text:
Radiation mutation breeding in plant seeds: practical aspects
I did read some seed irradiation papers and they all use Gy as unit of measure, however I have never seen seed weights reported.
How did they calculate that, since Gy is J/kg?
Differencies aside between using gamma and X-rays, is there any equivalent dose I can apply using an X-ray tube fitted with a dose area product meter?
I am not sure if I can assume that spreading seeds in an area and then irradiating up to a certain dose area product would mean that each of those seeds was exposed to a certain amount of radiation.
Suggestions welcome, thank you.

It might help if you shared a link to one of the papers you're talking about. I don't work with seeds, but I wouldn't expect to see the actual weights reported since the unit is already normalized to weight. For example, if I'm reporting on arsenic concentrations in the liver, I'm analyzing the normalized data in units like ng of arsenic per gram of tissue, and my methods section describes how those values were calculated prior to analysis. I would imagine that whoever makes the instruments used for irradiating seeds have standard protocols available online.

I see. So should I assume that they weighted the seeds and irradiated until they reached a certain amount of J/kg, hence being Gy?

Here are some links: http://en.cnki.com.cn/Article_en/CJFDTotal-JXNY200709006.htm https://inis.iaea.org/search/search.aspx?orig_q=RN:41095572 https://www.actahort.org/books/1067/1067_9.htm

As a general rule, you shouldn't have to assume things when reading a scientific research article. They should include some indication of the methodology or protocols used. Saddly, that's often not the case. I'd try reaching out by email to the corresponding author on a paper your interested in and politely requesting their protocol. Most people are usually willing to help. You could also try contacting the manufacturer of the instrument you are working with for support. Sorry this didn't really answer your question.


text:
Why is a cell in anaphase (without a nuclear envelope) be considered as a eukaryotic cell?
Can anyone shed some light on this? All I can think of is that it has something to do with the chromosomes being paired

Related, possibly could be considered a duplicate though it's a bit parallel rather than directly duplicated: https://biology.stackexchange.com/questions/10404/are-mature-erythrocytes-prokaryotic

Does this answer your question? Are mature erythrocytes prokaryotic?

Organisms are classified as either eukaryotic or non-eukaryotic, not individual cells. This organismal classification does not change with momentary alterations of cell physiology during the cell cycle.

It is still considered a Eukaryotic cell because the daughter cells and mother cell are both Eukaryotic; the chromosomes will condense and be contained in a Nucleus after Telophase and Cytokinesis. Furthermore, Prokaryotic binary fission does not involve the assembly of Spindle Fibers, whereas dividing Eukaryotic cells in Anaphase use Spindle fibers to transport the Chromosomes towards the poles of the dividing cell.
I hope this answers your question!! :)

Only eukaryotic cells are able to under go a mitotic/meiotic cell cycle, in which, after an interphase of variable time length, such cells enter M-phase, and one of the regarded phases of such stage is anaphase, so in order for a cell to undergo chromosome segregation in the form of anaphase, it has to be eukaryotic.

source: Stack Exchange

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

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text:
What is this soil digging insect?
It is in Texas(Month: May). Are these flying ants?termites? or Cicada Killers?

Certainly not cicada killers--those have yellow stripes on them, are considerably larger, and also have a very different shape of abdomen. Here's a good pic of one of those: https://bugguide.net/node/view/1721236/bgimage.
They certainly look to have a hymenopteran "waist" so that means they aren't termites, they are some kind of winged ant. Possibly carpenter ants due to the large size (for ants) and the reddish-brown color (like this one https://bugguide.net/node/view/1056576/bgimage).

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


text:
Does endocrine noradrenaline stimulate sympathetically innervated cells?
Cells that are innervated by the sympathetic nervous system, does endocrine noradrenaline target the same receptors on them? Are they dually activated by both nervous and endocrine noradrenaline?

Welcome. Is this a homework question?

Nope. Norepinephrine happens to be both endocrine and neuronal, technically the endocrine circulation should reach same receptor sites as the neuronal. Was interesting. Asked.


text:
The role of duration of infectiousness in SIR models
I refer to J.H. Jones' Notes on R0.

The basic SIR model - as described in Jones' Notes - considers three factors that make up the reproduction number:

$\tau$ = the transmissibility (i.e., probability of infection given contact between a susceptible and infected individual)
$\overline{c}$ = the average rate of contact between susceptible and infected individuals
$d$ = the duration of infectiousness

The (basic) reproduction number then is
$$R_0 = \tau \cdot \overline{c} \cdot d$$
The duration of infectiousness enters the basic SIR model as the so-called removal rate $\nu$ which is nothing but the inverse of the duration of infectiousness: $\nu = 1/d$:
$\frac{ds}{dt} = -\beta s i$
$\frac{di}{dt} = \beta s i - \nu i$
$\frac{dr}{dt} = \nu i$
with

$s$ = the fraction of susceptible persons
$i$ = the fraction of infected persons
$r$ = the fraction of removed persons (recovered or died)
$\beta = \tau \cdot \overline{c} = R_0/d$ = effective contact rate or infection rate

My question concerns the way that $d$ enters the SIR model, because I
  find it not so plausible:

to consider all persons that are infected today and take a fraction $\nu$ of them that will have recovered tomorrow.

Wouldn't it be much more plausible

to consider all persons that became infected $d$ days ago and let these be recovered tomorrow?

The latter approach would be especially valid when the death rate can be neglected, i.e. when "removed $\approx$ recovered".
My impression is that most papers using a variant of the basic SIR model let enter the duration of infectiousness in the first way - leading to significantly different predictions than in the second case.
I implemented both and this is the difference (only due to the different ways that $d$ enters the progression formula, i.e. the values of $\beta$ and $d$ are fixed):

(In case that you wonder why the curves oscillate: I have modelled some sort of acquired immunity with finite duration of only some month - but in the very same way in both cases.)

This question reminds me of the equations for radioactive decay (see http://hyperphysics.phy-astr.gsu.edu/hbase/Nuclear/halfli2.html). Over there, we assume that a constant fraction of particles decay per unit time. A particular particle can have a lifetime varying from zero to infinity, but the average lifetime of all the particles is simply the reciprocal of the decay constant. Perhaps something similar applies here? (Think of infected persons as particles, removal as radioactive decay, and $\nu$ as the decay constant.) If that is so, the first of the two approaches you mentioned is correct.

I guess the main difference is that radioactive decay follows a Poisson distribution, but recovering of a disease does not:  I assume it is somehow Gauss distributed around a characteristic maximum.

While the number of decays in a given time period for a sample follows a Poisson distribution, the particle lifetimes do not. In fact they have an exponential distribution. Also, how can recovery times for a disease have a normal distribution? A normal distribution stretches infinitely in both directions, whereas recovery time can never be negative.

Thank you, you are right in both cases. Nevertheless the distribution of recovering times might be "almost Gaussian" - because nobody recovers immediately after having been infected. So maybe THIS distribution is Poisson - as opposed to exponential?

My question concerns the way that $d$ enters the SIR model, because I
  find it not so plausible:

to consider all persons that are infected today and take a fraction $ν$ of them that will have recovered tomorrow.

Well, it is in fact not very 'realistic' as you point out, but in the assumptions of the model, we see that the population has no structure (it is well-mixed, constant) and there are no birth-death events. So, in this case, it is not so problematic to take $v$ as a constant across the entire simulation, because what you are trying to calculate is the rate at which the three sub-fractions of $N$ ($s$, $i$, and $r$) change, not really which individuals are moving from one class to another (which you cannot really know anyways, if you talk about fractions of $N$).

Wouldn't it be much more plausible

to consider all persons that became infected $d$ days ago and let    these be recovered tomorrow?

So, considering my previous comment, it would not make much sense really to take a time-delay form on $d$, because you cannot really know which individuals got infected at any given point, you can only talk about fractions of $N$ (there is no population structure, as they say in the model formulation). So, the fact that your formulation seems to have a slower dynamics might not be very informative, because what you did is simply applying $d$ to a fraction-of-the-fraction of the population classes, so it makes sense mathematically that it runs slower, but as per the model formulation it does not make much sense, unless you have population structure defined from the beginning (which in this case is not), and unless you can explicitely know individual-per individual class transitions. In fact, I believe that taking the fraction-of-the-fraction would lead to an artifactual 'undercounting' of these individuals that actually needed to be in the $i$ class (and overcounting of the other classes).

I don't see it problematic to take $\nu$ as a constant. I don't understand what you mean with "constant across the entire simulation". Furthermore, there is no single rate at which $s$, $i$, and $r$ change but two: $\beta$ and $\nu$. And I don't understand your which-individuals-argument. All I want to say: When "duration of infectiousness" does mean what is seems to be supposed to mean, it makes sense to remove all those newly infected $d$ days ago as recovered tomorrow, and not a fraction $\nu = 1/d$ of those that are infected today.

The persons infected today  consist of some newly infected yesterday, some newly infected the day before yesterday, ..., and some newly infected $d$ days ago. And only the latter will have recovered tomorrow (in the mean).

You want to treat the model as it had population structure, but it doesn't. That's the main problem as I see it.

So, it's not a problem with the model but how you use it.

Sorry, but I still don't understand your argument. And I still don't understand what's wrong with my argument. The only structure I am supposing is a "timely" structure: that it does matter when a person got infected.

I am not sure if I quite understand your question, but I think your problem is here: removal (and your d) is a rate (time/removal). It does not matter what time you choose; a day, a week, a year, as long as you adjust your c (which is /time) to same timescale. In other words, if you wish to use d over several days, you need to calculate your contacts over several days, and changing only one will erroneously lead to different results.

I'm afraid this misses the point.


text:
Identification and odd leaf anomaly
We're in the process of welcoming sheep, thus setting up the fences, now inside on of the areas, there is a small tree. Never seen leafs like this before. I suspect this to be some sort of anomaly/disease ?.
I identified 2 oddities : the branches are chorros-like and some leafs have small, vivid red appendices growing on them

Could anybody identify the tree?
are the branches and leafs 'normal'
3 is there any danger for the sheep? (toxicity) ?

Region : South-west France
Size: About 2 meters
Overall picture :

Details :

Closeup:

Not sure about the tree identification. But regarding the oddity I had to think about galls

Could you post it as an answer so I can accept your answer? it's indeed galls on a Ulmus minor.


text:
Have I identified this species correctly? Weird ocean blob
I often comb the beaches in Santa Cruz (central California coast) for weird stuff that washes ashore. The waves have been a lot stronger than usual the last few days, and the today the beach was covered in a thick layer of kelp and other seaweed. There were even two dead seals washed up on the sand. Most intriguing however was this translucent oddity:

Reverse side:

It's about two inches across at its largest. I moved it to a concrete wall to photograph so I could turn it over without coating it in sand, but I found it down much closer to the water. It seems all but certain that it was ripped up from the seabed. I think there's a tiny snail attached to it, visible in the first picture.
Having done some digging, my best guess for the identity
of this species is some kind of ascidian tunicate. The closest comparison I find is this picture of Ciona intestinalis:

due to the orange hue and the distinctive black cord running through it. However it seems much fatter and I didn't notice a siphon on my specimen. Additionally, most images of the species show a much paler color and even more prominent siphon. My specimen might have shriveled from being out of the water though.
So, my guess is Ciona intestinalis. Can anyone confirm or refute?

A coworker of mine was able to identify the specimen as a Lightbulb Tunicate, Clavelina huntsmani. The distinctive "lightbulb filaments" that give the species its name can be clearly seen in the pictures I posted:

So it was indeed an ascidian.


text:
How is in-vitro fertilization technically achieved?
I failed searching on Google technical details about how in-vitro fertilization is achieved. I'm referring to the toolset and its use, rather than the chemical or biological aspects of the process. I often watch on TV how a needle penetrates into a human egg to fertilize it with sperm, but provided that a human egg sizes about 100 microns, I come up with the following questions:

Do there really exist needles so thin to penetrate a 100 micron cell? In such case, how are these needles manipulated without breaking or losing them in the lab?
How do technicians manipulate the needle with such micrometric precision?
How do technicians keep the human egg still so they can break into it with the needle without pushing the egg away?

Not sure if these questions sound naive, but I haven't been able to find any simple answer to them on the Internet.

Have you read the Wikipedia article on Microinjection and followed up the references there? Remember the word needle does not imply any particular material or mode of construction, and of course the first needles were used for sewing (rather than injection) and made of bone.

@David, thank you! Actually Google never dumped the result for this Wikipedia's page and I also didn't come up with the "microinjection" word. I will check it out and follow up the references. Thx again!

After following user David's hints, I have collected some videos that answer the questions I posted:

Regarding to needle manufacturing, there exist machines able to create micropipettes (this is how the needles are actually called) by heating glass cilinders and pulling them to create very thin tubes (capillaries). Click for featuring video.
Regarding to the high-precision manipulation, technicians use mechanical devices able to convert macroscopic motion (eg: human manipulation) to microscopic motion (eg: using reduction gears). Click for featuring video.
Regarding to how they keep the egg still, technicians use another type of pipette that slightly "sucks" the egg in a vaccuum-cleaner style. For a full-feature video of how the egg and sperm are manipulated, check this video out.


text:
What is blood pH for different animals?
So we all know that humans average blood pH is 7.4. But is it the same for the animals?
I need examples of animals with the same blood pH as humans and the ones with different blood pH.
I guess dogs and cats have almost the same pH am I right?

This question has been asked before -- Chart of blood pH across different animal species?.  However, since there is no answer to the original question, yours is not technically a duplicate.  I recommend looking at the comments on the older question, as they link to some resources for blood pH of reptiles, insects, and birds.

It would be helpful to know which species or groups you are interested in. Can you be more specific than "the animals"? Note that many animals don't even have blood! e.g. insects and hemolymph. For example, sharks have relatively acidic blood: https://www.researchgate.net/figure/A-Mean-SEM-blood-pH-levels-in-the-Atlantic-sharpnose-shark-during-a-60-min-stress_fig2_226732907, https://academic.oup.com/conphys/article/5/1/cox012/3055083. But I don't know if that is something that you are interested in.

I'm interested mainly in carnivores v/s herbivorous. The alkaline diet claim that as we humans have a slightly basic pH we shouldn't eat acidic food like meat. It would be a nice counter-example if carnivores have a similar pH as herbivores.

@heracho a little confused as you are different from user Jane who posted the question. But it would be helpful to have this directly in the question rather than in comments discussion.

I don't think I should edit the question to my particular interest. Although I believed that my question (Is there any correlation between species diet and blood pH?) is too close to this one as to be a new one.

The alkaline diet claim that as we humans have a slightly basic pH we shouldn't eat acidic food like meat. It would be a nice counter-example if carnivores have a similar pH as herbivores. -- I think a question concerning animal diet and blood pH is more interesting and easier to answer than the very general question posted above.  This seems to be an XY problem.

Good point @acvill, I'm going to post this specific question.


text:
Is the 6th rib attached to 7th rib, and 7th rib to 8th?
I'm just confused between a lot of pics that draw the thoracic cage in their way. what are these white things that I've shown?
or why the 7th rib is attached to the 8th?

Those are just a part of the costal cartilage, which is only found at the anterior ends of the ribs, providing medial extension. This connects the ribs to the sternum and is made of hyaline cartilage. Here is a clearer diagram of the cartilage part:

Ribs 8–12 are called false ribs (vertebrochondral ribs- attached to vertebra and cartilage). The costal cartilages from these ribs do not attach directly to the sternum, but are all attached to the cartilage of the 7th rib. For ribs 8–10, the costal cartilages are attached to the cartilage of the next higher rib. So, in a way, you are right in saying that the 8th and 7th ribs are attached.
The 6th and 7th ribs, though, are not attached. There are just cartelagenous bridges present in between them. The first seven are called vertebrosternal ribs. (attached to vertebra and sternum)

Sources:

https://opentextbc.ca/anatomyandphysiology/chapter/7-4-the-thoracic-cage/

https://en.wikipedia.org/wiki/Rib

https://www.pulsus.com/scholarly-articles/cartilaginous-bridges-between-the-adjacent-costal-cartilages--a-case-report.html

thanks man really thank you


text:
High concentration of primer in PCR
Why is it that higher concentration of primers than the DNA template in PCR will favor the annealing of a template to a primer?

Using high concentration of primers ensures that after denaturation template DNA binds to primers instead of binding to each other. Also higher primer concentration enhanced product yield, as primers act as limiting factor for annealing.
(Reference: https://academic.oup.com/nar/article/24/5/985/1047654)

To simply put it, higher concentration of primers means more primers in the mix, therefore more chances of it annealing to your DNA template, however more is not always good. The optimum concentration of primers in a PCR reaction is between  0.1 and 0.5 µM. For most applications 0.2 µM suffices. Using very high concentration of primers can be troublesome as it can cause your primers to bind to partially complementary sites resulting in non-specific PCR products.
https://www.embl.de/pepcore/pepcore_services/cloning/pcr_strategy/optimising_pcr/


text:
Cloning using pET28a and Protein Expression in DH5alpha and BL21
Can someone please direct me to an e-resource or a book that will help a newbie like me learn in depth about Cloning using pET28a and Protein Expression in DH5alpha and BL21. Though I have done cloning using TA vectors, pET28a is very new to me. I need to design primers with restriction sites to insert my GOI into pET28a, so would like to learn how to choose these sites too.

Did you try google? The pET28 systems manual and plasmid maps are easy to track down.
https://research.fhcrc.org/content/dam/stripe/hahn/methods/biochem/pet.pdf
https://www.addgene.org/vector-database/2565/

I did come across these, but they don't answer questions like how the choice of restriction sites will influence your protein. A fellow researcher was asked to justify his choice of restriction sites. If I remember correctly he had used a combination of SacI and HindIII for which a review a reviewer suggested replacing the SacI site as it might cause non-specific proteins to be expressed. It has something to do with codons, but I am not too sure, hence the query!

I can't think of a reason this would matter for this plasmid specifically. It's possible they were concerned about potential coding regions adjacent to your gene of interest, especially if it contained something like a promoter or an extra start codon. If your colleague sequenced their construct, it should be easy enough to spot any unwanted elements upstream of your GOI.

Thanks, i'll read more about this.


text:
Assessing beta diversity variations with time
I'm just starting in the field of ecological statistical analysis and I have a few doubts regarding a dataset that I'm working on.
The dataset is composed of several samples collected at a single location during a few months multiple times per day.
From my data I have estimated the beta diversity (Bray-Curtis dissimilarity) and I'd like to know if there is a monotonic trend with time and how much of the diversity can be explained by the different sampling hours or days.
My questions are the following:
- Is the estimation of Mantel's Rho using Spearman correlation is a valid estimator for the linear temporal trend?
- To estimate the source of the diversity (days/hours) would it make sense to run a npmanova analysis (as I'm using R I'd run adonis in particular) using as explanatory variables the sampling hours and dates?

I think the Mantel test is a valid way to test for a correlation, but Spearman is a non-parametric measure of correlation, and will not necessarily test for or estimate a linear trend. A Pearson moment would be better, but you might need to look at your data distributions to see if they fit the assumptions.
In response to the first answer, I don't think Procrustes is the right test for this. It's used for comparing different ordinations, which are dimensionally reduced representations of your dissimilarity matrix data. You lose information when you ordinate a data set, and you want to include as much information as possible when testing hypotheses. Constrained ordination approaches like cannonical correspondance analysis (CCA), or distance-based redundancy analysis (dbRDA) might be more suitable. These are actually analagous to some of the functions performed in adonis.
You should be able to use adonis the way your described. You'll want to make sure you also run betadispersion, which can help assess how suitable your data are. You'll also want to consider how you code your time data. It's simplest if time values are considered as discrete (day 1, day 2, etc.) or categorical (morning, noon, night) variables. Since times of day are cyclical, there's a trick with treating them as a continuous linear variable. Unless you tell it otherwise, a model will treat 23:55 (11:55pm) and 00:05 (12:05am) as being parametrically more distant in time than say 06:00 and 08:00. Depending on your daily sampling window, this might not matter much, but if you want to treat time a continuous, there's a workaround that involves sin() and cos() transformations of the time collections were taken.
It sounds like you're already using Vegan, which is a great package. You might also consider looking into LabDSV, which has a fantastic tutorial page that's more in-depth than most R vignettes. It has good examples of some of the different approaches I mentioned, as well as some others that might be of interest to you.

Thanks for clarifying my doubts! I used Spearman as a more general approach to see if the correlation was monotonic. I used categorical data for both dates and hours, but I will give the sin/cos transformation a try!

Rather than Mantel, I would suggest doing a procrustes analysis. I didn't know much about it (and still I don't) but a reviewer required it for a paper I submitted, so I used the implementation in vegan package. You can also give a look at this nice tutorial
The idea of procrustes is similar to Mantel's but it should perform better for this case.
I don't what to say about the second question, sorry!


text:
Animal body size determination for abundance
Does an animal being small or large determine its abundance?

Welcome to Biology.SE! There is an expectation that question-askers show that they have done preliminary research prior to posting. There appear to be many good and free-to-read papers addressing your question, found by a simple Google Scholar search.  See -- Relationships between body size and abundance in ecology (PDF)

closely related https://biology.stackexchange.com/questions/24482/how-big-should-the-human-population-be-as-predicted-by-body-mass/24495#24495

I'm sympathetic to @Dirigible that this seems like the kind of thing that should be easy to research, but I was surprised to see that there's not an answer to this already on SE.Biology. So very quickly:
Yes, there is what is known as an "allometry" relationship between body size and abundance in which the two tend to be inversely related.
Here is one meta-analysis that attempts to describe the relationship across food webs. Here is a review article that may be easier to read describing the law in somewhat more general terms. Here is a figure from the review with plots showing the relationships in different kinds of organisms from different studies:

In some cases people talk about the population density in some area rather than overall abundance, as density is easier to estimate and can be thought of as a local measure of abundance. From the review you can see that there are some equations that people have derived to describe the relationship:

For large compilations of population densities, the relationship between the average mass of a species (Msp) and its average density (Ncomp) is generally well fit by a power function ($r^2 > 80\%$), with an exponent near 0.75 so that $N_{comp} = cM^{\frac{-3}{4}}$, where c is a constant (also known as Damuth’s Rule)...


text:
What are some good books on oncology?
I'm looking for some book suggestions on oncology, preferably I want them to be fairly recent. I am not worried if they are fairly technical, as long as they have good accurate content and layout.

You could try DeVita, Hellman, and Rosenberg's Cancer: Principles & Practice of Oncology. It has detailed information on both biological and clinical aspects of cancer. Apparently, the publishers regularly release online updates to cover the latest developments in oncology.
Reference to the current edition:
DeVita VT, Rosenberg SA, Lawrence TS, editors. DeVita, Hellman, and Rosenberg's cancer: principles & practice of oncology. 11th Edition. Philadelphia: Wolters Kluwer; 2018. 2432 p.

The must-have textbook: The Biology of Cancer from Robert Weinberg
https://www.routledge.com/The-Biology-of-Cancer/Weinberg-Weinberg/p/book/9780429258794
The Second Edition was published in 2013, I didn't heard about a newer Edition yet but the current one is well recognized in the field


text:
How to download omic data from ncbi? (SRA data or any suggestion?)
I proposed myself to replicate the results in this paper with an accession number PRJNA325650. So, I'm trying to download the data. Which will be the best way to do this?. I tried with the sratoolkit, and the SRAdb package in R but doesn't work.
My code:
In sratoolkit
Input:
prefetch PRJNA325650

Output:
prefetch.2.10.5 err: error unexpected while resolving query within virtual file system module - failed to resolve accession 'PRJNA325650' - The object is not available from your location. ( 406 )

In R (SRAdb)
Input:
rs = listSRAfile(c("PRJNA325650"), sra_con, fileType = 'sra')

Output:
Error in sraConvert(in_acc, out_type = c("study", "sample", "experiment",  :
  Input type shuld be in 'SRA' 'ERA' 'DRA' 'SRP' 'ERP' 'DRP' 'SRS' 'ERS' 'DRS' 'SRX' 'ERX' 'DRX' 'SRR' 'ERR' 'DRR'

Any suggestions or methods?

I’m voting to close this question because it is off-topic. In particular, this question has no biological component, but it might be suitable for migration to [bioinformatics.SE]. Please revisit the [tour] and read the [help] for details.

Sorry, but the tags "bioinformatics" and  "ncbi" are here and not in StackOverflow.

The fact that there is a tag is irrelevant to whether a question is or is not on topic. That is set out in the Tour. People here are happy with bioinformatics questions where the biological problem is to the fore, but less so with questions on particular software or coding. In any case you are more likely to get an answer on SE Bioinformatics, so I would advise you to move your question there.

Ok, I'm going to move it

I had a look, I can see the data in FASTA format.
The accession number is for a project with 50 samples, each of them a sequencing run.
First I went to genbank at
https://www.ncbi.nlm.nih.gov/
search that accession nunber selecting "all databases" to get the project page here
https://www.ncbi.nlm.nih.gov/bioproject/325650
Under "resources" there is "sequence data" "SRA experiments"
to the right I clicked on the number 50, taking me to:
https://www.ncbi.nlm.nih.gov/sra?linkname=bioproject_sra_all&from_uid=325650
I see the list of 50 samples, Clicking on the first I get to:
https://trace.ncbi.nlm.nih.gov/Traces/sra/?run=SRR3667045
Clicking "Runs" takes me to a page with the data viewable in many forms.
hope this helps.


text:
What proof do we have that visual attraction to other humans is a natural biological trait?
There's another question answered that relates to this, but the sources don't show enough evidence of how it is a natural biological trait that we're born with.
Even though there's evidence that culture influences some of our behaviors on visual attraction towards other people, is there any evidence this stems from something that is a natural biological trait?

I think your question might fit on a sister stack, but you need to better define "natural biological trait". You mean if it is 'pre-programmed' in our brains? If it is genetic? What are you looking for? Secondly, and not less importantly, what do you mean by visual attraction? What kind of outcome measure would you use for that?


text:
Exact definition of single nucleotide polymorphism (SNP)
So, I know on a higher level what an SNP is but I'm a bit confused about the details.
Firstly, our professor said that an SNP has to have at least a prevalence of 1% in the general population to be considered an SNP and not just a mutation. Wikipedia says the prevalence needs to be 0.5%. Is this actually a strictly followed cutoff? And which of the two values is correct?
Secondly, he said that SNPs never cause a disease but can only predispose you to one. However, the wikipedia article mentions thier role in diseases that are clearly caused by single mutations (cystic fibrosis, sickel cell anemia, and beta thalassemia). So, can SNPs cause a disease or not?

1% v. 0.5% is unimportant and arbitrary. The databases of SNPs need an actual cutoff. If you think of the millions of SNPs added to database by automated genome sequencing projects, the idea of weeding out any related to a mono-genic disease seems improbable,

In genetics, a SNP (Single Nucleotide Polymporphism) is the substitution of a nucleotide with a different one.
A SNP can have phenotypic effects or not.
A mutation, in genetics, is any kind of inherited change in DNA. Mutation types are: SNPs, indels, structural variants, translocations and so on.
Sometimes researchers (especially in the field of medical genetics) call "mutation" (meaning "pathogenic mutation") a SNP which is responsible of a disease (especially in case of a Mendelian disease). Since mutations causing severe Mendelian diseases are usually rare, several people use the arbitrary threshold of 1% to discriminate between a "SNP" and a "mutation".
So, probably your professor is stating that SNPs cannot cause a Mendelian disease because he uses the last definition I gave. However, while this definition may be useful for medical genetics purposes (i.e. I also agree that a very common variant is unlikely to be causing a rare Mendelian disease), it is arbitrary, if not wrong.

Single nucleotide polymorphism is the most common type of alteration in DNA, this occurs when a single nucleotide is replaced with another. SNPs are normally present in our genome, with prevalence of one in every 1,000 nucleotides, making approximately 5 million SNPs in a our genome.
These variations are commonly found in the DNA present in between the genes and act as markers for locating different genes. But when SNPs are present in gene sequence or in the regulatory region, this directly effects functioning of genes and can result in disease.
It is reported that SNPs effect person's susceptibility for developing various diseases like heart disease, diabetes, and cancer.
SNPs can also be used to track the inheritance of disease genes within families. These alterations also controls individual's response to environmental factors and response to various drugs.
Reference
https://www.snpedia.com/index.php/SNPedia
https://www.sciencedirect.com/topics/medicine-and-dentistry/single-nucleotide-polymorphism)


text:
Same target receptor different mechanism of action?
If different drugs have the same receptor as a target, does that imply that they have the same mechanism of action?

Not necessarily!
Biased agonism
It's reasonable to start with an expectation that agonists at the same receptor have the same effect, but that's not necessarily true due to biased agonism. Biased agonism occurs when binding of different agonists to the same receptor results in different downstream activation of second-messenger systems.
Psychedelics and serotonin receptors
A particular example I am familiar with (besides the Jarpe paper) involves the 5HT2a serotonin receptor. This receptor is a shared molecular target of several psychedelic drugs: LSD, psilocybin/psilocin, DMT and others. However, this receptor exhibits biased agonism (Berg et al 1998).
In fact, it seems like agonists at the 5HT2a receptor neatly segregate into those with psychedelic effects (eg: LSD/psilocybin) and without (eg: lisuride/ergotamine, also serotonin itself) based on the different downstream molecular signalling pathways that they trigger, despite binding to the same general site on the same receptor.
Other considerations
Drugs' mechanisms of action can also depend on concentration and on all the other possible targets for those drugs. Pharmaceuticals are often small molecule drugs and while they may have preference for certain receptors, they are rarely (probably never) purely specific.
For example, the NSAID class of anti-inflammatories all work through inhibition of cyclooxygenase enzymes, but they differ in their relative specificity for COX-1 and COX-2. If you are looking at two drugs that have the same effect on COX-2, but don't compare their effects at COX-1, you might be surprised to find they have different results.
For another class, SSRIs used as antidepressants also have effects on other monoamine transporters (dopamine and norepinephrine) but vary in how specific they are.

Berg, K. A., Maayani, S., Goldfarb, J., Scaramellini, C., Leff, P., & Clarke, W. P. (1998). Effector pathway-dependent relative efficacy at serotonin type 2A and 2C receptors: evidence for agonist-directed trafficking of receptor stimulus. Molecular pharmacology, 54(1), 94-104.
González-Maeso, J., Weisstaub, N. V., Zhou, M., Chan, P., Ivic, L., Ang, R., ... & Sealfon, S. C. (2007). Hallucinogens recruit specific cortical 5-HT2A receptor-mediated signaling pathways to affect behavior. Neuron, 53(3), 439-452.
Jarpe, M. B., Knall, C., Mitchell, F. M., Buhl, A. M., Duzic, E., & Johnson, G. L. (1998). [D-Arg1, D-Phe5, D-Trp7, 9, Leu11] Substance P acts as a biased agonist toward neuropeptide and chemokine receptors. Journal of Biological Chemistry, 273(5), 3097-3104.

Thanks for this enlightening answer.


text:
Can I find out what resistance bacteria has based on strain? where do I look for that info?
I have a list of strains across various organisms for example:
Escherichia coli - ATCC 25922, CGSC 6152, W3110RL.
Pseudomonas aeruginosa - ATCC 27853, PAO1, APAE1111.
I'm failing to find any resistance information on these strains, as in what strain is resistant or susceptible to what antibiotic. Is there a way to find out?
Thanks.

There are many official websites that holds information and collection of microbial strains, here you can find a selection of them: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4241729/

@Dirigible Answers should be in answers rather than comments.

@Dom, are you looking for a database of resistance genes carried by these strains, or do you want information on minimum inhibitory concentrations?

Start with the ATCC product sheets (Just google the ATCC Number). They have lots of information about common uses, history of the strain, references, and sometimes some antibiotic susceptibility info. Keep in mind, if it has been kicking around a lab for a while, you might want to double check some of the MIC values, as they're known to change with serial passaging in broth cultures. But that's mostly if you need rather exact values.

If database and literature searches fail, you can plug the GenBank accession numbers for your genomes into the CARD Resistance Gene Identifier. It takes either protein or nucleotide sequences, though nucleotide seqs. undergo ORF calling first. For example, plugging in NZ_CP009072.1 for E. coli ATCC 25922 gives 7 perfect hits to known antibiotic resistance genes. Granted, carrying the genetic determinants of resistance is different from phenotypic resistance, but it's a place to start.


text:
Why is urine acidic (equilibrium of I/O, input <=> output)
Urine pH is on average 6.0, net excretion of acid. Is that in balance with net input of acid?

Welcome to SE Biology. The answer to your question is, of course, no. Have you tried to research this question yourself? Acid–Base balance is an important topic and there are numerous introductory articles such as this one about it on the web. If after doing a little reading, you still have specific problems, repost letting us know precisely what they are. (There's no chemical law of conservation of acidity, you know.)

consumption of meat (acidic) will be handled by increased excretion of acid via the lungs though, carbon dioxide, and since the kidney is the major organ for acid-base regulation, it seems very likely that its normal rate of excretion of acid was a result of equilibrium of "acid-in, acid-out", since it will increase acidity of urine to respond to acidosis, or alkalinity for alkalosis, etc.

Please finish reading the Tour to find out how this site works. If you wish to answer your own question you may do so, but as an answer, not a comment. My own comment was an attempt to improve your question by making it more specific, given that this is such a wide area. Although I expressed an opinion, I was not answering your question (by explaining why) but suggesting where you could read about the counter-view to the one that seemed implicit in your question and may have been the result of erroneous chemical assumptions.

well if average kidney pH has nothing to do with acid-base regulation (while urine pH clearly does often reflect acid-base regulation), and it is more about antibacterial properties or similar, that'd be an answer too. idk if the question is out of place, since clearly acidic diet (or, one that generates surplus acid in body) would tend to acid-base regulation compensation by acidic urine.


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What’s the name of this insect that looks like a leaf? I found it in Taiwan
Found it in a tea plantation. It can jump.

It appears to be a Tituria planata nymph.

The adults look like this:

At first I thought it was a treehopper, but it turns out that it was a leafhopper (they are similar but different).
Tituria planata is one of the most common leafhopper species in Taiwan.
https://www.inaturalist.org/observations?place_id=7887&taxon_id=49025&view=species
Image source 1
Image source 2


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what kind of lizard is this
Found on ground by house in residential neighborhood in Fort Pierce FL. looks mature maybe 17".

Nice find. It's a common basilisk or jesus christ lizard, distributed throughout central america, they grow to 27 inches and can run on water, the male is bigger than the female:
https://travel.mongabay.com/colombia/images/colombia_1513.html

haha nice downvote. :) i have only 6000 points left. can we go to 6666 plz.


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Is there anyway from which we can measure the viscosity of honey using a refractometer?
Is it possible to use a refractometer to measure the viscosity of honey because as we know, a refractometer is used to measure moisture and therefore water influences the viscosity of honey so is there a way that we can use to measure the viscosity of honey that way or using any other method apart from time since time has a high percentage of uncertainty?

Theoretically, if refractive index and viscosity are both simply functions of moisture content, you should be able to use one to approximate the other using an empirical standard curve. However, based on this paper, it looks like the relationship between moisture content and viscosity at 25C can vary quite a bit between different types of honey, expecially down below ~18% moisture. So I'd be pretty hesitant to rely on refractive index for acurate viscosity measurements unless you first rigerously validate your methodolgy against empirical viscosity measurements.


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How can a homozygous mutation, considered pathogenic, occur on a gene such as HFE without the disease developing?
What happens when you have a homozygous mutation on a gene (eg. a swapped base), that is considered pathogenic, but without developing the disease?
It it were a heterozygous mutation I would get it, because we still have at least one healthy/wild-type copy of the gene, so at most the disease will just manifest in a more mild form, but with a homozygous I have no idea how is it possible to NOT develop the disease.
Also, what happens when heterozygous mutations develop the disease? In these cases why does the healthy version of the gene goes "quiet"?
One example is HH caused by HFE gene mutation (mostly C282Y and H63D), and not everyone develops the disease, doesn't matter if they are heterozygous or homozygous.

What happens when you have a homozygous mutation on a gene (eg. a swapped base), that is considered pathogenic, but without developing the disease?

It may be an example of incomplete penetrance of variable expressivity. Simply, you are probably dealing with a complex trait in which either more than one gene is involved, or there is interaction between genetics and envronmental factors.

Also, what happens when heterozygous mutations develop the disease? In these cases why does the healthy version of the gene goes "quiet"?

I assume you are still talking about a putatively recessive disease. One possible explanation is haploinsufficiency, i.e. the WT allele alone doesn't produce enough transcript and the heterozygous individuals has "problems"

One example is HH caused by HFE gene mutation (mostly C282Y and H63D), and not everyone develops the disease, doesn't matter if they are heterozygous or homozygous.

And indeed HH is an excellent example of complex disease, in which genetics is involved, but the inheritance is not purely Mendelian.


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Can aflotoxin presence be inferred from the mild discolorotion at the middle parts of a hazelnut?
Can aflotoxin presence be inferred from the mild discolorotion at the middle parts of a hazelnut?
For instance, how likely is it that the hazelnuts pictured below contain Aflotoxin?
P.S.: these hazelnuts were fried before packaging in a vacuum sealed plastic bag. ( I am not sure whether the color change in the middle part comes from fungal activity (e.g., aflotoxins) or from the frying process?)

Welcome to Biology.SE! Please take the [tour] and then go through the help pages starting with [Ask] questions effectively on this site and [edit] your question accordingly. In particular note that personal medical questions are not appropriate for this site. ——— We also encourage 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!

This is not a personal medical question, sir, to put it in other words: Can aflotoxin presence be inferred from the mild discolorotion at the middle parts of a hazelnut? I was gonna edit the question but I could not see an edit option.

@NerdyNerdie Your question is fine except for the question "is it safe to eat?". This very much is a question that falls under the umbrella of asking for advice that may impact your health. Please see here. As such, your post will likely be voted closed unless you remove that portion of your post. You can [edit] your post by clicking on [edit] at the bottom of your question.

Reformed the question accordingly.

related (how to test it cheaply?) https://biology.stackexchange.com/questions/104505/how-to-reduce-the-quantity-of-carcinogenic-mycotoxins-in-oatmeal/105022#105022

Depends on who you bought them from and how you stored them.
Molds can grow in nuts and nutmeats and produce mycotoxins (from toxin-producing strains such as aflatoxins by Aspergillus flavus). The mold is usually visible and below is picture of Aspergillus flavus growing on a nut product. Source

The amount of aflatoxin produced by the mold is dependent on weather conditions and storage. We can only account for or control the storage conditions. When food substances are not well preserved, fungal growth may occur, leading to the production of mycotoxins.
The pictures presented could also just be an improper storage (with no health risks). There's indication that storage of wet nuts in poorly ventilated silos increases the potential for developing kernel brown centers. Source
If these nuts were stored in improper conditions from farm to store and the farm has been associated with a breakout of Aspergillus flavus then there's chance, but slim. QA/QC and aflatoxin levels are regulated. Codex Standard 193-1995 mentions the maximum levels of aflatoxins and sampling plans.
If the nuts had mold on them and they were washed to get rid of the surface mold, they could have spores from Aspergillus flavus capable of producing alfatoxin. Aspergillus fungi can case discoloration of  certain grains (rice), but that implies that you're able to see them on the product (the mold growth). The nuts in the picture seem quite clear.
In terms of where you bought the product, street vendors are at higher risk of having their products present alfatoxin problems rather than commercial enterprises, because of the location the product is sold at. Source


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strange creature
We live on the Gulf Coast in Corpus Christi, Texas. There was a big thunderstorm that dumped several inches of rain at our home. We live about a quarter of a mile from the bay.
My daughter found it in a shallow puddle on the sidewalk. The creature is about 2-3 inches and about as big around as a pencil. Not sure where it came from or what it is, any ideas?

Welcome to Biology.SE! I suspect this could be part of a plant rather than an animal. Did you see any sign of movement from the organism? Were there any flowering plants in the vicinity?

I agree with tyersome, it has green on it and it looks like a root from a plant. There are water animals with tails charmingly called rat-tailed-maggots, which are hoverfly larvae, although they are different.

you should take it home and plant it in a semi submerged soil and see what grows from it. probably a small plant that flowers.

It is a penis worm!

https://en.wikipedia.org/wiki/Priapulida

Priapulida (priapulid worms, from Gr. πριάπος, priāpos 'Priapus' +
  Lat. -ul-, diminutive), sometimes referred to as penis worms, is a
  phylum of unsegmented marine worms. The name of the phylum relates to
  the Greek god of fertility, because their general shape and their
  extensible spiny introvert (eversible proboscis) may recall the shape
  of a penis.

I am not positive, but you are close to the Gulf where these live, and maybe the weather swept some up from the bottom.  If that is what it is, it would need a seagull to drop it or some kind of Fortean rain to get any distance from the beach.


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Triangulation number of the SARS CoV-19 virus
Is the triangulation number of the SARS CoV-19 virus capsid, in the sense of the Caspar-Klug theory, known?   In case the Caspar-Klug theory does not apply to it, is it known what is its tiling, in the sense of the viral tiling theory of Twarock (and coauthors)?
I am a mathematician, trying to learn the geometric and group-theoretic aspects of virus structures.

Coronaviruses, like many viruses with a lipid membrane, are pleomorphic. The individual particles don't have a consistent shape. Here is a cryo-electron micrograph of SARS-CoV-1:

It might not be obvious, but each particle seen here is unique, they are not different rotations of identical copies. Since there is no consistent symmetry, there can be no triangulation number.
The image is from the following reference: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1563832/

Thank you very much for your explanation.  It is very helpful for me!

After reading just about every paper on SARS-CoV-2 structure I could find, I think the answer is a bit more nuanced.  The coronavirus capsid is probably somewhat regular, but not perfectly regular.  Calling it "pleomorphic" is probably more confusing than descriptive here - it's not that the virus can be produced in several distinct forms by cells, but rather it can rearrange itself (eg under mechanical forces), and it can also be damaged during preparation of samples for microscopy which can create the appearance of having different forms.  Carefully collected SEM images show a very uniform and narrow distribution of particle sizes and shapes.
There are a couple of bits of information which may help:

A broken open virus releases an apparently helical strand of RNA+N protein which is about 15nm in diameter and very long, and
There are some regular arrangements of N proteins visible inside intact particles by cryo-EM tomography, typically a hexagon plus one protein in the middle (these are also 15nm in diameter)  (Source: Yao 2020, Molecular Architecture of the SARS-CoV-2 Virus)

The most likely way to combine those two observations is that the strand folds itself into a hollow sphere, perhaps in a way similar to examples from other enveloped viruses (eg PDB ID 3J3Q).  Looking at a snapshot at any point in time, the strand winds around such that most of the copies of N form a lattice, although the lattice may be distorted, and probably has a few places where the spacing changes and/or there are defects in the lattice; but also this may not be a fixed arrangement over time.


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Are endorphins addictive?
Endorphins are among the brain chemicals known as neurotransmitters, which function to transmit electrical signals within the nervous system. Stress and pain are the two most common factors leading to the release of endorphins. I wanted to know if they are addictive, and found some contradicting answers:

If people can get addicted to risky sports just for the thrills they
  provide, they can also get addicted to painful activities where
  endorphins provide relief, "despite the harm to self and/or others,"
  says Dr. Anna Lembke, chief of addiction medicine at Stanford
  University School of Medicine in an email interview. "For example,
  someone who compulsively cuts herself for the endorphin release is
  causing self-harm. Someone who compulsively runs, even to the point of
  causing musculoskeletal injury, is causing self-harm."

Source:
https://science.howstuffworks.com/life/inside-the-mind/human-brain/can-be-addicted-to-endorphins.htm

In contrast to the opiate drugs, however, activation of the opiate receptors by the body's endorphins does not lead to addiction or dependence.

Source: https://www.medicinenet.com/endorphins_natural_pain_and_stress_fighters/views.htm#
If they are not, how can we explain the 'love' for pain in (this content might be sensitive for some of you) some people?

Wiki suggests that they haven't found a root cause for exercise addiction: https://en.wikipedia.org/wiki/Exercise_addiction#Mechanisms

Addiction specialists and others who study human behavior often catageorize addiction into the two broad categories of physical dependence and psycological dependence. They are not always mutually exclusive, and they can both manifest in serious or mild cases of addiction depending on the person and a number of other factors.
What differentiates them is how they affect your physiology. A person severly addicted to alcohol or opioids can become extremely ill or even die from the withdrawl of those substances, due to the strong physical dependence their body has developed. To my knowledge, people do not experience a physical withdrawl after cessation of compulsive pain seeking behaviors. Since they didn't cite any source, we can only guess as to the intended meaning of your second source, but it's probably related to this lack of withdrawl. A quick search on PubMed shows publications referring to certain endorphins as mediating this type of addiction. Meaning that the endorphin is not addictive per se, but a compulsive or addictive behavior can be communicated to the brain in terms of a native neurochemical pathway which is otherwise a normal part of a healthy brain.
I think the lesson here is to be somewhat skeptical of online sources that don't link to peer-reviewed science. Attempts to simplify a topic for the purposes of communicating with a lay audience often result in more confusion than clarity. And if you search something on PubMed or google scholar, you'll probably find an answer in the same amount of time it took you to post your question here.

Pain is not an endorphin but p substance triggers reactions to form opioids and those are endorphins. There is a lot of research about serotonin and dopamine being highly addictive.
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4028699/
Here they review this and explain it a little bit
From a psychological point of view people harm them self because they want to sentence themselves, but there are very much deviations and you can not put anybody in the same pot...

Hi and welcome to biology.se. Answers are expected to explain and give an answer to the question, not mainly link to another source. Please edit your question accordingly to avoid its deletion. Also please have a look into the Help center on answering questions.

I have huge problems dealing with you guys here, there is the explanation Substance P triggers opioid secretion, what else do you need?

It‘s now 2020 and before 1970 they already knew the biomolecular way how pain triggers addiction, and you can not take my 3 words - opioid - substance p - secretion and make a quick google research it‘s awful how you guys are here on this channels.

If you like it or not - in this community an answer is expected to answer something and not point to another resource or a google search only.

Anyway I gave an accurate answer  substance p leads to expression of opioids. Opioids make addictive what do you need more? All the stuff after is just some other stuff to read because it‘s interesting for me and has not a real link to the question above... his question is inaccurate pointing to an interview and not to science, so what do you want from me?

I will review how to answer questions and try to change it I try to help not to disturb threads. And Itms not my goal you feel disappointed by my answers


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Technical term for a mutation that only occurs after a preceding one
Consider a hypothetical population of 1000 organisms.
(a) 300 of these 1000 have a T to G substitution at a specific position 1.
(b) 200 of these 1000 have an A to T substitution at a second position 2.
(c) All of the 200 with the substitution at position 2 (b) also have the substitution at position 1 (a).
As a non-geneticist, I would call the second mutation a refinement of the first mutation. Would that seem reasonable, or is there a specific technical term for this phenomenon?

Can you clarify why it would be a "refinement"? Why do you suppose that there is any connection between the two mutations? Why not just a second-site mutation that occurred later in the same clone as the first mutation? I'd recommend looking into previous work tracking mutations across time, e.g. https://www.genetics.org/content/200/2/619

Your question needed a little tidying up and someone had suggested some changes. I have tried to lay it out in a more concise and readable fashion. In particular I have removed the term "refinement" from the title as that really begs the question. Better, I think to describe the phenomenon and then give it your own description in the body of the question. But you are free to revert as you see fit. (But use SE's own tool console for emphasis. Whatever you did, didn't work for me.)

Yes, good point. Refinement is a bad word because it has a value to it. I don't suspect that there is any relation between the two mutations. As a mathematician I'd say that the set of organisms that have a mutation in position 2 is a strict subset of the set of organisms that have mutation in position 1, but this is also bad notation somehow. (Thanks @David for great edits).

I am not a geneticist either, although a molecular biologist, so cannot be sure whether there is a term for what you describe. For my part, I would describe the results in a factual manner before considering possible explanations of the type suggested by @Dirigible.

The description of the second mutation depends on the nature of its relationship to the first mutation.

If the first mutation reduces fitness of the organism, and the second mutation tempers the fitness reduction, then the second mutation would be compensatory.
Compensatory mutations are common in bacteria that acquire antibiotic resistance.  Consider a strain of E. coli that acquires resistance to streptomycin by mutating the rpsL gene, which encodes a 30S ribosomal protein targeted by streptomycin.  In the presence of streptomycin, the rpsL mutant is obviously more fit than wild type E. coli.  In the absence of streptomycin, however, ribosomal mutations lead to inefficient translation.  Compensatory mutations may then arise elsewhere in rpsL or within another gene involved in the ribosomal complex, partially alleviating the fitness defect caused by the initial mutation to rpsL.

If, instead, the mutations are synonymous and otherwise unrelated in their functional potential, I would simply call those mutations coincident in the genome, though this isn't really a "technical" term. If you wish to describe the relevance of these synonymous mutations in context of the three distinct genotypes given in the question, you could say that the first T to G transversion differentiates strain X from ancestral Wild Type, and the second A to T transversion differentiates strain Y from ancestral strain X.  This assumes that both of these mutations occurred once in the genetic history of this population.

Thanks - I am not thinking about the fitness though. What would you call it if all mutations were synonomous.

@FrederikRavnKlausen, I've updated my answer.  Do you have a specific organism or system in mind, or is this truly hypothetical?

Thanks, I have the Sars-Cov-2 in mind. Here there is a very specific strain the Wuhan reference and with respect to that one can track the mutations one after another so they actually quite accurately behave as the example above. @Dirigible

@FrederikRavnKlausen, That's helpful. I'd recommend editing your question to include that information.  At the moment, your question is very abstract, and reads a bit like an XY-problem.


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How is minimum infectious dose defined?
I'm a bit confused by the concept of a minimum infectious dose (MID). It seems from what my research so far has turned up, that while any dose greater than 0 could potentially cause an infection, for most pathogens the likelihood of this occurring is low enough to be dismissed.
What I'm now trying to figure out is, what metric is used to define the MID? Is it the amount of the pathogen which is expected to cause an infection in 50% of those exposed (similar to an LD50?) Is there some other value used instead?
Secondly, is there a specified relationship between the received dose, as a multiple of the MID, and the likelihood of infection (for example if the MID caused an infection in 50% of people, then perhaps 2 MIDs would cause infection in 75% and 3 MIDs would cause infection in 87.5%).
Note, I am not asking about how the MID is empirically measured, but rather about the conceptual underpinnings of the concept itself. Also, any links you can provide to additional resources would be most appreciated. Google is useless these days now that the search results are flooded with nothing but SARS-CoV-2 specific articles.

Minimum infective dose is the minimum number of infectious particles that causes infection/illness in 50% of those given that dose.
Practically this is only really measurable in a controlled laboratory setting, but one can estimate it for real world circumstances as well.
It isn't easy to know how exactly the probability will vary around the MID - there are too many factors related both to the individual and the pathogen to make simplistic assumptions (like assuming each individual infectious particle has an independent probability of leading to infection). It is typical that higher initial exposure (particularly for foodborne illness, but seems to be an issue with SARS-CoV-2 and other respiratory viruses as well) leads to more severe illness, however.


text:
What species mimics two others?
Richard Dawkins in 'the selfish gene':

But there are species of mimic that do something very strange. Some individuals of the species mimic one nasty species; other individuals mimic another. ... One butterfly may mimic species A while his brother mimics species B.

What is an example of such a species, along with the two species its members mimic?

How about Mimic Octopus? they mimic sea snake, lionfish, and others.
https://en.wikipedia.org/wiki/Mimic_octopus

Thanks Polypipe wrangler.  Dawkins seems to have something else in mind:  One allele in the gene pool that makes the butterfly look one way, another allele (for the same gene or gene complex) that makes the butterfly look another way.  Not a shape-shifter!  I'd like to know a specific butterfly species like that.


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Crossover Value and Genetic Mapping
In my textbook and most of the sources I have checked, it is stated that recombination frequency in eukaryotes give us knowledge on the location of the loci. I don't understand the direct correlation between the distance between the genes we are investigating and the recombination frequency. Assume that the recombinant gamete frequency of is around 35%, why does it mean that those genes would be located on the opposite ends of the chromosome? Do all crossover events take place with a single break on one chromosome? I have searched the crossing over mechanism for a bit and have seen diagrams in which two breaks occured and the DNA chunk acquired seemed to be transplanted, although it was in general a tad too complex for my understanding. If you have a link to a clearer and more concise explanation of the mechanism, it would be much appreciated! Please forgive my ignorance if that's a very basic question, I'm just a high school student.

Welcome to Biology.SE! For this question, you should be able to find answers quite easily from reliable sources and as such this question seems to fit this sites criteria for "homework". I encourage you to start with the basics — see my next comment for suggestions. That will allow you to ask more focused questions and make you have the background to understand the type of answers you are likely to get here. ——— Please also take the [tour] and then go through the help pages starting with [Ask] questions effectively on this site. Thanks!

I have found that when learning about a new area starting with a relatively accessible and reliable source like Khan Academy is very helpful. Wikipedia is also generally a good starting point and you can then check their references. Online platforms called MOOCs offer free (or very low cost) courses on a wide variety of subjects — two I am familiar with are Coursera and edX. Finally, textbooks with a good level of detail are also freely available online e.g. from NCBI.

As a silly example:
Let's say that you are traveling along a road where you know there are bandits and thieves. You want to finish your journey quickly, and spend very little time on the road, because the more time you spend on the road, the more likely it is that you are robbed and they take your money away. If there are more thieves around one day, you still want to spend as little time on the road as possible, it's just that the risk is higher.
Using this logic, you can then try to figure out how far away two cities are on the road by how likely you are to be robbed by thieves while traveling between them.
Just substitute "chromosome" for "road", "crossover" for "robbed by thieves". You measure how far away two loci are by how likely there is to be a crossover between them.
It may help to think of it in a different way. There is nothing preventing multiple crossovers, but having more crossovers saturates with increasing distance. Here is one plot of how you can think of linkage (I just generated this, it's not mathematically accurate, only for demonstrating simple point):

Figure 1.
Basically, the closer two loci are, the less likely it is that there will be a crossover between them. So if you compare three loci, two of which (A, B) are close when the third (C) is far away, you will see few AxB crossovers/recombinants but many AxC and AxB crossovers/recombinants. This is because the probability of crossovers is fairly uniform across the genome. The more distance, the more opportunities for crossover.
Another confusing feature is that the maximum number of recombinants (usually) is 50%, because at that point the two loci are assorting independently, e.g. completely unlinked and behave as if they are on different chromosomes. However, two loci can be "unlinked" and still be on the same chromosome, they are just quite far apart then.
This is not really changed by multiple crossovers. The same principle of "loci further away" --> "weaker linkage between loci" is the same no matter how many crossovers occur in a chromosome. More crossovers just means that the map is "expanded", because everything is more weakly linked than with fewer crossovers per chromosome.
Update:
It may help to be very specific about what we mean by "same chromosome" vs. "different chromosomes". Recombination happens between two molecules that can be considered the "same chromosome" even if they are different molecules. We call them "homologous chromosomes" because they pair and recombine. On the other hand, when we talk about 23 chromosomes in human cells, those are "different chromosomes", but they are actually 23 pairs of homologous chromosomes, so there are in total 46 chromosome molecules, which can be arranged in 23 homologous pairs. For each pair, we get one from each parent ("paternal" and maternal").
Recombination only occurs between homologous chromosomes.
So when recombination happens, the locus doesn't transfer to a different chromosome. It stays on the "same" chromosome, it's just a different version of the same chromosome. See this image (Figure 2):

Figure 2.
You can think of a chromosome as a collection of loci in some linear order. This will arrangement will be the same (or close enough, for our purposes) for each chromosome of a homologous pair. It may have different versions of the locus on each chromosome of the pair. We call these different versions "alleles", which in Figure 2 are labeled "A" and "a" for locus A or "B"/"b" for locus B. So we start with types AB and ab, but if recombination happens then we would observe types Ab and aB. The loci didn't move between chromosomes, they just exchanged alleles.
In terms of how loci "split", think of them as two chains of the same length. When recombination happens you cut one link of each chain, exchange pieces, and rejoin the chains. See Figure 3:

Figure 3. single recombinant: a single recombination event occurred between maternal and paternal chromosomes at coordinate x = 1.0 to yield a recombinant. Double recombinant: two recombination events occur, at x = 0.8 and x = 1.0

Thank you a lot for the detailed answer sir, the analogy did help a lot! What I can't fully grasp is how a crossover incident between two loci guarantees that they would end up in different chromosomes. For example, for A, B and C genes located in that order on a chromosome, if a crossover happens on the gene B, does it automatically mean that A and C would be split?

@TarıkAkçin if there is only a break at B, then yes A and C would always be on different chromosomes. However, it's entirely possible that there could be more breaks between  A and B or B and C and whether A and C ended up on the same chromosome would depend on whether the total number of breaks between A and C was odd or even.. The probability of additional breaks depends on the distance between A, B, and C. In human chromosomes there is always at least one crossover, and typically between 2 and 4.

@TarıkAkçin see update to answer.

@TarıkAkçin and to directly answer your comment question, the answer is "yes" as long as the number of breaks is odd, and "no" if it's even. I am hunting for a good image that shows this.

@TarıkAkçin I gave up and made it myself. see figure 3.

There are two main question: (a) dependence of the frequency of recombination with the distance that separates genes and (b) do all crossover events take place with a single break on one chromosome?
Let's give some context. In gametogenesis, chromosome crossover takes place in every tetrad in prophase I. Tetrads are constituted by a pair of homologous chromosomes which are paired by a particular complex (synaptonemal complex). Such complex allows one chromosome to be very close to the other. This intimacy permits chromosome crossover to occur between non-sister chromatids and sister chromatids. This interchange is random and can potentially take place in any place of the chromatids and it begins with the breakage of the two chromatids in a common site, so there are two breaks per event (question b). It must be said that there are generally multiple chromosome crossover events per tetrad.
Even though chromosome crossovers can potentially take place at any site, the probability of such events occurring is proportional to the distance that separates two genes, which implies that genes that are separated by a great distance (one in the p-arm and the other in the q-arm, for example) are more likely to be split apart than any pair of genes which are closer to each other. The classical explanation is that there are physical impediments to the formation of chiasmata when genes are close to each other, such that the chromosome crossovers between neighboring genes is unfavorable, while the formation of chiasmata when the genes are far away lacks such physical impediments, and is therefore more favorable (question a).

    https://i.stack.imgur.com/2LbJT.png. A non-sister chromatid with three distinct genes (A, B and C). In addition, 1,2,3 and 4 are other genes.
A more intuitive way of understanding such dependence is by considering that chromosome crossover is random. Let's consider a non-sister chromatid, like the one in the figure above, whose genes A and C are far from each other. In order for recombination to take place between A and C, there would have a break in the space between the two genes. Because this distance is big, such break could take place in 1, 2, 3 or 4 (and many more), in the other hand, if we consider a recombination between the genes A and B, the only possible way to achieve this is by a break in 1. Because crossover is random, since there are a lot more possible sites of breakage between distant genes, it is more likely that one of these many places is selected as the site of crossover. Crudely speaking, it is analogous to the throw of a dice. The probability of getting a 2, 3, 4, 5 or 6 on a single throw is much bigger that the probability of getting a 1, simply because there are more possible outcomes in consideration.
Regarding the mechanism, it all depends in the depth you want to cover, nevertheless, I would advise to read the section of chromosome crossover in Introduction to genetic analysis by Griffith


text:
Does dormant poison ivy contain urushiol in the above-ground portion of the plant?
I recently had a run-in with poison ivy (late spring; Canadian shield).
The poison ivy plants had not yet leafed-out so I failed to identify them as a hazard.

I think I must have either trampled and broken the stems of the plants, or dug up and broke the roots (or both), and therefore was exposed to the poisonous sap.
While the plants had not leafed-out, they were also not truly dormant (it wasn't the middle of winter).

Question:
I'm wondering if there is a time of year when the above-ground portion of poison ivy plants would not contain urushiol.
In other words, in the dead of winter, when the plants are dormant, do poison ivy twigs contain the poisonous sap?

Let's tackle your second question first. Yes, leafless poison ivy still contains Urushiol, and still can give you a rash. Here are three sources supporting this statement: a first-aid sales company, a newspaper, and a non-peer reviewed infosheet from a university. Be careful with poison ivy all year.
Your first question has slightly more nuanced implications. To know if there is a time of year where above-ground poison ivy doesn't contain Urushiol, first we have to think about when and where the urushiol is produced in the plant cell, where it is stored, and how it degrades. Some studies have shown that Urushiol and like compounds are present throughout the plant. In this older article, they extract it from both the leaves and the twigs, but more current advances have been able to focus on urushiol in just the stem. I have seen no evidence that it reduces at any time of year, and very little publication on how it is produced biochemically, although people are working and have worked on the topic. I am interested to learn more about this aspect from other answers to this question.
(An aside: you can also pick up a Urushiol rash from some cheap furniture, so this compound can stay poisonous on a wood surface for quite a while. Unfortunately, I'm speaking from first-hand experience, which is backed up by this informative article about Urushiol!)

Thank you. That clears things up. And the Japanese furniture thing is quite interesting/horrifying!


text:
Alzheimer's disease - Hyperexcitability
I am trying to read literature on Alzheimer's disease.
A very important phenomenon that occurs in AD patients, is hyperexcitability in neurons close to A-beta concentrations.
Some authors only describe the phenomenon of hyperexcitability in excitatory cells as an indirect phenomenon, which results due to the suppressed function of inhibitory cells.
Some other authors only describe it as the direct result of excessive concentration of Glutamate in a synaptic cleft which, due to the dysfunction of Astroglia, remains there and causes hyperexcitability and excitotoxicity.
I haven't found yet a paper where both are mentioned as distinct ones. At least I haven't found any that I could comprehend, given that my background is not biomedical.
I would like to know if these two cases I mentioned before, are indeed distinct ones, or if they are the same, and I cannot see it due to lack of knowledge.

The answer would require expertise in that specific field. I would suggest you to get in touch with some of the authors whose papers you mentioned, you read.

We can help, do you have the refs handy? otherwise i will look it from scratch.

@PolypipeWrangler thanks a lot! The references are the following:
as an indirect phenomenon: link
as a direct phenomenon: link

I  might be a week, is this still useful?

of course! many thanks for the willingness to help


text:
What animal classes has also "Like Humans" XY Chromosomes for Males and XX for Females?
Are other mammals. birds, reptiles, or even insects same to humans in that the male organisms have XY Chromoson at the end and female XX?
Thanks for the ansver

https://en.m.wikipedia.org/wiki/XY_sex-determination_system

specifically from that Wikipedia link: " humans, most other mammals, some insects (Drosophila), some snakes, some fish (guppies), and some plants (Ginkgo) tree"

Does this answer your question? Do males of all sexual species have Y chromosomes?

In mammals, Y chromosome determines the sex. SRY gene present on Y chromosome is responsible for sex determination. And, in absence of this gene results in female sex. Non-human mammals use several genes on the Y chromosome.
Platypus and Drosophila also uses XY sex determination system, but in different way. Like in platypus, combination of genes present on XY chromosome are used to determine sex characteristics. And in drosophila, two X chromosome gives female characteristics, and Y chromosome determines maleness.
Reference:
https://en.wikipedia.org/wiki/XY_sex-determination_system


text:
Can amount of gene share in descendants be easily calculated?
I saw on the web an explanation on how to calculate amount of certain genes in a person.
For instance: if your grandfather was French and your granny was an American then your father is 50 French and 50% American. Then he met an american woman and their child going to be 50/2=25% French and 50% American. And so on... dividing each time by two.
Is it truth?

Just so we know: how far down the rabbit hole do you want to go? That calculation is... approximately true, on average, but there are plenty of exceptions and a lot of terminology needed to make it all clear.

@downvoter can't say why somebody would downvote it.

@bashsane not too deep.

Every parent passes half their DNA onto their kids. There is a not infinite, but very high, amount of DNA. This means for the first generation it is precisely true: if Mom has 100% red genes and Dad has 100% green genes, child will have 50% green and 50% red genes. For the second generation, for people with mixed genes, it becomes true only on average. So if child has 50% green and 50% red genes, by passing on half its genes it could theoretically pass on all red genes, or all green genes. It very likely won't pass on  exactly half of each. But because there are a lot of genes, the law of averages does that in practice you can say they pass on half of each, meaning if the other parent has all green genes the resulting child will be 75% green genes, 25% red. This indeed goes on through the generations for awhile until you run into the finiteness of DNA; at some point the amounts will be small enough that they no longer follow the laws of averages, and it become much more variable whether a child gets the full complement of their parent's red genes, or none, or some intermediate amount.
This is further complicated when we aren't talking about abstract "red" or "green" genes, but "American" or "French" genes. What the heck are "American" or "French" genes anyway? The human gene pool is fairly well-mixed, with most genes being widely shared. Those that can be used to identify specific ethnic or even national origins are low enough in number that what I said earlier about the law of averages no longer applying happens earlier if you look at specific subcategories of genes. Still, it works for several generations I believe.

What the heck are "American" or "French" genes anyway? The human gene pool is fairly well-mixed, with most genes being widely shared. Those that can be used to identify specific ethnic or even national origins are low enough But there was a company in the US, you could sent it a sample of your slime and see results on the web-page, that you have 30% of German genes, 20% African...

@RS that's right, but those depend on small numbers of genes that are characteristic of certain groups - meaning people in that group tend to have them and people outside of them don't. Those groups don't map perfectly to nationality, and how well they map depends on said nationality - I've never heard of them assigning people to "American" for example, and I doubt most French people would get "100% French" either.


text:
In what ways does the number of legs affect an animal's functioning?
After much research, I've only been able to find specific examples of leg-number's impact on locomotion and dexterity (and/or object manipulation). I feel as though there must be other ways it has a role in an animal's anatomy and function.
Examples I imagined but couldn't evidence include;

Respiration rate (relating to S.A. for tracheoles in Arthropods).
Similar to no. 1 but not quite the same - the structure of the circulatory system.
Insects'/tetrapods' stabilty (especially regarding an ant's capacity for load-bearing).
The brain's capacity for higher order thought processes (does conscious control of more limbs limit this?).
Efficiency of thermoregulation (also related to differences in S.A.).

I would most appreciate an explanation for how a given animal's number of legs gives it an aptitude for a type of locomotion (such as sprinting, climbing or burrowing). I would also like simple yes/no answers to the ideas listed above - as to whether they are implicated in the number of legs.


text:
How do you biologists draw a protein when you write a paper?
The following is one example of protein structure diagram that I want to put in my research paper. I took this from

Koniev, O. & Wagner, A. “Developments and recent advancements in the field of endogenous amino acid selective bond forming reactions for bioconjugation.” Chem. Soc. Rev. 44, 5495–5551 Jan. 2015, DOI: 10.1039/C5CS00048C

As a Chemist, the only drawing tool I have used so far is ChemDraw and it does not provide such protein structure; The only protein diagram it provides is a Y-shaped IgG. How do you biologists draw such convoluted proteins when writing a paper? Do you use a specialized software for this?

They're not drawn they are produced by software from crystal structure data. Look up PyMOL.

Does this answer your question? Molecular graphics, if not, try this Mac-specific one or this one. Also look at the PDB link in my answer to this one.

As mentioned in the comments, diagrams like these are generated by software. The one I use is Chimera, it is free. The structure of the protein is recorded as a list of atoms and their 3D coordinates, as well as bonds, helices, sheets, etc. When a structure file is loaded, the software generates a 3D model based on the data. The user can rotate the model, move it, zoom in, change the color, an many other options, then export a 2D image when they are satisfied. If you want to use structure data files other researchers have generated, the Protein Data Bank is probably the best resource. Research articles that involve new structural data will list the PDB numbers of their structures near the end. In the article you link, the authors include pdb accession numbers for the structures they used for their figures. For the image you use as an example, here is the caption:

Fig. 56 PEGylation of four solvent-accessible Tyr residues of chymotrypsinogen (pdb: 1EX3) reported by Francis et al.

There are various software programs available to design a protein structure based on your requirement.
These programs can be used to:

Design atomic model based on the amino acid sequence of particular protein.
Predicting protein's 3-Dimensional structure.
Determining secondary and tertiary structure of protein based on it's protein folding properties and statistical tendencies of conformational features.
For checking whether protein contains transmembrane domain or signal peptide.

I have used Rosetta to design specific antibody for my protein.
Reference:
https://en.wikipedia.org/wiki/List_of_protein_structure_prediction_software


text:
Frequency modulation of parasympathicus and sympathicus
According to my literature, the sympathetic nervous system accelerates heart rate and modulates < 0.1 Hz, whereas the parasympathetic nervous system decelerates heart rate and is modulated 0.04 - 0.5 Hz.
According to this, heart rate accelerates in sympathetic which means the frequency should be higher than that compared to Parasympathetic. Though Parasympathetic starts with 0.04 it goes up to a value higher than 0.1Hz. Why so?
Here is the source (Physiological Sensing of Emotion by Jennifer Healey in the Oxford Handbook of Affective Computing):

Since it is known that the parasympathetic nervous system is able to
  modulate heart rate effectively at all frequencies between 0.04 and
  0.5 Hz, whereas the sympathetic system modulates heart rate with significant gain only below 0.1Hz (Akselrod, Gordon, Ubel, Shannon, &
  Cohen, 1981; Berntson, et al., 1997), the relative strengths of the
  sympathetic and parasympathetic influence on HRV can be discriminated
  in the spectral domain.

Can you cite and quote from your source? Your logic doesn't make much sense but it would be helpful to see what is actually said to help you understand it.

@BryanKrause I have added the source


text:
What is multiplet nuclei capture rate?
I met this terminology in a publication.https://core.ac.uk/download/pdf/226940818.pdf.
It's in the last sentence of the second paragraph in the text.
I tried to search for it but didn't get a conclusive definition.
Is it an important parameter whiling processing snRNA-seq data?

It is multiple nuclei capture rate. They talk about it in the supplementary section near the bottom of the article. They diluted the processed sample to get an estimated 2000 nuclei per microlitre. They then want the machinery to process individual nuclei, but cant tell from the results if two or more nuclei are processed simultaneously (which would give a mixed signal). That's why they estimate the multiple nuclei rate using a separate experiment with nuclei from a mix of mouse and human cells.


text:
Can the innate immune system defeat a pathogen by itself? Fast enough that we don't develop antibodies, etc.?
Would we have any way of knowing if our innate immune system destroyed a pathogen without involving the adaptive?
Could a symptomless person who tests positive for COVID-19 with the RNA test, e.g., later test 'negative' for exposure on the antibody test?

Generally antibodies are formed, but it is possible that innate immune system has cleared out the pathogen. But antibodies will be formed even after that, as adaptive immune system has received  the stimulating signals from helper T cells, which are matured during the innate immune responses triggered by an infection.
This signal triggers B cells to produce antibodies. Antibody production is activated because of signals from innate immune system.
So, even if infection is cleared by innate immune system, still antibodies will be synthesized.
Reference:
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3399021/
https://medicalxpress.com/news/2020-05-dont-antibodies-immunity.html

If the innate system is very fast at clearing the pathogen out, the memory B cells, responsible for antibodies production won't be numerous enough to provide with a good immunity.
Reference:
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4159104/


text:
Why exactly would a big, tropical, dangerous spider not thrive if imported to a "cold" climate location such as Sweden?
Whenever I have put forward the idea that somebody could capture a bunch of disgusting, huge spiders from Australia, fly them to Sweden and just let them out in the woods nearby houses, and they will naturally replicate in huge numbers in no time and take over the place...
... then I get a reply such as: "They would not survive for long because they are out of their natural habitat."
What does that mean exactly? Would they not be the "spider kings" of this new place where all other spiders are smaller and weaker? Would not the imported spiders, as disgusting as it is to think about, rule and spread? Not die out at all?
Why exactly would such monsters not be "fit" for Sweden? If the problem is that it snows here but not in Australia, then what makes it unable to dig itself into the ground like the other spiders (I assume) do? And hibernate?
I don't understand why they would die out and not thrive, but I certainly hope that they would quickly die because even the native spiders here are gigantic and disgusting IMO, and I would simply not be able to live in Australia with its monster spiders... nor would I ever go on vacation there, for this reason alone.

Downvoted primarily because spiders are not "disgusting",

welcome to the biology SE! Please try to maintain neutral language in your questions and avoid opnion-based "facts" (like saying spiders are "monsters").

I believe this page from Khan academy explains pretty decently why temperature is important to living organisms:
https://www.khanacademy.org/science/biology/principles-of-physiology/metabolism-and-thermoregulation/a/endotherms-ectotherms
It comes down to biochemistry. Temperature affects the molecules that make up our bodies and do everything in it. At very low temperatures water freezes and that messes up everything in the body for obvious reasons (molecules can't travel around and react with each other in solid ice the way they can in liquid water; ice takes up more space than water so the process of water freezing will break cell structures...). At very high temperature complex proteins will tend to lose their shape which is vital to their function, meaning they become useless. And beyond those two "hard" limits, living bodies use chemical reactions to run (essentially you could argue a living body is a very large set of varied chemical reactions), those chemical reactions are usually helped around by complex molecules called enzymes, and enzymes often have certain temperature ranges they work best in. This further narrows the range of temperatures various organisms can tolerate or thrive in.
So I believe this addresses one aspect of your question - why tropical spiders might not do well in a cold climate. The enzymes in their bodies are just optimized for a higher temperature than that. Moreover, temperatures in Sweden fall below freezing and cold-resistant species tend to evolve specific adaptations for that that aren't just behavioral but also chemical. The abstract of this paper discusses different such strategies in insects (I assume spiders would be similar), which involves either chemical adaptations to avoid bodily fluids freezing, or adaptations to survive them freezing:
https://journals.physiology.org/doi/abs/10.1152/physrev.1985.65.4.799
So native Swedish spiders probably have adaptations of this kind that tropical spiders don't, and they're not adaptations that can arise in a single individual or even a few generations.
You bring up another question however, which is why can't tropical spiders adopt behavioral adaptations, like digging in the ground or hibernating? Well, for one thing "hibernating" is as much a physiological adaptation as a behavioral one. You don't just improvise the body slowing down that way by lying down for a nap. But more to the point, it isn't clear you can just improvise novel behaviors either, especially if you're a spider. Many behaviors like "burrowing to avoid the cold" are hard-wired evolved responses that organisms that haven't evolved them are going to do spontaneously. I don't know if the burrowing behavior you describe in spiders specifically is of that type. This paper makes the point that while spiders (like other arthropods) are traditionally thought of as having completely hard-wired behavior, more recent thinking shows they do display more flexible behavior as well:
https://www.sciencedirect.com/science/article/pii/B9780124159198000033
Still, arthropods do show more such instinctive, hard-wired behavior than, say, mammals do. So while it's not impossible that some such spiders would happen to burrow in a way that avoids the cold (that's another point - they'd have to burrow at the right time, in the right places, in the right way... things that might not be obvious), and if they didn't have huge physiological barriers to surviving the cold even while buried, and enough survived this way to reproduce and multiply and weren't outcompeted by native spiders who weren't freezing their cuticles off this whole time... Then I suppose they could spread, but that's a lot of "ifs" and I think a tiny minority of introductions of tropical species would satisfy them, if any.


text:
Should I consider [H+] as substrate in MCT transport equation?
I'm trying to model the transport of lactate in cells (in both direction via Monocarboxylate transporters):
[Lactate]intra + [H+] <----> [Lactate]extra + [H+]
I found some data on kinetics of Lactate itself (Km and Vmax) but I don't find anything on [H+].
My initial thought was to consider [H+] as a substrate, and model the transport as a sequential ordered Bi-Bi reversible reaction (from this paper: Poole & Halestrap (1993). Transport of lactate and other monocarboxylates across mammalian plasma membranes. doi:10.1152/ajpcell.1993.264.4.c761)
But it require a lot of parameters (Ki, Km, Vmax) for each substrate involved (especially H+).
So my question is: Should I consider [H+] as a substrate or just as an external parameter that impact the direction of the flux ?
Thanks everyone
(first question on Stackexchange)

To include or exclude the H+ basically depends on the scope of your model. The H+ can be used as external parameters if you assume that both sides of the membrane are well buffered and the pH will not change. If you want to simulate a condition during which the pH changes, like for example strong exercise in muscle or ischemia, then you would need separate H+ for each side of the membrane.

Thank you for your answer. Yes the pH will change at each side of the membrane (I simulate cancer cells with high glycolytic activity). But if I consider H+ as a substrate like lactate, should it follow a michaelis-menten kinetic (or derivatives) ? If so do you have any idea of where I can find this information about H+ ? I didn't find any paper measuring such parameters for H+.

I think this article can give you some kinetic data on proton symporters with different pH. There is a lot published on the subject but it is difficult to find the best search term... perhaps this paper or this paper may also give some usefull parameters.

Thank you ! I already downloaded the second article but didn't saw Km values for H+, a second read is usefull :) The cell's paper seems really promising, I'm going to read this right away.


text:
Cell image database for citotoxicity test
Is there any cell image database for citotoxicity tests? I know that there are several image databases available (like this, this and this one), but none of them have the images for citotoxicity tests.
Thanks in advance,


text:
Why does hypocalcaemia cause increased muscle contraction?
Calcium is needed for  muscle contraction, so how does hypocalcaemia cause increased sustained contraction?

Consider the pathophysiology of tetany, which is the involuntary contraction of muscles caused by hypocalcemia.
From the tetany wikipedia page:

Low ionized calcium levels in the extracellular fluid increase the permeability of neuronal membranes to sodium ion, causing a progressive depolarization, which increases the possibility of action potentials. This occurs because calcium ions interact with the exterior surface of sodium channels in the plasma membrane of nerve cells and hypocalcemia effectively increases resting potential (rendering the cells more excitable) since less positive charge is present extracellularly. When calcium ions are absent the voltage level required to open voltage gated sodium channels is significantly altered (less excitation is required).

So, when Ca2+ levels are low, action potentials are spontaneously generated, leading to muscle contraction.