmids at the end, do you get plasmid naturally present in that bacteria in addition to your vector? The standard plasmid purification kits (miniprep, maxiprep, etc.) aren't sequence specific in their purification (they just seem to isolate all plasmids in the cells). I would assume you want a constant purity of vector. Otherwise, for example, you could have 2 vials of plasmid at 1 ug/ uL plasmid while one has 0.4 ug/ mL vector and another 0.8 ug/ mL vector which wouldn't be good for reproducibility. Or is it that the bacteria used for cloning are devoid of naturally present plasmids which would fix this issue?

Very interesting question, Chris. What result do you see when you analyze a miniprep from non-transformed bacteria on an agarose gel?

I'm a bit newer to this area of biology techniques so I haven't looked at many plasmid preps yet. The plasmid prep that I have seen on a gel had one band (or 2 bands if cutting the insert out with a restriction digest). If this result is generalizable, it would suggest the vector was present in much greater quantity than any of the endogenous plasmid (if there was any endogenous plasmid at all). I can think of 2 reasons for this (if the result is generalizable):

Sorry I accidentally posted the previous comment before it was finished. I was going to say the 2 possible reasons that I could think of are (I don't know which reason is the primary reason though): 1) The strains used for cloning have less endogenous plasmid. 2) The bacteria had to express a lot of vector to get sufficient antibiotic resistance such that the vector was present in much greater quantity than you would normally see in endogenous plasmids.


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If a cell has two different GPCRs, how does the cell differentiate between the phosphorylation cascade caused by each?
In my biochem course, we learned that GPCR receptors trigger a phosphorylation cascade, with the end result being a large amplification of the signal in the form of cAMP. We never studied any particular GPCR individually, but we were told that GPCRs always end in the formation of a large amount of cAMP, which will go on to phosphorylate key targets that achieve the end result.
My question is as follows: If there are two GPCRs on the same cell membrane (let's say GPCR-A and GPCR-B triggered by substrates A and B respectively), how does the cell "know" which GPCR triggered the phosphorylation cascade if the end result is the same (large amount of cAMP). In theory, couldn't substrate B bind to GPCR-B and cause a phosphorylation cascade identical to that of GPCR-A, thus triggering GPCR-A's cellular response?
Is there some deeper specialization/uniqueness to each type of GPCR receptor that we didn't cover in my course? Does each GPCR produce a slightly different cascade that ends in something similar, but not exactly cAMP? Or is there some restriction, like each cell limited to only one GPCR (I would find this surprising, if this is the case)?

First, it would be an oversimplification to say that GPCRs act only through increases in cytosolic cAMP. This is true for receptors coupled to Gs proteins, but there are other G proteins like Gi, Go and Gq which act differently [1].
Now, a cell can have receptors coupled to many different G proteins. Vascular smooth muscle, for instance, has Gs, Gi and Gq-coupled receptors [2]. Further, a cell can have different receptors coupling to G proteins of the same type (e.g., hepatocytes have glucagon and beta adrenergic receptors [3], which both couple to Gs).
In such situations, the effects of different hormones add up. The final effect is a function of the total cytosolic concentration of second messenger (e.g., cAMP). Thus glycogen breakdown in a hepatocyte depends on the overall effects of glucagon and epinephrine [3]. The hepatocyte has no way of 'knowing' which cAMP molecule was formed by which hormone.
References

https://en.wikipedia.org/wiki/Heterotrimeric_G_protein
https://cvphysiology.com/Blood%20Pressure/BP026
https://www.nature.com/articles/emm2015122

So, if cells have several different GPCRs of the same G-type but triggered by different substrates, the effects must be additive and can't be unique (i.e. the different substrates can't trigger entirely different cellular responses)?

@SullyChen No, I think. They can't be unique. Do you have any particular counter-example in mind?

I don't have a particular counter-example, but I can faintly remember a professor remarking that a single cell could have dozens (or hundreds? not quite sure) of GPCR proteins on its membrane, so I was curious if they were all duplicates of the same receptor or if they could possible all be unique. I think you've answered my question, thanks!

Actually, there is the phenomenon of 'spatiotemporal signalling'. Basically, the cAMP or other signal is restricted in space, so that it can only activate certain proteins. It has recently been shown that GPCRs can create cAMP signalling domains of nanometer size. So very much the cell can tell which cAMP molecule was formed in response to each hormone. Its extremely complicated and researchers are only just beginning to understand the significance of such signalling, but just imagine, all these receptors being located to distinct regions of the cell (cholesterol rich lipid rafts in the plasma membrane, endosomes after internalisation, cilia), and that each downstream signalling molecule or protein can only get so far before being down-regulated. As such, you can get very distinct signalling paths between different GPCRs, even in the same cell. (It gets much more complicated but).

Excellent answer, but we do ask that answers for anything beyond basic textbook info contain sources/references to support what is written and allow avenues for follow up reading.


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How is energy stored in the cotransport of molecules down to its electrochemical gradient?
I am talking about symporters and antiporters, that transport usually an amino acid against its concentration gradient while at the same time transport another molecule down its electrochemical or concentration gradient or both. It is said that "cotransporters use the energy stored in electrochemical gradient", but I do not understand what do they refer to when talking about storing energy.
Thanks in advance.

Hey Laura not sure what exactly your question means. Please read the theory about electrochemical potentials in general and ask your question again.

Please give a source for your quotation, with a link if possible.  For one thing, it lacks context, and for another the lack of an article before “electrochemical” suggests you are paraphrasing or quoting from memory. We need more and precise information if we are to help you.


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Why viruses "die" outside the host?
Why viruses "die" outside the host after sufficient time? I want to know the biological process behind it. What role being exposed to air plays in virus destruction? What role sunlight plays in the same?
Now there might be many biological processes behind this phenomenon, please mention the same and explain about any specific virus.

Answers on that post doesn't explain the biological process involved.

But the question covers your point. Sorry, the message is autogenerated to be polite, but in doing so misses the point that SE Biology doesn't do duplicate questions as the idea (at least in principle) is to amass a definitive collection of questions.

@fghjkl: Virus "death" isn't really a biological process, it's a chemical one.  Think of viruses as complex chemicals, and those chemicals degrading in the presence of UV light & oxygen, or just drying up because they aren't in a liquid environment.

Viruses are metabolically inactive outside the host cell. They bind to the specific receptor to be activated. They cannot replicate without a host.
For example, in case of HIV, the protein envelope of the virus binds to CD4 receptor fo T helper cells and thus supressing the immune system gradually.These viruses are only active when it binds to CD4 receptor and not any other receptor.


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Why did we lose our fourth type of cone cell (in the eye)?
Most species of birds, reptiles and fish have four types of cone cells in their retina, thus they have four independent channels for conveying color information. They are:

short-wave (S) cones: sensitive to colors with short wavelengths.
middle-wave (M) cones: sensitive to colors with medium wavelengths.
long-wave (L) cones: sensitive to colors with long wavelengths.
ultraviolet (UV) cones.

This condition is called tetrachromacy. Wikipedia mentions:

It was the normal condition of most mammals in the past; a genetic change made the majority of species of this class eventually lose two of their four cones.

We have only three. My question is, why did we lose our UV cones? I searched a little about this and here's what I found:
Scientists Have Found a Woman Whose Eyes Have a Whole New Type of Colour Receptor

According to estimates, that means she can see an incredible 99 million more colours than the rest of us, and the scientists think she's just one of a number of people with super-vision, which they call "tetrachromats", living amongst us.
They took 25 women who had a fourth type of cone cell, and put them in a dark room. Looking into a light device, three coloured circles of light flashed before these women's eyes.
To a trichromat, they all looked the same, but Jordan hypothesised that a true tetrachromat would be able to tell them apart thanks to the extra subtlety afforded to her by her fourth cone.

Which means some of us still have it. What I don't understand, though, is why this isn't a more common trait? Evolutionarily, is being able to perceive vision using three cones "enough" for humans?

we lost more than that, primates only have 3 cones cells due to a mutation creating a new cone cell, other mammals including the ancestors of primates only had two cone cells.

Let's be clear: most mammals, including basal primates, had only 2 cone cell types. Primates evolved a new cone cell becasue frugivores have a distinct advantage being able to distinguish reds and yellows. The mammal lineage may have never had a fourth cone cell, if they did it was lost early.
Eutherian mammals lost the third cones cells likely because we spent several hundred million years as small nocturnal animals during the dominance of dinosaurs. In small nocturnal animals, there is a strong competition between having more rods for better low light vision vs having cones for color vision, so a loss of some cone cells may have been neutral or even beneficial. There was some work on bats that seemed to contradict this, but the researchers failed to control for frugivory in the bat lineages they studied; So there is an issue with their results. There is a lot of variation in color vision across vertebrates so it is no surprise a consistent selective pressure could have a lasting effect.
source

The source you cited mentions -"The recent gene duplication and mutations that have given rise to the series of longer-wave pigments in primates also appear to have occurred independently in some teleosts and probably within some reptiles," which clearly means I had some conceptual misunderstanding about the evolution of cones. (sorry for that) Thanks for your quick answer and the amazing source! :)

the evolution of the different receptor proteins is very complex in the details, there are mutations all over the animal kingdom. worse the gene is fairly easy to duplicate so you often have animals with both the original form of the gene AND and mutant form at the same time.


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Have Bonobos and Chimpanzees competed?
After reading de Waal's "Our Inner Ape", I'm left with the impression that chimpanzees would easily drive away or kill-off bonobos, if they were to compete for the same territory.
Have there been any instances of that in the wild? Or have their habitats always been completely separated by the Congo river?


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Why does insertion of transmembrane domains occur in the rough ER?
To elaborate on that question, why in the secretory pathway does the insertion of transmembrane domains into the membrane occur in the rough ER as the protein is translated and threaded across the ER membrane? This is the answer to a problem from a science textbook. I thought that integral proteins are first produced in the rough ER, modified in the Golgi apparatus, and then shipped in vesicles that fuse with the cell membrane. If that's the case, wouldn't insertion of the entire protein into the membrane happen when the vesicle fuses with the cell membrane?

Why do you think transmembrane domains are integrated into a membrane as translation proceeds?  Can you quote something saying that?

Sure, the exact question and answer. "At which point in the secretory pathway would the insertion of transmembrane domains into the membrane occur? Answer: It occurs in the rough ER as the protein is translated and threaded across the ER membrane."


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What is the mass of a single erythrocyte?
I really have been searching through internet on different languages, but can’t find any article that answers on the question what is the single erythrocyte mass. I don’t know, I think it’s pretty easy to calculate experimentally, but I didn’t find anything.
Has anyone measured single erythrocyte mass, and if yes, what is the value?
My try
Experimentally
I am not biologist or medical student. What do I know: blood consists of liquid part(water, salt) and solid part(red blood cells, white blood cells and thrombocytes). If It is possible, the white cells and thrombocytes can be moved off the blood in some test tube, so that will left only erythrocytes. Then, there should be medical statistical value like erythrocyte density or number of erythrocytes per liter.
We have some blood with only erythrocytes, we know how many erythrocyte are there. We can measure that blood weight, substrate the liquid weight(somehow), divide by erythrocyte number and will get the mass of a single erythrocyte.
Theoretically
About 90% of erythrocyte mass is hemoglobin. Hemoglobin is a molecule. Molecule is a countable thing, so, perhaps there is information about how many hemoglobin molecules, in average, is in one erythrocyte.
According to Angelo D’Alessandro, Monika Dzieciatkowska, Travis Nemkov, and Kirk C. Hansen article Red blood cell proteomics update: is there more to discover? it is about 270 millions per red blood cell. Molecular mass of hemoglobin is about $64 kDa$, absolute mass equals $1.106*10^{-22} kg$.
If my assumptions are correct, then 90% of erythrocyte mass is about
$$2.97*10^{-14} kg$$

If you can’t find the mass (and I wouldn’t imagine there’s a lot of interest in that, but obviously it interests you) you could presumably calculate it from the cell dimensions, assuming a density of about 1. Not a simple sphere, I know, but it should be possible.

Is your problem that you wish (or have been asked) to separate them? If so, you need to search for a term like "centrifugation of blood" or "fractionation of blood". Is this Wikipedia article any use as a starting point? And the English in your title is misleading: I would suggest you replace "separate" by "individual" or "single".

@David, I am not a biologist, or medical worker, I can’t do that

The volume and the density of erythrocytes should be known.

OK, I've made a calculation. You could check the arithmetic. But do tell me, why do you wish to know this?

@David doing some modeling for diploma work

Had another try. Checking the paper I see I misread the figure legend.

About 90% of erythrocyte mass is hemoglobin.
According to Angelo D’Alessandro, Monika Dzieciatkowska, Travis Nemkov, and Kirk C. Hansen article Red blood cell proteomics update: is there more to discover? there are about 270 millions hemoglobin molecules per red blood cell. Molecular mass of hemoglobin is about $64 kDa$, or $1.106*10^{-22} kg$.
From the given, 90% of erythrocyte mass is about
$$2.97*10^{-14} kg$$
Now, using the proportion, calculate that the average erythrocyte mass is
$$m=\dfrac{2.97*10^{-14}kg*100\%}{90\%}=3.3*10^{-14} kg$$
$$erythocyte\space mass=33 pg$$

@David calculations result is also pretty similar to mine, He got $83 pg$

It’s not my kind of biology, and I tend to make mistakes in arithmetic, I’ll have a go…
I found a paper by Leblond and Shoucri published in the Journal of Microscopy (1978) 113, 161-170, entitled Calculation of surface area and volume of human erythrocytes from scanning electron micrographs. You need institutional access to read it, but for the human erythrocyte shown below they calculated:
Volume = 85.5 μm3

They found a range of sizes (65 μm3 in another image) so I shall take an average value of 75 μm3.
75 μm3 =  75 × 10–18 m3
Assuming a density of 1.1 g/cm3 for erythrocytes, i.e. 1.1 × 106 g/m3
Mass of an erythrocyte = 83 × 10–12 g (0.08 ng)
This is the same order of magnitude as that calculated later by the poster.
(Apologies for initially quoting the volume in pm3. No idea how I did that — it’s clearly μm3.)

Unfortunately, wrong. $75pm^3=7.5*10^{-35} m^3$.

RBCs have a density of approx 1.110g/mL. Source: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5516969/

Also, volume, that equals $85 pm^3$ is interesting, because I found range $70-100 um^3$

According, to that(another) “article “https://en.m.wikipedia.org/wiki/Mean_corpuscular_volume, average volume is $92.8 fL=92 um^3=9.2*10^{19} pm^3$

@ArturKlochko  Mea culpa. I see now, it's the pm as a whole that are cubed. Hunting down papers I can do, simple arithmetic as another matter... However now I seem to get an impossibly low answer of the order 10^–29g. Am adjourning for the moment.

Yeah, it’s impossible because it less then any atom mass

Discovered it was cubic micrometers not picometers. Now corrected, and correct, I hope.

Pretty similar to what did I calculate. I think the fact that this two different ways gives very similar values proves that mass of an average erythrocyte is about tens of picograms. But, still I think, Your method is not as accurate as mine, because it depends on simultaneously two various value - erythrocyte volume, and blood density(much more various then erythrocyte volume). Thank You for help


text:
What is this insect seen in Northern Italy?
I am from Northern Italy, close to the border with Slovenia.
I saw this thing today on the window, and was sure it was a piece of a dry rosmarine branch carried there by the wind - until it started to move.
It looks like a cocoon of some kind, on the top of it there is an opening from which a head of something like a caterpillar comes out, sometimes together with some portion of its body with two (?) tiny legs on each of its body "segments". But I imagined cocoons as something attached to a branch, not moving.. While this thing moved from one point of the window to another, always attached to the window (not using what I think are the caterpillar's legs). (I must admit I am reluctant to open the window and examine it from a closer range :) ; the photograph is taken from inside the house).
What can this insect be? (the length is around 4-5 cm)

Related: Is it possible to identify this chrysalis? and Caterpillar(?) in Leaf Cocoon identification - Missouri.

This looks like some kind of bagworm moth. Their larvae would use silk and plant debris to construct a protective case around themselves. It’s hard to tell the exact species unless you open up the case or wait for it to emerge as an adult moth.
There are species on pretty much every continent and definitely some in Northern Italy. You can check out a list of observations and photos here: https://www.inaturalist.org/taxa/61415-Psychidae

As an aside, if you are interested in this kind of stuff. I highly recommend that you also join the iNaturalist community. There are many more naturalist experts of various beaches of life there to help with identification.


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Visual receptive fields
What I know about centre-surround type receptive fields is that depending on whether the region is on or off, the response to being stimulated is either excitatory or inhibitory respectively. So if a light shines on the centre of an on-centre/off-surround and off-centre/on-surround fields, spikes would be detected in the first case and not the second.
To my understanding, if both centre and surround areas are simultaneously stimulated, no spikes would be detected in either of the above-given fields. However, that means that if I am staring at what is essentially a blank white wall, I shouldn't be able to see anything. But that is obviously not happening. What am I missing here?
Also, on a related note - do on-centre & surround or off-centre & surround fields exist? What function do they serve, if any? What are the other types of visual receptive fields in humans, or other animals? Is there a major difference in properties of visual fields across species?
Edit: While browsing a few resources on receptive fields, I found this very-helpful image here.

This image perfectly illustrates my question: what happens to the grey areas in the right image? How are they processed by the retinal ganglion cells?

The centre + surround do not cancel completely, as you can see from these mudpuppy recordings. [Image 1] (Werblin and Dowling, 1969, I believe)

One function of a centre-surround set-up is to highlight the contrast at borders.  Most of the useful visual information is from borders/outlines, so this is a method of ignoring redundant information.  The highlighting of contrast borders and ignoring of redundant information explains why the neural image appears different. [Image 2 - right].
Another function of centre-surround fields is to avoid saturation, but this is more complicated to explain. [Image 2 - left] (Diagrams from Cambridge MVST Part IB lecture series by Hugh Matthews)


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Mapping of genes: are genes for physically close things close to each other?
I am not sure how to google this but the question is pretty simple: would the genes for the index finger be located "near" the genes for the thumb? Would all genes concerned with the heart be clustered together?

There are no “genes that code for the index finger” as such†, but the question is valid in more general terms.
In short the answer is no (or, at least, not necessarily).
This sort of principle is valid to a large extent in bacteria, where genes that work together are part of one transcriptional unit called an operon. The most famous example of this is the lac operon of Escherichia coli which contains a group of genes all concerned with the utilization of lactose as an energy source for this bacterium.
However in higher organisms, this need not be the case, a good example being the genes for the two chains which associate to form the human blood protein, haemoglobin. Despite their similar structure and probable evolutionary relatedness, the gene for alpha globin is located on chromosome 16, whereas that for beta globin is on chromosome 11.
Nevertheless there are some examples of what are termed gene clusters in higher eukaryotes. These are often genes of a single family that have arisen by relatively recent gene duplication. Over longer periods of evolutionary time they can become separated by recombination. One reason that this may not occur so frequently in prokaryotes is that groups of prokaryotic genes are often transcribed into single so-called polycistronic mRNAs — mRNAs that encode all the proteins of the cluster. This allows expression of the genes to be co-ordinately regulated.
Eukaryotic genes do not normally produce mRNAs of this type, and co-ordinate regulation (e.g. for alpha- and beta-globin chains) is achieved in a different manner. Thus, there is no strong selection against disruption of an ancestral cluster.
As always in biology, there are exceptions. Some eukaryotic genes need to be close together, for example those involved in the class specificity of immunoglobulins (the part that determines whether an antibody of the same specificity if in the cell membrane, or in mucous tissues etc.). These need to be close together for the process known as class switching.
–––––––––––––
† Particular related organs or parts of the anatomy like the different fingers are not encoded by different genes. They are different because of a development programme that determines the fate of precursor cells. That sort of thing lies in the general field of development and embryology, I believe.


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Do people with higher body hair growth (eg. Women with hirutism) need more protein?
Hair is protein. Does that mean that the body of a woman with hirutism is using more than usual protein to make hair and thus she needs more for building and repairing muscles?

Welcome to Biology.SE! Please take the [tour] and then go through the help pages starting with [Ask] questions effectively on this site. This seems likely to be true, but I would guess the extra amount is trivial (think about how little your hair grows each day). If you really want an answer to this I suspect [medicalscience.se] might be a better choice (please don't repost — instead request migration). ——— We also expect you to do some research on your own and then, informed by what you have learned, ask any questions you still have (ideally with references to reliable sources). Thanks!

Not significantly.  Most people should have roughly 50g of protein a day, and most diets provide plenty.  Larger people require a little more,  and activity levels are another factor.
Hair grows fastest on the head, but when talking about "hirsutism" you are referring to body and facial hair, not head hair.  Now consider shaving all the body hair, the total mass is pretty trivial, and the increase in mass per day is a fraction of a gram. Now consider the difference between a "hirsute" and "less hirsute" person, and there the extra protein requirements disappears into triviality.  One extra lentil a day, not something worth measuring.
So the amount of body hair someone has naturally is not a factor that needs to be considered when calculating the protein requirements. In fact, one doesn't need to calculate protein requirements at all, unless you are on a very strict diet (in which case you will likely be under the care of a physician.)


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How are large snails able to climb trees?
In answers to What kind of hot pink eggs are these? and the linked duplicate I found out that snails that live in the water will climb up a smooth stick or branch to deposit their eggs. Today I saw several large (8 to 10 cm) snails climbing trees both a relatively smooth one and one with considerably rough bark.
How do these large and heavy snails manage to adhere safely to the sides of trees and climb so high? Is it adhesion? Is suction involved?

click images for full size view
above: June, northern Taiwan lowlands in a damp area. They look similar to the species discussed in answers to What are these four large snails doing? below: from What kind of hot pink eggs are these?

The foot of the snail secretes a sticky mucus which allows the snail to climb even the smoothest surfaces. The mucus have two states: one in which it is almost liquid to lubricate motion, and the other - a very viscous one, in which the mucus is sticky and "glues" the snail to the surface. The mucus can alternate between these two states via the pressure the snail activates on it. The gluey state sticks the snail to the surface via adhesion.

Researchers discovered nearly 30 years ago that snail mucus has some unusual properties. It allows the animal to stick to a surface while moving, with the mucus changing its characteristics according to how firmly the snail presses on it.  The slime initially acts like glue, sticking the snail to the surface. But when the snail's foot presses down hard enough on the mucus, it becomes more liquid, allowing it to flow underneath the moving snail. Existing theories assumed that this special characteristic of snail mucus was always necessary for the snail to push off and move forward.

Cited from: https://news.stanford.edu/news/2011/april/snail-slime-trails-040611.html

How does it alternate between these two states? Does this information come from some source?

It comes from Prof. Joseph Heller's Land Snail monograph, which I don't have with me right now. See also the following research: https://news.stanford.edu/news/2011/april/snail-slime-trails-040611.html

I didn't see your comment until now for some reason, it may be that the @reply was necessary. From FAQ see How do comment @replies work? I'm still looking for an understanding of the mechanism that holds these snails against gravity from falling off the trees; is it adhesion, or suction, or a combination of both, or if something else is also involved, so I've added a bounty.

@uhoh The sticky mucus works as a glue, that is: as an adhesive. See https://en.wikipedia.org/wiki/Adhesive

I've adde a bounty, asking for a "more detailed answer". if you think that adhesion is the primary mechanism for climbing trees and suction and/or gripping are less important then please feel free to include that back into your answer post rather than a comment. Thanks!

@uhoh I added it to the answer.


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Which animal dug this 5 cm diameter hole deep into mud and build a large mound around it?
I noticed the large structure below today at the edge of a very small pond in northern Taiwan lowlands. It is June and it has rained a bit the past few days, and this 15 cm mud dome with a 5 cm diameter hole going straight down looked fresh and wet and glistening.
It is hard to tell for sure but it looks like the borough went deep enough to reach the water line of the pond next to it, but I could not tell because it's dark inside and I did not have a flashlight.
The mound is large, perhaps 15 cm tall and wide, which suggests that a lot of material has been removed and the tunnel could be quite deep.
The pond is only about 3 x 5 meters in diameter.
Question: Snake? Crab? Mole? What further information can I collect about it that would help to identify what produced this?
click images for full size view

A crustacean (land crayfish). There are a lot to choose from.
http://web.nchu.edu.tw/~htshih/crab_fw/fw-crabe.htm

Cool link, thank you! I certainly do see land crabs around from time to time. Can you add a little more to your answer though, perhaps a link demonstrating that they do indeed build chimneys or whatever this is? I found this while googling after your answer, perhaps it can help https://www.semanticscholar.org/paper/Burrows-with-Chimneys-of-the-Fiddler-Crab-Uca-and-GUSM%C3%83O-JUNIOR-Machado/5de43358797ebf5a6b5156f36b15b8e28e77f3df

I haven't found a ref for this, just now talked with an old farmer from Taiwan, he says they are shaped  more like crayfish, with a tail.

I'm quite sure this is the right answer, thanks for checking on that!


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Can CRISPR be used in editing primary cells? How is the transfection efficiency?
Sometimes people wanna use primary cells to do gene-editing because the cells normally have more interesting characteristics, but can we really do so?

The most efficient CRISPR-based editing of primary cells that I've read about used a technology called prime editing, developed in 2019.
Search-and-replace genome editing without double-strand breaks or donor DNA (PDF download)
Normal CRISPR-Cas9 protocols involve generating double-strand breaks (DSBs), and then either introducing a template for homologous repair or allowing the cell to repair the break without a template, leading to insertions or deletions at the lesion site.  Off-target cutting is common, so normal CRISPR-Cas9 produces undesirable or lethal mutations in a majority of transfected cells.
Prime-editing uses a catalytically impaired Cas9 (generates nicks instead of DSBs) fused to a reverse transcriptase.  The fusion protein is guided to its target by a prime-editor gRNA ("pegRNA") that contains a normal targeting domain at its 5' end and a template for reverse transcription at its 3' end. A nick is generated by the Cas9 on the exposed strand (i.e. the strand not bound by the gRNA), and the 3' portion of the pegRNA partially hybridizes to the the 5' side of the nick, providing a free 5' end and a stretch of ssRNA for DNA polymerization.  Resolution of the resulting "flap" by endogenous nick-repair mechanisms results in editing at the target site without DSBs or exogenous DNA template.
This method was assessed for its efficiency in several cell types, including primary mouse cortical neurons, which are post-mitotic and terminally-differentiated.  The authors observed the desired edit of DNMT1 in 7.1% of cells, with 0.58% indels on average.  Cas9 nuclease editing of the same cell type with the same lentivirus transfection system resulted in 31% indels, on average, an error rate more than 50 times that of prime-editing.

Theoretically, CRISPR technology is not restricted by species cells, but primary cells have limitations of passage and monoclonal jumping, so it is generally cell lines that are used for gene editing.


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Identify this insect with a big "face" pattern on its brown fuzzy wings
Hiking in low mountains in northern Taiwan in early May I noticed that something seemed to be looking at me from the ground, and it turned out to be the pattern on an insect's wings.
The wings are fuzzy like a moth or butterfly but they fold back.
There is also a striking face-like pattern on the wings, one "eye" with heavy upper eyelid on each and a "mouth" across both, and it has very long black (or blue?) and white densely-striped antennae or feelers which project straight forward, and it's legs were also black with several white bands. The length from head to wingtips (not counting antennae) was about 2 or 2.5 cm.
I also got the distinct impression that its orientation was not flat (parallel to the leaf's surface) but oriented with its rear high, so that something in front of it could see the "face". I don't have a photo from the side but based on judging things from what is and isn't in focus I think it's pretty clear.
Question: Is it possible to identify this insect with a big “face” pattern on its brown fuzzy wings? Is it also possible to know if the pattern has some underlying structural function within the wings, or is it only for appearance?

I fully admit that I am not an expert on Asian insects but having trawled through various species identification keys and collections I am fairly certain that the insect you observed was:
Deltoplastis commatopa
I lifted the following species description from Wikipedia and I think it matches your description & photo rather well:

Deltoplastis commatopa is a moth in the family Lecithoceridae. It is
  found in Taiwan and the provinces of Jiangxi, Hunan, Hubei and Sichuan
  in China.
The wingspan is 16–22 mm. The forewings are light lilac-fuscous with
  blackish-fuscous markings, edged ochreous-whitish. There is a large
  subtriangular antemedian blotch from the dorsum nearly reaching the
  costa, connected with costa by an angulated mark. There is a large
  triangular postmedian blotch, its base posterior, reaching the costa
  and the dorsum, its apex cut off by ochreous-whitish to form a
  tadpole-shaped mark. The terminal area beyond this irrorated
  (speckled) ochreous-whitish, a blackish marginal line round it. The
  hindwings are fuscous, darker posteriorly.

Here is a screenshot of the entry in the Global Biodiversity Information Facility:

You can see from the entry that several occurrences have been reported (with images) by people in Taiwan.
I also found this Taiwanese biodiversity website (in Traditional Chinese) and thought I would include it here (although I have to admit that I am not able to read Traditional Chinese).


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What happens to intrinsic factor exactly at the terminal ileum, where B12 is absorbed?
IF is very important for IF-dependent B12 absorption in the terminal ileum, the mechanism by which most of dietary B12 is absorbed. The B12-IF complex bind to IF receptors on enterocytes, but does the complex in its entirety get absorbed, or does B12 alone get absorbed and the IF is left outside?
The latter mechanism I came across in source 1 (see below), which stated the following:

IF-B12 complex binds to specific receptors. Following this, the vitamin B12 is absorbed into the cytosol of the enterocyte by endocytosis, leaving behind the IF at the brush border.

However, several other books and articles (like 2-4) rather vaguely state that the IF-B12 complex is absorbed into the enterocyte. I've found two articles that discuss the existence of these two viewpoints, (5 and 6), but they are kind of old (from 1965 and 1989 respectively) and I don't know if the "mystery's been solved" as it were.
Sources:

Concise Textbook of Human Physiology (this specific page)
The Mechanism of Absorption of Vitamin B12 (cobalamin) in the GI Tract
Marks' Essential Medical Biochemistry (this specific page)
Textbook of Pharmacology (this page)
Intrinsic Factor
Vitamin B12 absorption and malabsorption

After reversible attachment of intrinsic factor-cobalamin complex to its ileal surface receptor, an energy-dependent
process prevents removal of the complex from the cell surface by EDTA or acid; cobalamin dissociates
from intrinsic factor and, as suggested by previous
workers, binds to a molecule antigenically similar to
transcobalamin II; and  intrinsic factor is slowly(after some hours)degraded and forms breakdown products that are detectable in ileal extracts.
References
Textbook of Pathology Page 318
One article
Intrinsic factor mediated absorption of cobalamin
Recent articles-
Physiology of absorption of vitamin b12

This article is also quite old, newer articles than it suggest that the issue was still controversial at the time

@Dahen yes I agree. Though I have added one recent article proving the degradation of IF. However upon more research I found some articles stating the controversial fate of IF.

Thanks for going out of your way to look for so many sources, I appreciate it.

@Dahen thanks. I too got to know about this. It is a good question.


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Reverse oxidative phosphorylation?
I noticed that all of the cellular energy production methods that I covered have a fixed ratio of ATP to NAD(P)H out. For example, in the combined process of glycolysis, pyruvate oxidization, and the Krebs cycle, 10 NADH, 2 FADH2, and 4 ATP are produced (based off of my high school's bio text book, if I'm adding that right). In this way, NADH and FADH2 can easily be exchanged for ATP through oxidative phosphorylation. That got me wondering what would happen if a cell was using so many electrons (from NADH and/or FADH2) that there is too much ATP. (Just as a hypothetical: It seems fairly unlikely to me)
I was looking for a way that oxidative phosphorylation could be reversed, but I didn't find much. I did find that anaerobic bacteria can oxidize nitrite in this way, but I couldn't find much evidence of an O2-forming version. Does such a thing exist?

I am not clear whether you understand how ATP is produced in oxidative phosphorylation when you talk about producing oxygen. If you are still following a course you should wait until you have learned how a proton gradient, produced by the oxidative electron transport chain, is used to phosphorylate ADP. When you are at that stage you will be in a position to appreciate how hydrogen ion transport can be accomplished by essentially the reverse of this process. (If you need to learn this yourself, we can suggest suitable reading.)

Sorry, should've clarified... My question is basically whether there is a mechanism in any organism to split H2O (into H+ and O2, like PSII) using energy from an existing H+ gradient, possibly created by an ATPase.

I cannot see any biological rationale for what you are suggesting (much less any chemical likelihood), but I should point out that the production of ATP (like other biochemical processes) is tightly regulated. If there is sufficient ATP, there will be a switch from energy generation to energy storage.


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Can human pathogens present on plants become plant pathogens?
Since human pathogens sometimes live on the surface of plant leaves(read here and and here), and there are plant-pathogen microbes also living on leaf surfaces, is it possible for plant virulence genes to transfer to the human pathogens (perhaps via horizontal gene transfer) and make the human pathogen also pathogenic to plants? Has there ever been evidence of this happening?
This review paper addresses why plant pathogens haven't "crossed the Kingdom border" to being human pathogens, but what about the other way around (human pathogens affecting plants). Since there is such a wide array of plants out there with a wide range of pathogen interactions, it seems to me that it would be statistically more likely that a human pathogen could mutate to be pathogenic to some plant, than some plant pathogen could mutate to be pathogenic to specifically humans. Is that assumption valid? Also, I am talking about human-animals specifically, since it looks like there is a known virus infects both animal and plant cells in the lab (Lepidoptera/ cow pea)
As a currently-relevant example, could some plant virus, say Southern Bean Mosaic Virus, somehow share genes with a coronavirus strain and become a morph plant-human pathogen? (I know this last question is a little "out-there"). I chose that example plant virus since it is a positive-strand RNA virus like SARS-CoV-2. Thank you!


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What causes rashes to appear in specific parts of the body without a site specific trigger?
Why do rashes appear randomly at highly specific locations (and not others), without location specific triggers? Like, if it's a systemic issue, then it should be distributed to other areas on the body too.

It appeared on the back of my right hand, and nowhere else, and then died down. I've had similar rashes in the past where they appear without any obvious trigger, on a highly specific location and nowhere else, then disappear spontaneously after a few hours.
I'm curious what, in theory, can possibly cause this observation. If I have sensitive skin, they should not be localized like this.
I'm not asking for medical advice, just curious as to how exactly this even happens.

Welcome to Biology.SE! Please take the [tour] and then go through the help pages starting with [Ask] questions effectively on this site. In particular note that personal medical questions are not appropriate for this site. Saying it isn't personal is not enough when the text of your question contradicts you! This also seems likely to generate opinions rather than facts (also against site guidelines). Finally, we expect you to do some research on your own and then, informed by what you have learned, ask any questions you still have (ideally with references to reliable sources). Thanks!

I've pared your question down a bit but it could still use some prior research to improve it. Keep the personal anecdotes out of it.


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Why do we see colours when we close our eyes and press our hands against them?
Whenever we close our eyes and press our hands against them we either see some colours or sometimes some weird patterns(similar to hypnotic patterns).
What is the cause of this phenomenon?
Also, is this the right place to ask this question? Does this question have more to do with biology than physics?

Does this answer your question? What do you see when your eyes are closed?

Yes, this is a biological phenomenon, not a physical one, because the phenomenon depends on a cellular response. Pressing your eyeballs (mechanically stimulating them) causes you to see phosphenes.

What is the cause of this phenomenon?

The increased pressure in the eye causes activation and inhibition of cells in your retina (retinal ganglion cells). These cells are intermediates between the light-sensitive sensory neurons and the brain which interprets information into an image.
Quoting a well known study from 1989:

Eyeball deformation [pressing] in total darkness led to an activation of the
  on-center ganglion cells, while the off-center ganglion cells were
  inhibited. The latency and strength of this activation or inhibition
  varied considerably between different neurons, but were fairly
  constant in the same neuron when the eyeball indentation was repeated
  after a pause of 1-3 min. The latency and strength of neuronal
  activation or inhibition seemed to be dependent mainly upon the neuron
  location relative to the point of eyeball indentation. Some on-center
  neurons also exhibited a short activation at "deformation off". [...] We assume that the activation of on-center and inhibition of off-center ganglion cells by eyeball deformation are caused by retinal stretching, which also leads to horizontal cell stretch. Stretching the horizontal cell membrane probably generates an increase in membrane sodium conductivity and a depolarization of the membrane potential [neuron firing]. This depolarization of the horizontal cell membrane potential is transmitted either directly or indirectly (via receptor synapses) from the horizontal to the bipolar cells.

This is a phenomenon at the retina (periphery), i.e. not in the brain region associated with vision processing (occipital lobe). You can achieve the same visual effect by vigorously sneezing or blowing your nose, stimulating the same cells electrically (by injecting current with electrodes) or magnetically (with coils that generates a local magnetic flux, whereby currents are locally induced). It is also possible to duplicate the effect by stimulating only the visual cortex, but it is likely due to the fact you are simply approximately replicating the retinal firing patterns coming to the brain via the visual nerve.

I recommend to use the biology.SE search bar at the top with the term 'phosphene'; there are some archived answers on the topic already.


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What large "package" is carried by this large spider underneath itself?
One night in early May in northern Taiwan a strange looking spider carrying a large white "package" underneath itself ran in front of me and stopped, so I photographed it. The package is roughly the size and shape and color of a round dental floss dispenser that one would carry in one's pocket, perhaps a little smaller, about 2.5 cm in diameter.
I took some photos with a flash and without. The total span of the spider's legs was about 10 cm.
I'm guessing this would be an egg case, but it's surprisingly large, could it be prey? I suppose if a spider didn't have a home of any kind it would have to carry its meals with itself. It seems to be well adapted to this and moved quickly even with the large load.
Question: What kind of spider is this and what is it carrying underneath itself?

It's a Huntsman spider. The genus is  Heteropoda but not sure of the species (pingtungensis?) Yes, it is an egg case she is carrying.
Ask a local if it is the white barred spider, LaYa 喇犽, Mandarin is 白額高腳蛛. If so then it may be veratorias as in below article.
Wikipedia article on one species at
https://en.wikipedia.org/wiki/Heteropoda_venatoria
If you get more good photos, put them on wikipedia or somewhere. Until then, here's Heteropoda venatoria (Fam. Sparassidae) from here:
 click for full size

Oh, comments are on again. I fixed the link thank you, feel free to edit the answers yourself to do so. The good photos can go on wikipedia, and maybe iNaturalist. I dont know any other good place to put them.

Okay this certainly seems close enough for me considering the quality of my snapshots, thanks!


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If there is such known "Mitochondrial Eve", does it means that all the mitochondrial dna in everyone's body is same?
P.S. I know not that much, just some basics, but this question really interested me :)

Hello and welcome at Biology SE!
Can you edit your question and define 'same'? It is important to clarify what do you mean by this term. Since every cell in your body can acquire mutations independently and this is also true for cell organelles like mitochondria, in the strict sense of same = identical, then the answer is no. Based on the above logic even two mitochondria can have different DNA due to individual unique mutations.

The mitochondrial genome has a nonzero mutation rate, though estimates differ according to method. Estimates are approximately $10^{-8}$ per bp per year on average, and the mt genome is $\approx20,000$ bp. So we can do some math and expect that many (or most) people experience heteroplasmy, which is to say that they carry various different mitochondria (in the same person).
Note also that you inherit multiple mitochondria from your mother, not just one.
So- no, not everyone has exactly the same mitochondria, even if we can trace them all back to a single hypothetical human.

The M.DNA mutates about 1% in a million years, and because our Mt-Eve is 150,000 years old, our mitochondria are 0.15% different, or 99.85% the same globally, and 99.95% the same in Eurasia.
The variation of mitochondrial DNA between different people can be used to estimate the time back to a common ancestor, because mitochondrial DNA accumulates mutations at the rate of approximately one every 3,500 years per nucleotide. They can measure the differences in a tree:

Good answer, but I think it would be improved with some reference for those figures and a link for the tree.


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When did humans or their ancestors gain the instinct to take shelter?
I was going to ask if seeking shelter in a constructure dwelling or natural formation was instinctive to modern humans or if it is a learned sociatal behaviour.  By shelter I mean seek routine issolation from elements by being "inside" some structure or formation that encloses the individual or group on multiple sides and above.  A small shelter would be expected to trigger Claustrophobia and being outside of a shelter would be expected to trigger Agoraphobia in people that experiance such conditions.
It was highlighted that "nest building" is considered a part of a shelter instinct.  I am looking for when this behaviour develops not just during child rearing (as many birds do) but routinely (as great apes do with bedding).  Unlike forming a bed in an open space it seems common place for modern humans to form their beds inside a shelter and to choose to perform many other actions in this shelter such as eating.
Perhapse the first part of that should be to ask if there are any current or recent groups of poeple that do-not routinely occupy a shelter?
Many nomadic peoples seem to go to the trouble of transporting shelter with them but perhapse some do not if there is not an environmental driver to do so.
Not knowing where to look I did some searching and found a couple of websites that dicuss human instincts but not all of them list sheltering as instinctive so perhapse that is still debatable?
Herding but not sheltering is mentioned on Wikipedia.  Shelter is mention in this Harvard Business Review article about How Hardwired Is Human Behavior? but it seems that we could learn to shelter driven by other instincts.  This website was one of the more prominant ones to list seeking shelter as instinctive but I would not call it a reliable source.
Following on from that would be the harder question of when did the instict to shelter first evolve in humans or an ancestory of humans if it is instinctive?
I am not looking for a calendar date but whether there is some point in the ancestry where it is possible to say these early humans did prefer indoors and these ones did not.  We often hear about finds being located in caves which suggests those humans were sheltering in the cave.  I would accept those as signs of habbitation inside a shelter.
It seems obvious that other mamals like Rabbits and Foxes instinctivey live in burrows or dens either perminantly or following a "Nesting Instinct" but it is not so clear for humans it seems.  I could find more references to humans having a "Nesting Instinct" so perhapse that is where the instinct began or maybe it is the limit of it in humans.  There are examples of nesting or sheltering in fish speacies to so it is clearly something that develops multiple times in evoluionary processes, unless the Nesting Instinct is common all the way back to some aquatic species long ago for our line.
Sorry this is a bit rambling and not well resurched.  I have no background in biology, sociology or the study of human evolution so I am a bit stumped as to where I would begin to look for an answer.
I did look into the H2DB from a suggested similar question but noting in there seemed obviously linked to shelter to me besides "conditioned place preference (CPP)" & "housekeeping ability".  Housekeeping being a predominantly female trait could suggest a genetic factor in shelter, possibly from earlier "nesting" instincts?  Although I would have thought both male and female might have some protection of mate & young instincts beyond those for our habbit of forming herds or family groups.

Why must seeking shelter have evolved in humans? As you note, mammals (and other vertebrates) routinely seek shelter. So humans likely do this because they inherited it from their ancestors.

@kmm I am unsure how how to correctly ask about humans or their earliest known ancestors.  AFAIK there are no modern day relatives that do more than make a bed so it seems to be something specific to our line.  Could you suggest how I best rephrase the question in a way that would widely be understood to include everything running up to a "modern day human" in our genetic lineage?

Nest-building, which you are arguing is no more than making a bed, is considered part of shelter behavior (and therefore all great apes shelter). Either you're going to need to be much more specific on what "shelter" means, or, more likely, you'll have to recognize that pretty much every evolved trait, including behaviors and even those that are encoded culturally rather than genetically, occurs gradually, so there is no way to put a date on such a thing.

@BryanKrause I have tried to improve my question to make clear that by "shelter" I mean some kind of "indoors" instead of "outside".  We find remains of ancestors in caves which suggests to me sheltering indoors of a kind.  If there are certain ancestors that are only found outside of caves that would be an indicator of when to me. Not concrete as we only get small numbers of finds but it would be a start.


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Why do nattokinase and serratiopeptidase remain effective when given orally, but not insulin?
Why do nattokinase and serratiopeptidase not break down in the stomach and intestines?
Article says that serratiopeptidase is absorbed in rats intestines after oral intake - https://iubmb.onlinelibrary.wiley.com/doi/abs/10.1111/j.1470-8744.1994.tb00308.x

Added reference to the body of the question, thanks


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I would like help Identifying this insect
We found this in our house after coming in from outside but we are unsure if it came in on one of us (riding our coat) or was in our house before. We live in Massachusetts if that helps. We would like to know if anyone can ID these poor quality images.

Please [edit] your post to include an approximate size and any other contextual info you can think of. Additional better photos are also always useful for future visitors to comapre to. Thanks.


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Cellulose structure
In cellulose structure, some beta glucose are inverted. I’ve read that therefore the hydroxyl groups stick on both sides, but aren’t there hydroxyl groups on both sides anyways whether it was inverted or not and whether it was alpha and not beta? So why is this considered so special about cellulose?

Although cellulose is an important bio-molecule, this question concerns polysaccharide structure, and I believe it would garner more attention on chemistry.SE.

@Dirigible — Structural Biology is on topic here.  The question, however is unintelligible to me as it stands. What does the poster mean by “the structure is inverted” and “stick out on both sides”? Unless and until he presents molecular structures — which would probably answer his problem — it is a waste of everyone’s time considering his question.

Indeed, there would be hydroxyl groups in both sides independently of the orientation in space of each glucose monomer. The alternating inversion of each glucose residue reduces the steric effects between each monomer, simultaneously allowing the formation of more hydrogen bonds between each glucose. So it is a matter of molecular stability, and this is not special to cellulose, as it can be seen in other polysaccharides (e.g. chitin).


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Can hand sanitizer kill a fertilized human egg cell?
If you took a human egg cell that was fertilized in vitro and sprayed some hand sanitizer on it would it die?

Hello and Welcome at Biology SE! Please take our tour to see how to ask good questions on this site.

Yes, most likely.  Alcohol-based hand sanitizers are at least 60% alcohol (ethanol or isopropanol).  Alcohol concentrations as low as 15% are efficient at killing cultured mammalian cells.
See: Toxicity of Ethanol in Low Concentrations: Experimental Evaluation in Cell Culture

All cells were killed by a 15-s exposure to 30-40% ethanol while a concentration as low as 15-20% gave a total response after 5-10-min exposures.


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What Software could I use to create Diagrams of Biochemical Processes like these?
Cross-posted at GraphicDesign.SE here
Is there any software software that I could use to (closely) create pathways as depicted in these diagrams?

Or does anyone happen to know what software was used for these diagrams specifically? [Sourced from Harper's Illustrated Biochemistry (31e) and Murray's Medical Microbiology (8e) respectively]
I would like to be able make alterations such as adding extra steps, changing color, including newer pieces of data and such-like for the purpose of making my own notes.
I assume that knowing which software was (or can be) used to create these, I'd have greater versatility making the edits I need, or creating something in similar from scratch for other processes/pathways.

I've cross-posted on Graphic Design SE (since it seems like another good place to ask); however I'm under the impression there are Users here on Bio.SE that may have better recommendations, since I want to create/recreate pretty much only biochemical and biologic processes; there might be software for this very purpose popular among people in the field :-)

Cross-posting is typically frowned upon, see https://meta.stackexchange.com/questions/64068/is-cross-posting-a-question-on-multiple-stack-exchange-sites-permitted-if-the-qu I'll let each community decide whether this one is okay with them or not.

By posting to this forum, I presume the question is whether the illustrators of this and other biochemistry books used software specifically designed for the purpose of drawing reaction pathways, or, if not, whether such software exists. From my experience of using such illustrations in my own teaching over the years, I believe that the answer is probably no (although there are a couple of what I would consider ‘almosts’ mentioned below.) The main reason I would not expect this is that it would not seem commercially viable (biochemistry teachers and book illustrators are hardly a huge market) and you can get by with more generic pre-existing applications.
The class of application I consider best for this is termed a vector graphics application (popularly known as a ‘drawing’ application), as opposed to a bitmap or raster graphics application (popularly known as a ‘paint’ application). Although today there are applications that combine both functions, vector graphics applications have the advantage that they are more easily editable and they scale to any print resolution. The professional applications in this area can be very expensive and have a steeper learning curve than bitmap graphics applications (such as Adobe Photoshop). Moreover, they may lack features needed for biochemical use. It is therefore be worth exploring cheaper offerings, or investigating specialist vector graphics applications more focused on engineering or computing diagrams.
For biochemical work I personally would require software to be able to provide the following:

Controllable geometric lines (Bezier curves)
Customizable arrowheads
Text control that at least allows subscripts and
superscripts, and ideally both simultaneously, e.g. for a charged
phosphate species.
Rotatable text (as in the upper example)
Basic graphic primitives (as in the lower example)
Export to vector formats accepted by other applications (PostScript or PDF) to allow output in formats and at resolutions required for print publication.

How do different applications satisfy these criteria? They all support basic graphic primitives, and most allow export at least as PDF, if not the more flexible PostScript.
Surprisingly the creation of a line with an arrowhead is not straightforward as one is dealing with a combination of two separate objects. Although all applications tend to provide straight lines with arrowheads, curved lines with arrowheads tend to be absent from the general applications (even the most sophisticated) because a curved line is not really a line as such, but is generated as an oval segment with a stroke (visualization of its drawn edge) but no fill (the body is transparent). I have tended to use this sort of application (going back to MacDraw II of the Classic Mac) and fudge the arrows on them by combining them with straight lines of the same length as the arrowhead. However they are provided by more specialized diagramming software like OmniGraffle (mentioned in another answer) or the dedicated ChemDraw (which I find too limiting to use other than for export).
Text handling is the other problem. Placing a superscript directly above a subscript is a page layout operation that only dedicated mathematical software (e.g. MathType) is likely to support. Microsoft Word’s equation editor will do this, but export is only as PDF, and import into other applications varies in effectiveness. If you work in a generic application you will have to fudge it yourself with separate text boxes.
What are the choices for generic vector drawing applications? Adobe Illustrator is the most sophisticated, is used by most professional illustrators, but is very expensive (it is now subscription only). Other vector drawing applications that I am aware of but have not used include the commercial Corel Draw (cheaper than Illustrator) and the even cheaper Affinity Designer. As mentioned in a comment, there is also the free application, Inkscape. Free trials are available with most applications, so I would recommend seeing what is the best solution for your personal situation.
Addendum
I have just had a quick look at BioRender, which was mentioned in another answer. It has many different modules, including ones for biochemistry (including a Glycolysis pathway template) and seems quite attractive. However if you want to use the results for publications you need a $35 per month personal academic subscription (or your institution to buy a site license). I guess you tend to get what you pay for.

I find the absence of any "dedicated" software for the job a bit disappointing. Your answer's fairly comprehensive, and it didn't immediately occur to me to use ChemDraw, but I guess I could  use something similar (MarvinSketch) to craft some elements of the diagram. And thanks for the last bit about transferring vector graphics between apps; my brain was fixated on finding the One Perfect App, that it didn't occur to me. Thank you very much! +1

You’re welcome. I was going to extend and reorganise my answer a bit but have been tied up this morning. Will probably do it later.

Have done a 'final' tidy up, reorganizing a little, adding a few more titles, and explaining some of the technical stuff.

In the scientific community, we mostly use a couple tools to draw publication-quality pathway figures:

OmniGraffle
BioRender

These tools are optimized for making the kinds of figures shown in your question.
Others have also used Adobe Illustrator, Inkscape, or PowerPoint.
Like OmniGraffle, Illustrator and Inkscape can export resolution-independent vector graphics, ideal for publication on screen and paper. They do not make it easy to draw pathways, because unlike OmniGraffle, they lack "magnetic" points to lock arrows, lines, text, and other elements.
In Illustrator and Inkscape, you have to do a lot more work by hand with these tools to make nice figures. Tweaking the appearance of some element over in one layer will force you to spend a lot of time cleaning up other layers.
Microsoft PowerPoint is good for making slide decks, but it is not ideal for publication-quality work. It can be used to draw the kinds of primitives in the example figures in your question, but it exports high-resolution TIFF files, and these are very large files and so are difficult to distribute.

I've had a look at BioRender, and it looks like a tool that's very close to what I'm looking for. In addition, it looks like it'll help me with a whole bunch of other things as well. Great find! (That and the Nature article you linked).

I've accepted @David's answer because it provides me with general guidelines on using multiple apps to be able to create the diagrams I want (i.e: It gives better versatility than any one app). However, I'm still very pleased that you recommended BioRender to me. I to hope award a bounty on your answer for that (when the bounty window opens). Thanks!

I have used Draw.IO for similar tasks involving flow charts from scratch.
I've also used Adobe Illustrator, usually to modify figures when I have them in a compatible vector graphics format.
Finally, I've often made similar graphics directly in PowerPoint when I needed them only for a slide presentation and not a paper-quality figure.
As @David mentioned, you're unlikely to find any purpose-built tools, but there are a whole array of vector-based graphics programs. My main advice would be to try to pick one and use it, these are tools with massive feature sets that you tend to learn gradually. You can do a lot with just the basics, but the more you learn about a specific tool the faster your workflow will be.

I spent a few hours fiddling with draw.io the other day, it was considerably frustrating (primarily because it was my first time using it). The thought of using PPTs to recreate something  like this scares me (aesthetics matter to me, I'm afraid). I might give draw.io another shot later on; and @David's suggestions look promising. Thank you! :-D


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What is this insect? (Location: Bangkok, Thailand; found on a rambutan; size: 8 mm long, 4 mm wide; color: black)
What is this insect? (Location: Bangkok, Thailand; found on a rambutan; size: 8 mm long, 4 mm wide; color: black)

On the rambutan:

Videos:

https://youtu.be/WwB0B_PdOT8
https://youtu.be/0DZ8nXcJIkI


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Universal clock for humans contained in the telomeric sequences?
I don't know if this would make sense, but imagine that we could only suffer from natural aging (not diseases whatsoever involved). Is there an estimate of what is our natural maximum lifespan that a human can have?
I learned that the telomeric sequences protect sensible information in DNA, and that somatic cells suffer from a cut of these sequences in each replication. So I wonder if this is a natural clock, and if it has been estimated how much time do we have naturally.

If the clock is universal, it obviously doesn't run at the same rate for everyone.

I should have written on average for the human beings.


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If species are reproductively isolated, then how are interspecific hybridisations carried out?
during fertilisation there is compatibility test done so that both sperms and eggs are of same species. the zona pellucida of egg bears sperm specific receptor proteins(ZP3 receptor proteins) which bind with species specific proteins (bindin) present on sperm. so during interspecific hybridisaton( for example mule which is hybrid of donkey and horse) how fertilisation between gametes of different species carried out? what is exactly the mechanism behind this?

Mules existed for quite a long time - maybe 5000 years? - before any of the relevant biology was known: https://en.wikipedia.org/wiki/Mule  Apparently there is enough similarity in sex pheromones &c that male donkeys are quite willing to mate with female horses.  But that's not saying much, since a couple of my female acquaintances who have donkeys have told me that they just don't ever bend over when they're in the same corral as a male.

Hello and welcome at Biology SE! Please take our tour to see how to ask good questions. Can you please clarify your question? Are you interested in the specific molecular mechanisms behind egg and sperm cell interactions or you would like to know how is it possible that different species can mate?

i want to know about specific molecular mechanism behind egg and sperm cell interaction during interspecific hybridisation processes.

Why do you think that molecular mechanism would be different compared to intraspecific matings?

i am not able to understand that how gametes of different species involved in fertilisation. what about species specificity? how is it compatible?


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gene inversion and DNA directionality
The directionality of the DNA goes from the 3-prime end to the 5-prime end.
Thus, the inversion of a gene would connect a 5-prime to a 5-prime. How could that be?
Maybe inverting a gene also switches between the two strands of the DNA?
Thus, if one stand goes from 5 to 3, and the other goes from 3 to 5,
Inversion would make the first go from 3 to 5, and the other from 5 to 3,
And then each strand would be able to connect to the other?
Does inversion both changes direction, and switches stands?
If not, then how is gene inversion possible?
Thanks!
edit:
My main question arises from the contradiction between:
1) The DNA has a direction (3-prime to 5-prime).
2) inversion inverts the direction.
Thus, my question is: How can an inversion mutation happen?
How can a piece of the DNA, after being inverted (i.e., it is now in the wrong direction), connect back to the DNA?

Hello and welcome at Biology SE! can you please clarify your question? It might be only me but it's hard for me to figure out what do you mean by inversion and 'different strands go from'. You also have multiple questions can you please narrow it down

Thank you!
I updated my question to narrow it down to the main thing that bothers me.

Draw yourself a sample gene of say 10 base pairs marking 5’ and 3’ ends of the strands. Invert it — voila! Hint — I wrote base pairs and strands.

As you know, chromosomal DNA has two strands, with each strand running in opposite 5' <-> 3' directions.  When a chromosomal segment is inverted, both the 5'->3' sequence and its complementary 3'->5' sequence from the other strand are inverted together.  When reattached to the two strands it came from, the segment will have effectively switched its orientation on both strands by switching strands.  This happens exactly because a 5' end must mate with a 3' end.  This diagram should help make this clear (although it shows a duplication with inversion instead of an inversion in place):

Source: Wikipedia Commons

Awesome! Thank you!


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Are peppers on the same plant genetically identical?
I'm a hot pepper growing enthusiast and on one unknown super hot cross there is significant variation in pod size and shape.
What causes significant variation of pod shape and size on the same plant? Environmental factors? Genotype/genetic factors?
Also, what is a hot pepper phenotype? What makes a phenotype a phenotype?
Appreciate any input!

Hello and welcome at Biology SE! Please take the tour to see how to ask a good question. You have multiple questions in a single post. Can you please narrow it down, clarify your example a little bit. Thank you!

Also, what is a hot pepper phenotype? What makes a phenotype a phenotype?

Phenotypes are the quantitative or qualitative characteristics that arise from the interaction of an organism's genetics with the environment.  For pepper plants, height is a phenotype, as are leaf color, average fruit weight, and pretty much every other characteristic you can measure. Capsaicin concentration (mass of capsaicin per unit mass of fruit) is a phenotype that is relevant to hot pepper enthusiasts.

What causes significant variation of pod shape and size on the same plant? Environmental factors? Genotype/genetic factors?

It's hard to know.  There could be a genetic component that results in inequitable distribution of resources to individual fruits during plant development. There could be environmental factors that determine why one fruit is larger than another -- perhaps the larger fruit developed during a time when water and sunlight were plentiful to the plant.

Are peppers on the same plant genetically identical?

See this excellent answer given by mgkrebbs to the question Are the seeds in a single capsicum fruit genetically identical?