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Why people carrying the same SNP doesn't have the same Promethease report
I'm a frequent user of Promethease to run health analysis based on MyHeritage SNP data dump.
I ran two people through Promethease and both have the same SNP:
rs4307059 (T;T)
In one report we see an Elevated Autism risk and in the other report we don't even see this SNP mentioned.
Does anyone ran into this same problem?

counterbalancing snips that reduce autism risk/lower some polygenic score?

Are the two VCF files from the same testing company and did they use the same version of the test?

Welcome to Biology.SE. Please take the [tour] and then go through the [help] pages starting with [Ask] questions effectively on this site. In particular, this question seems like would be a better fit for [Bioinformatics.SE], but please do not crosspost, instead request migration. This site is intended for questions about biological process or mechanisms, but your question seems to be entirely about a software product and is thus off-topic for this site.

can you migrate it please?

I can't migrate as I am not a moderator — you can request migration of this question by flagging your post for moderator intervention and explaining what you want and why. ——— Also, if you want to notify a poster who isn't the original poster you need to @ them (e.g. @ppaulojr).


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Abilities used to survive against natural enemies: directional selection or frequency-dependent selection?
Regarding abilities used to survive predators and parasites, are they subjected more to directional selection or frequency-dependent selection?
It's usually that host-parasite coevolution is represented to be characterized by frequency-dependent selection, such that rare traits in hosts select for traits in parasites subject. That would make the phenomenon of female choice for "good genes" males surprising because one might instead expect healthy males to be more likely to yield sickly offspring or grandoffspring. Is this a simplification and are there some aspects of host immunity subject to directional selection? If so, which?
Same with anti-predator defense traits:  only frequency-dependent selection or some substantial percentage subjected to directional selection?
Thank you for your time.

Both. These are sometimes called "arms race" or "trench warfare" (directional) and "Red Queen" (freq-dependent).

Would you be able to offer more, such as what sorts of characteristics are selected on directional vs freq-dependent?

source: Stack Exchange

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

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What is the thickness of the mucous, submucosal, muscular and serous membranes of the stomach wall of a piglet aged 60-75 days? (Large White pig)
There is publicly available data on the thickness of the layers of the stomach wall of piglets aged no more than 20 days. But at an early age, the thickness of the layers of the stomach wall increases extremely non-linearly and there is no way to predict how the layers will change by 60 days. Maybe there are specialists among the community who participated in the experimental determination of the thickness of the layers or those who have met studies on similar topics?
I will be glad of any constructive answers on the merits of the question. Thank you in advance for your response.
For those who are interested, I attach drawings with the dynamics of the thickness of the layers in the cardiac (a) and pyloric (b) parts of the stomach of piglets.

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


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What type of bacteria can I use to break down motor oil for a high school biology experiment? Any suggestions where I can find this bacteria?
I am experimenting to determine the optimum conditions for microbes to break down motor oil. The conditions I am going to test are different pH levels to resemble freshwater pH and saltwater pH. I will be using the chemical NaCl to adjust the salinity of the solution.
I have researched and found companies that provide oil-eating microbe powder. However, there is no information on what type or strain the microbe is in the power.
I'm failing to find information on what type of microbe would be best for this experiment and additionally where these types of microbes are supplied.

hit number one on google https://response.restoration.noaa.gov/about/media/who-thinks-crude-oil-delicious-these-ocean-microbes-do.html after searching for:bacteria that breaks down oil ,you can do a search for the different bacteria mentioned in the article

If you have the time, run an extra replication using dirt from a place where oil has been spilt for many years.


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how to perform ligand and DNA alignment in pymol
I need help in inserting ligand to specific base pair in DNA. I have a drug molecule and want to insert in between the base pairs I am interested in (it is dsDNA). Please note that it is a customed sequence dsDNA so it does not have any intercalation site for the ligand to bind itself. I tried to follow the tutorials but cannot find something where I can insert ligand into the custom DNA sequence I have generated.
I will appreciate if you can please help me or guide me where I can study and understand how to do it.

Welcome to Biology.SE. Is there some reason you are asking this here rather than in [Bioinformatics.SE]? If you agree that site seems more appropriate please either delete from this site and repost there or request migration. Please do not crosspost as that is considered to be impolite.

Could you clarify? Am I right in thinking that you are trying to answer the hypothetical question: “If ligand L were to insert itself between two specific base pairs in my custom dsDNA structure, what molecular interactions would it make?” If so, have you any reason to  think an application to display molecular structures can do this? I would except to have to use some high-powered energy minimizing program to compute possible structures first. Are you sure Pymol has such a facility?


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Are antibodies labelled with fluorescence that have not attached to an antigen visible under light microsocopes?
I came across this thought while studying histology, what happens to fluorescence labelled antibodies that do not bind with an antigen, can we see them? or are antibodies activated upon antigen binding which in turn activates the Fc region to which the fluorescence molecule is attached.

By far the most common IHC protocol, in my experience, is using a primary antibody which binds to your target of interest, followed by a secondary antibody (which carries the fluorescent tag or labeling enzyme) to bind the primary antibody.
An example protocol from one manufacturer is found here:
https://www.rndsystems.com/resources/protocols/protocol-preparation-and-fluorescent-ihc-staining-paraffin-embedded-tissue
Summarizing:

Apply primary antibodies diluted in Incubation Buffer according to manufacturer’s instructions...

Wash slides 3 times for 15 minutes each in wash buffer.

Incubate with the NorthernLights™ secondary antibody diluted in Incubation Buffer according to the manufacturer’s instructions...

Wash slides 3 times for 15 minutes each in wash buffer.

The "wash" steps are intended to remove from the tissue any primary antibodies that are not bound and later any secondary antibodies that are not bound.
You may still get some residual background fluorescence either due to non-specific binding of the secondary antibody, or unbound primary antibody that isn't washed out (I believe in typical use the non-specific binding of the secondary antibody is going to be the most relevant contributor to background, but I don't know a good citation for that), but you use "blocking" steps to attempt to reduce non-specific binding, and the assumption is that anything remaining contributes to a fairly even background stain.
You can further use negative controls that omit the primary antibody to estimate non-specific binding of the secondary antibody and check for any unexpected partitioning that may contribute to an artifactual signal.

Oh wow! Beautiful! Thanks a bunch!


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How would it be possible to engineer cows to have more offspring?
Cows usually only give birth to one calf per year and only several in their lifetime. What would we have to genetically alter so they can have more offspring, more frequently. I read that their is a record for most births from one cow at once: 16. How could we possibly genetically engineer a cow to make this them give birth more frequently?

High potential of being unanswerable due the large number of physiological aspects likely to be involved and our lack of understanding of them.

With a couple of notable exceptions, the vast majority of agricultural "genetic engineering" is by selective breeding; the answer would typically be "continually mate cattle from lineages with high fecundity together". Little knowledge of biology beyond that is necessary.
However, you could also look for particular alleles involved in increased fecundity; here's a paper talking about one example:
Kamalludin, M. H., Garcia-Guerra, A., Wiltbank, M. C., & Kirkpatrick, B. W. (2018). Trio, a novel high fecundity allele: I. Transcriptome analysis of granulosa cells from carriers and noncarriers of a major gene for bovine ovulation rate. Biology of Reproduction, 98(3), 323-334.
If you wanted to raise a herd that had a high rate of this gene, again, you could use selective breeding alongside genotyping to propagate that particular allele.
It's a bit more complicated than just making lots of bovines, though; if you're doing this for agriculture, it's going to be quite important that the offspring have healthy development so they can be used for milk or meat. I'm not an expert in the field so I may be mistaken, but it doesn't seem like fecundity is a crucial limiting factor for cattle.


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Where to find morphometric data for fish?
I need data regarding the aspect ratio for caudal fins of different Elasmobranchii. It should be some easily retrievable information but apparently fishbase doesn't have this type of data for many species.
Do you know any other database maybe that is specific for morphometric measurements?

update: the answer below describes a database for freshwater ray-finned fish (Actineropygii), which does not cover the taxa you want (elasmobranchs are a subclass of the cartilaginous fishes, Chondrichthyes, which is a separate taxon). I'm going to leave the answer up anyway in hopes that it's useful/interesting to someone.
(Searching for elasmobranch morphometric database finds a description of the MEDLEM database (Mediterranean elasmobranchs, Mancusi et al 2020) which (1) doesn't seem to be publicly available and (2) probably has only overall length measurements, not the details you need ...)
Brosse et al. 2021 report on a global fish morphology database. I think you can almost but not quite get aspect ratios of caudal fins from this database. Specifically, they state that they have taken all of the measurements listed in figure 1a:

I'm not sure exactly how you define aspect ratio of the caudal fin, but I'm assuming that it would be something like (tail length/tail depth), or based on the measurements here, ((max body length - body length)/caudal fin depth) = (MBl - Bl)/CFd. However, the authors don't make the raw morphometric measurements available, only derived values that are listed in their figure 1b, which include MBl (in centimeters), "body elongation" = Bl/Bd, and "caudal peduncle throttling" (CFd/CPd).
If you had the raw morphometric values you would almost have what you needed (I'm a little surprised they're not included in the database along with the derived measures), but you'd have one more big problem. To get caudal fin length you would need max body length measured in pixels rather than cm (MBl is taken from Fishbase; the rest of the measurements are taken in pixels, since they're derived from analysis of images with unknown scales). If the authors measured max body length in pixels when they did their image analysis, you could derive what you need from that ...
One could contact the database maintainer / contact (their e-mail is in the README file from the database, which you can get from the link below) and ask for help.

Data availability statement

FISHMORPH is publicly available through figshare (https://doi.org/10.6084/m9.figshare.14891412). We kindly ask users to cite the
present paper in any published material produced using these data.
Users are free to use the FISHMORPH data and to contact the au-
thors for details or collaborations. We also encourage any potential
data contributor to contact S.B. with potential datasets to expand
the database

Brosse, Sébastien, Nicolas Charpin, Guohuan Su, Aurèle Toussaint, Guido A. Herrera-R, Pablo A. Tedesco, and Sébastien Villéger. “FISHMORPH: A Global Database on Morphological Traits of Freshwater Fishes.” Global Ecology and Biogeography 30, no. 12 (2021): 2330–36. https://doi.org/10.1111/geb.13395.
Mancusi, Cecilia, Romano Baino, Caterina Fortuna, Luis Gil De Sola, Gabriel Morey, Mohamed Nejmeddine Bradai, Argyrios Kallianotis, et al. “MEDLEM Database, a Data Collection on Large Elasmobranchs in the Mediterranean and Black Seas.” Mediterranean Marine Science, April 28, 2020. https://doi.org/10.12681/mms.21148.

Thanks for the answer, it's very detailed. Aspect ratio is the ratio between the maximum width of the fin to the power of 2 ($Cfd^2$ in this case) and the actual surface area of the fin. From data you described I don't think it's possible to obtain this metric. Thanks though, its definitely useful in other cases.


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What is the importance of radiation hybrid (RH) mapping in terms of genes?
I'm currently reading about radiation hybrid mapping with a TSP (traveling salesman problem) application in order to find an ordering of the genetic markers (i'm a mathematics student) and was wondering about the usefulness of the procedure. If the end result determines the proximity of certain genetic markers then we can draw inferences about genes which are in close proximity to each other and genes which are separated with a larger distance. I'm wondering for certain set of genes if they are closely related distance wise then are the properties for the genes often related to each other? I believe there are also genes which are dependent upon having other genes in close proximity in order to function properly if I am not mistaken. Is this true?
I'm also curious as to what we may say if we have for instance two genes which are separated by large distance? May this be related to the fact that the farther away two genes are the more they act like they are unlinked?
Any help is appreciated.

One might say that this question is too basic for this list, and I feel that it must have been asked before in some form, but I can’t locate an example. So here is a short answer.
First, it should be mentioned that Radiation Hybrid Mapping is an old technique which, judging by the brevity of the entry in Wikipedia, is little used today. The main reason for this is the availability of the genomic sequencing. It may make a good example for algorithms, but that’s probably about it.
However, the basic question is still valid, “Does human gene proximity suggest interaction, and lack of proximity not?”
At one time it was thought that this might be so because of the clustering of bacterial genes e.g. involved in a single metabolic pathway in operons. However, this is generally not the case in higher eukaryotes like humans. A good example is the locations of the genes for the two subunits of adult human haemoglobin which associate in the tetrameric protein α2β2. The gene for the α subunit is located on chromosome 11, whereas that for the β subunit is located on chromosome 16. Another example is the genes for the approx. 80 proteins that assemble into the protein-synthesizing organelle, the ribosome. This 1998 paper (which, incidentally, used radiation hybrids) concluded:

Though functionally related and coordinately expressed, the 75 mapped
genes are widely dispersed: Both sex chromosomes and at least 20 of
the 22 autosomes carry one or more rp genes.

So, although there may be counter-examples, no general conclusions about human genes can be drawn from mapping alone.

Thank you very much for your answer. I was wondering in relation to genomic sequencing  which also seems very much to be a quickly evolving field what are the most popular used techniques today? I assume cost and efficacy very much play a role here.

@PianoMath — That's another question. Depends what question you are asking in your research.


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Animal models to study depression
Is there a non-invasive animal model to study the pathogenesis (i.e., the development of) depression?

Welcome to Bio.SE! What attempts to answer this question have you already taken? We ask that all question posters here attempt to search for an answer to their own question and explicitly indicate what research they've already done, what they learned, and what is still confusing or unknown to them. Our goal is not to simply be an answer site, but rather a site that promotes self-learning with some expert help along the way :). Please take a moment to edit your post with this additional detail, and it will likely be received more positively by our community. Thanks!

You might be interested  in Scientists investigating the DNA outside our genes - the ‘dark genome’ - have discovered recently evolved regions that code for proteins associated with schizophrenia and bipolar disorder. (from the University of Cambridge web site)

TL:DR: A simple question doesn't usually have a simple answer in science.
To a great extent, the answer to your question depends on what, exactly, you mean by non-invasive. Please know that it is exceedingly difficult to study the pathogenesis of depression by non-invasive methods.
If by non-invasive, you mean the animal is not killed and the brain examined, then yes, there is a great deal of literature studying depression without sacrificing the animal. Blood tests can examine the presence of specific hormones, etc. and imaging studies can see brain changes associated with depression to localize which areas are affected, etc.
But if you consider blood tests to be invasive (which, technically, they are), that narrows it down greatly.
In studying animals and depression, the researcher must treat the animal in a way which is highly likely to result in depression, or the study will be fruitless. If you define treating the animal with means that would be considered unethical in humans (or outright cruelty) as invasive, that puts most serious research into the illness outside of the scope of reliability. In designing a study, the researcher must ask themselves, "What events might make an animal become depressed?" It can be as minimally cruel as prolonged social isolation, or can be stepped up to discomfort  (e.g. a repeated shock) when performing pleasant tasks (e.g. eating something tasty), or repeated restraint of an animal significant enough to cause distress, or stepped up to discomfort when performing life-necessitating tasks (getting to food), etc.
If you accept certain stress-inducing events as non-invasive, the researcher can certainly wait until the animal dies of natural causes to do a post-mortem exam, but that becomes problematic in that the more time passes from the event, the more questionable the findings are as related to the event.
If you allow a non-life threatening but technically invasive procedure as acceptable, e.g. a fecal transplant from depressed humans to gut-microbiota-depleted rats to see if depressed behavior occurs due to the gut microbiome, it is still invasive, depending on the definition.
Depression is defined by a number of parameters. Most animal studies will not meet all the criteria to begin with, but a non-invasive one will most likely be severely deficient in meeting any of the criteria for pathogenesis of depression.
PET scans are non-invasive and can be/are used to study depression, but the pathogenesis may remain unclear. For example, a dog's beloved caretaker dies, and the dog exhibits clear signs of depression (lack of appetite, energy, anhedonia, etc.) A PET scan will correlate with that seen in humans who suffer deep losses. But, short of waiting for a lot of people beloved by their pets to die and seizing their dogs to do PET scans, it doesn't give us much information that we don't already have in humans or can intuit.
The link below is a fairly recent (2021) overview of animal models for studying depression and their limitations (including animal-sized imaging machines). Still, the animal must be stressed into depression, which can be considered invasive/inhumane.
All this to say that a simple question doesn't usually have a simple answer in science.
Benefits of animal models to understand the pathophysiology of depressive disorders


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Distinguishing between yeast and bacteria
Can hematoxylin stain be used to tell apart yeast and bacteria cells
Are there any other method to tell apart yeast and bacterial cells?
I know hematoxylin stains histone protein but I am not sure how does it affects the bacterial cell so not sure if it will be full proof method to tell them apart( and it’s given that the cell I have is yeast cell or a bacterial cell)
Other method to tell them apart  I thought of is through microscope I think there will a size difference in yeast cell and bacteria cell but are there any other morphological features which can be used to tell them apart
So my first thought was to use a stain which only stains nucleus through which I came came across H&E staining but was not sure what affect it has on bacteria and I also saw other alternatives for hematoxylin but not sure about their affect their affect on bacteria for that I am thinking of setting up control (as stated in comments) will this be sufficient there may be other variables need to be taken into account?
And for antibiotics I was thinking was using a mixture of them but then I came across an answer in research gate saying chloramphenicol is used
So my main question is are the above stated method sufficient to distinguish between bacteria and yeast or are there any other efficient ways to distinguish them?
And the hematoxylin one too

Welcome to the site. What research have you done on your own to answer this question? The Biology.SE community has agreed that questions that show little or no prior research effort are off-topic on this site unless you have shown your attempt at an answer. Please [edit] your question and tell us where you've looked for answers, what you do know about the topic, and where exactly you still have questions. Unresearched questions may be subject to down-voting and closure. Please see our homework policy for more information.

Now is it fine?

Better, but it still needs work. What actual research have you done - web searches, literature searches through Google Scholar or your university's library, looking through microbiology textbooks? Have you simply searched for how to tell the difference between bacteria and yeast in the lab? What did you find when you did that? What do you still have questions about? Keep in mind that there are (roughly) two major kinds of bacteria - Gram positive and negative - and they have different types of cell walls. Also, remember that different bacteria range in size from tiny to gigantic.

So I am thinking I might not need to know how hematoxylin affects bacteria as I will stain the given sample in hematoxylin. And take a yeast cell and a bacteria cell  and stain them and compare these cell with the sample(which might be bacterial or yeast). And on comparison I make sure which cell is given in sample. This way there’s no need to know hematoxylin affect on bacteria

And also using antibiotics I have heard that chloramphenicol usually kill multiple bacteria but there might be some chances of survival is using a mixture of antibiotics recommended or chloramphenicol will be sufficient on its own

You should indicate whether you mean any possible yeast and bacteria, or specific ones of interest. Why are you trying to do this?

You should also include details of the research that you have done with references - in the body of the question. Comments are not permanent and should not be used as a substitute for editing the question with the relevant details.

I have made changes now is it fine


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Do homologous chromosomes have same rates of gene expression in a cell?
I was googling around and found only articles related to XY differences in expression. Can you please clarify if homologous genes/chromosomes have about the same levels of expression in a cell or one of them "stays silent" and another is "switched on" somehow?

It's a complicated subject. Try searching for "genetic imprinting" and also for "epigenetics" and for "gene regulation in cis and trans".

thanks for a feedback! Everything is a complicated subject, I'm a software engineer by the way ;)


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What characteristics identify modified 'plant parts' as the respective 'plant parts'?
I was learning about different modifications in plant parts such as modified leaves, stems and roots from my Biology textbook.
Modified parts differ as they are modified for different functions.
For example, the pitfall traps in a pitcher plant are called modified leaves. These have completely different function than normal leaves but are still referred to be leaves.

What characteristics identify such parts to be those parts?

Not an answer but helpful background/vocabulary: https://en.wikipedia.org/wiki/Homology_(biology)


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What is this small white insect on my plants?
Environment
I have a large amount of plants in an old industrial loft apartment.
I live in Rochester, New York.
I ship plants in from across the US, often exotic ones.
Observations
A few months ago, I noticed that two of my Sarracenia plants in my carnivorous plant bog were not growing anymore. Upon cutting them out as to not disrupt the live sphagnum moss grow medium, I noted that one of the insects in question had burrowed its way down into the core of the plant. I assume this to be the cause of the growing issue.
Today I noticed that one of my grape plants and Colocasia plants were covered in these bugs at different stages of growth. They range from white specs to ~3mm with the tail thing.
These insects appear sedentary. I have never seen one move, except when I cut the one out of the center of the plant.
Here is a picture of the bug, which was difficult to get due to the size.

Research
I looked through a variety of different "common insect" sites as well as some insect identification sites but I was unable to find anything remotely similar.
I have only elementary knowledge of insects. Any pointers in the right direction would be appreciated.

Mealybug; don't know much about them.


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Can arsenic contaminating calcium carbide enter banana skin during artificial ripening?
Calcium carbide which is used for ripening banana contains arsenic, is it possible for that arsenic to enter banana skin?

Welcome to SE Biology. Please finish reading the [Tour] and ask only one question at a time.  Your second question about the way calcium carbide ripens fruit is quite different from how it enters banana skins. Please edit your question to remove it and pose it as a separate question. That way it will be indexed as such.

Welcome. Can you add your findings so far? Apparently you did some research, linking the relevant web pages would help, as your findings so far on the permeability of banana skin to arsenic


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

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

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

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

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

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

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

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

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

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

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


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Feather identification

One of my sister's chickens was killed a few days ago.  This feather was left at the scene of the crime.  The location was Idaho, near Boise.
The death of the chicken leads us to believe it is a hawk or falcon but the vertical brown line has us all scratching our heads.  The current belief is it's from a juvenile, but we can't pick out the type.
Does anyone recognize it?

please add a bit more information like the size of the feather and what time of day/night was the chicken killed and what injuries did it have any information can help identify the bird.

Certainly.  The feather is 5 inches long.  The chicken was killed in the afternoon, the sun was still above the horizon.  While I didn't see the carcass, I was told it looked like it had been pecked over and over.  Likewise, she owns a very large, very grumpy rooster who was missing some feathers and had his comb ripped, meaning it had to be big enough to take on a large, angry rooster who was trying to defend.

perhaps try the feather atlas https://www.fws.gov/lab/featheratlas/idtool.php, or reddit/birdwatching reddit birds of prey it's too specialized for here

It's impossible to say definitively from a picture, but the feather looks very much like that of a Barn Owl (Tyto Alba). This also fits with the geographic location of Idaho.
Take a closer look at the trailing edge of the feather, it appears to have the soft "fluffy" edge typical of most owl feathers.
Here's an example that shows the similarity:
https://www.barnowltrust.org.uk/barn-owl-facts/signs-barn-owl-occupation/signs_feathers-male-female/


text:
Gametes produced after single and double cross overs
A female genotype, shown as abc / +++ produces 100 meiotic
tetrads. Among these, 68 showed no cross over (NCO) events; 20 showed
single crossover (SCO1) between a and b; 10 showed single crossover
between b and c (SCO2) and 2 showed a double crossover (DCO) between a
and b and between b and c. Of the 400 gametes produced, how many will be
of the following types? Fill your answers in the table. (Source)

According to me, the answers should be,
A. $68\times4=272$
B. $20\times4=80$
C. $10\times4=40$
D. $2\times4=8$
However, the answers are $336, 40, 20, 4$ respectively. What am I getting wrong?

You are not taking into account that crossovers happen at the four-chromatid stage and between cromatids. Take a look at the following picture1:

I suggest you draw down all the crossover events:

Now count the number of gametes that will be formed:
$$
\begin{align}
\text{(+++) and (abc)} &= 4\times 68+2\times20 + 2\times10 + 2\times 2=\mathbf{336} \\
\text{(+bc) and (a++)} &= 2\times20 = \mathbf{40} \\
\text{(ab+) and (++c)} &= 2\times10 = \mathbf{20} \\
\text{(a+c) and (+b+)} &= 2\times 2 = \mathbf{4} \\
\end{align}
$$

Introduction to Genetic Analysis 11th Edition, W. H. Freeman and Company, 2015.


text:
How do viral envelopes contain molecules coded for by viral genes when they are derived from the host cell's plasma membrane?
I have been studying viruses from " Biology: A Global Approach " by Campbell, Urry, et al. Regarding viral envelopes in animal viruses, the textbook writes, " ..the viral envelope is usually derived from the host cell's plasma membrane, although all or most of the molecules of this membrane are specified by viral genes."
I understand that the capsid proteins and glycoproteins on the surface of the viral envelope and coded for by viral genes, but the envelope formation happens in a process similar to exocytosis, where the new viral capsids are wrapped in the membrane as they bud from the cell. How can the viral envelope contain molecules coded by the viral genes (apart from the surface glycoproteins)?

I think by "all or most of the molecules" they are excluding lipid molecules. Is that what you are concerned about? Or are you asking how virus-encoded proteins can embed themselves in the plasma membrane?

@timeskull It wasn't clear to me which molecules the textbook was referring to me as viral-gene-encoded. I did consider the possibility that they were simply excluding the lipid molecules, and was seeking some solid clarification regarding the same. I guess that means that the viral encoded particles are the glycoproteins that embed themselves in the membrane?

I don't have access to the book, so I can't be sure how they meant that statement, but most likely "all or most of the molecules" in the lipid membrane excludes the lipid molecules themselves. One of the defining characteristics of viruses is that they don't do their own metabolism. Even if they did, viral genes could only specify the enzymes for lipid synthesis, and these wouldn't be included in the membrane.
However, viruses often DO manipulate the host cell's lipid metabolism. From this review of Lipid Interactions During Virus Entry and Infection:

Large enveloped viruses are not the only viruses that manipulate cellular lipid metabolism. Microarray analysis of HCV infected cells show significant changes in the expression of genes involved in lipid metabolism (Woodhouse et al., 2010). Recent transcriptomic and proteomic analyses indicate that the expression of host genes involved in lipid biosynthesis, degradation, and transport is profoundly altered by HCV; in particular cholesterol biosynthesis genes were found to be upregulated (Woodhouse et al., 2010). Parallel lipidomics analysis also showed changes in selected lipid species, particularly phospholipids and sphingomyelin (Diamond et al., 2010). This suggests that HCV reprogramming of host lipid metabolism attempts to maintain host homeostasis in spite of the elevated demand of metabolic precursors by the virus.

So, membranes in the cell are composed of different types of lipids, and they aren't equally good for making virus membranes. Some viruses have been shown to upregulate production of the lipids they need, so in that sense those lipids are products of virus genes. That's a bit of a stretch, though, imo.
For proteins in the viral membrane, they aren't necessarily all glycoproteins, though it looks like most are. M1 and M2 membrane proteins in influenza aren't glycosylated, for example.
Here's an image from another review showing virus budding through the plasma membrane:

One kind of virus budding. Viral glycoproteins, inserted into the cellular membrane at the endoplasmic reticulum and processed through the Golgi to the plasma membrane (see Figure 3), associate with the assembled viral nucleocapsid. The direct association pictured here is characteristic of togaviruses. For other viruses, possessing helical nucleocapsids, the association is mediated by a peripheral membrane protein. Cellular membrane proteins are excluded from the envelope of the mature virion. This may occur during assembly, as pictures, or by prior formation of a viral membrane patch (or raft), before the nucleocapsid arrives at the membrane.

In this image, you can see the host membrane proteins (the white ovals) being excluded from the patch where the viral proteins (black shapes) accumulate and which later envelops the nucleocapsid. This process is likely what your textbook is referring to.


text:
Actin-myosin cortex stiffness VS elasticity
I have two questions on the mechanics of actin-myosin network:
1- Actomyosin cortex as an elastic material is defined by its elastic modulus $E$. But I know that elasticity would be described by the stiffness of the material!
How do $E$ differ from cortex stiffness $k$ then?
2- What is the difference between passive and active mechanics? In this article, Box 1 page 3 (538), https://www.cell.com/trends/cell-biology/fulltext/S0962-8924(12)00111-0#:~:text=The%20cortex%20is%20a%20thin,role%20in%20cell%20shape%20control., they wrote in the second column "Actin networks differ from passive semiflexible polymers" but they already at the beginning said that "actin filaments are semiflexible polymers". This makes confusion for me in understanding the difference between passive and active properties in cell mechanics.


text:
Sodium-potassium pump (Na+/K+) time limit, endless without action potential?
As written in Wikipedia:

The sodium–potassium pump mechanism moves 3 sodium ions out and moves
2 potassium ions in, thus, in total, removing one positive charge
carrier from the intracellular space.

I know that thus the cell (neuron) is excitable, and due to an action potential, the ion concentrations will change since their flux is opposite as what the pump does.
But what happens if there is no action potential, and the pump tries to work forever until no sodium ions are in the cell anymore?
Presumably, this won't happen in reality but in theory then the pump could not keep the cell polarized?
Or are there other effects like leak currents that contribute, and why exactly that issue won't happen?

This won't happen, so if you want to ask about a hypothetical you're going to have to be very very precise.

Even if there is no leak or other currents there will be an equilibrium condition in which the ATP hydrolysis by the pump could drive no more ions due to the electric potential. Actually there are condition in which the pump can work in reverse, synthesizing ATP in the process.


text:
Price Equation in Evolution
I am trying to solve for $\text{cov}(w_i,z_i)+E(w_i\Delta z_i)$ as it apears in Price Equations in terms of the mean $\overline{w}$ and variance $\sigma_{w}^2$ of the fitness of a population where I am given the relation $\Delta z_i=-cz_i$. I don't understand how we can solve this because I do not know how I have any knowledge of the values of the $w_i$s given what I know about the $z_i$s. Any hints would be appreciated.
The Price Equation is defined as:
$\Delta z = \frac{1}{w} cov(w_{i}, z_{i}) + \frac{1}{w} E(w_{i}\Delta z_{i})$

It would help to know if you are working from data ("what I know about the $z_{i}$s", "values of the $w_{i}$s") or just as a theoretical exercise. If you have data, getting an example would be helpful. Usually my understanding is that the Price equation is applied when we have knowledge of trait values and of fitness. It does not sound like you are doing theoretical work but it's hard to say based on the question.

The question was intended to be theoretical. The problem I was given was to first find the expectation in terms of the mean and variance of the fitness, and then to compute the right hand side of the Price equation (which I presumed also meant to compute $\text{cov}(w_i,z_i)$. This was all the information I was given, and I am not sure if I misunderstood some element of the Price equation or if there was not enough information given.

Seems like it might be better to ask for clarification from the person giving you the assignment (and edit this into your question, if it's helpful). Of course, if you do come up with an answer on your own it's perfectly acceptable to self-answer your own question.

I'm not an expert here so I won't answer in much depth (and for homeworks we want to see some evidence of work usually, see here for more info https://biology.stackexchange.com/tour), but I would suggest the standard algebraic tricks. E.g. look into the definition of covariance, consider a case where covariance approaches zero,  consider a case where covariance is complete.


text:
How do I explain "effective number of types" to a lay audience?
I know how to calculate effective number of types. I can't figure out how to explain it to an audience that has no ecology training or background. Suppose one has 12 (for example) groups, each with a different population. Okay, so we calculate the effective number of types for that region and it's 5.7. How do I get across the concept that "out of twelve total types, with these population counts, that's the same as 5.7 types in that region"? The concept does sort of make the mind boggle a bit.

I appreciate this is a complex concept, but it would be useful if you gave a reference or two to this. I am not an ecologist and had never heard of this, but have some experience at explaining things. I checked out the top hit on a Google search, but that was clearly too complex for me. However if you suppled links to the accounts that you think are best, someone other than those in the field might be able to help.

For a lay audience, I don't think you need to explain too much of the math, just the general concept, and an example will work best.
Let's think about trees. You have 5 types of trees in a forest. If there's 200 of each, that's about as diverse as 5 types can get: we can say there are 5 species of tree in that forest. No controversy.
If, however, there's a different forest with 900 maples, 97 birch, one oak, one locust, and one willow, well, that doesn't seem nearly as diverse, does it? Sure, there are 5 tree types, but it's almost all maples with a few birch, so if you stood in that forest it might feel like there's only effectively one or two types of trees. You want to give that forest a "diversity number" that's smaller than the forest with 200 of each tree, but that somehow accounts for there still being more than just one tree type there: some number between 1 and 5.
There are of course different ways you could weight those rare versus predominant tree types (this would be q in the equation), and there's no single answer that's right for every case, but if you pick a number for how to do that (say, choose q=1), then you can get just one number that lets you say "this place has more diversity than that one" not by just counting the number of species, but also considering their proportions. It will equal the number of species if you have an even distribution, but be less than that if some are rare.
I'd give a couple concrete examples on a slide if you were presenting this to an audience (or possibly a table in a written work) with different proportions to demonstrate how it works out in practice.

(+1) I think your example with the tree species would be quite effective, and more persuasive to a general audience than considering formally-defined statistical estimates.


text:
Why does a respiring mitochondrion have less cristae?
I read the following-

Number of cristae is more in resting-state of mitochondrion, but
decreases with activity, hence less in the respiring state.

cited: GK Pal, Textbook of Medical Physiology

After looking up a few sites, I was still unable to find out why resting mitochondrion have more cristae. Why is it so?
Based on this paper, the cristae undergo morphological changes in response to metabolic state and/or matrix volume (cristae remodelling), but I don't think that explains why it does so.


text:
Why do eubacterial DNA Ligases use NAD whereas eukaryotic and archaeal DNA Ligases use ATP?
DNA ligases in eukaryotes are ATP-dependent (as is the enzyme from bacteriophage T4) but in Escherichia coli the DNA ligase is NAD+-dependent. I cannot understand the reason for this.
An extensive literature search just left me with more confusion. (I read NAD+ dependent DNA ligase have BRCT domains and was wondering if it is in any way related to this)

This difference is certainly intriguing, but, like many other general ‘why?’ questions, can be approached on different levels.

Because they evolved differently.

is one answer, and not a trivial one because of the shared cofactors of archaea and eukaryotes. But I imagine that the poster would respond by asking why they evolved differently — whether there is some functional or structural difference that can explain this. There isn’t, and the question is avoided in the papers I have looked at, so the answer would seem to be

Nobody knows. If there is a reason it is not evident from the function the reactions perform (which is the same) or the structure of the enzymes (which is similar at the active site).

Let us look at the thermodynamics of the reactions. In both cases a phosphodiester bond is being formed, a reaction with a high +ve ΔG. In ATP-dependent DNA ligases an overall –ve ΔG is achieved by the hydrolysis of ATP to AMP and pyrophosphate; whereas in the NAD-dependent DNA ligases it is supplied by the more unusual, but equally energetic, hydrolysis of NAD+ to NMN+:

The overall structures of the two types of DNA ligase are different:

But the catalytic site for the ligation reaction is remarkably similar in both cases:

(Both diagrams from Structure 1999, 7:35–42)
So explanations in terms of mechanism of reaction would seem to be ruled out.
Coda
There are several analogous problems in biochemistry, e.g. why GTP is generated in the tricarboxylic acid cycle in most (but not all) organisms, and why NADP is the cofactor for a particular oxido-reduction reaction in bacteria, whereas NAD is used in eukaryotes. In general one feels (or at least I do) that the explanation must be something to do with compartmentation of cofactors or coupling reactions to their availability. Perhaps a particular choice was advantageous to bacteria early in evolution, but this was no longer the case in eukaryotes, and in fact the reverse became true. But without any evidence to support such arguments they are merely hand waving, which is why professional scientists generally tend to avoid them in their research publications.

This makes sense why authors have avoided the reason behind this. And I feel, with the answer you have provided (which i feel is explained much much better than what i could find in different literature sources) i need to make peace with the fact that some things have just happened due to reasons inexplicable. I hope if there's a concrete reason behind the utilisation of different cofactors we do find it soon.


text:
Bug on wall identification request
I've been finding a few of these on the same wall of my apartment the path month. Size is maybe 3-5 mm.
I live in an apartment in Toronto Canada.
Thanks in advance!

Without clearer photos it is pretty hard to say, however, I think it is likely to be one of the Dermestidae family of beetles.
These include a bunch of common pests in the household, including "carpet beetles" (Anthrenus sp.), and the larder beetle (Dermestes lardarius).
I think this is most likely to be a carpet beetle, given the light/dark mottled pattern on the shell.


text:
Thymus & T-Cell Generation and Maturity
I am a beginner in immune system. I am trying to understand the connection between T-Cell and Thymus as person ages.
It is clear from Guyton & Hall that till teenage the T-cell from bone marrow comes to Thymus which further gets filtered so that T-Cell does not attack self antigen (normal antigen of body). In this process of filtering out T-cells about 90% of the T-cells produced in bone marrow is destroyed in Thymus.
And then its said that, after teenage Thymus gets partially inactive OR it can be removed. Now what I am unable to understand is if Thymus gets removed/inactivated, in say a 45 year old person, who is going to filter the T-cells produced in bone marrow; by filtering I mean kill off the T-cells which can attack self-antigen of body.
If anyone can throw some light, it would be great.


text:
Selective herbicides
There are several herbicides available that claim to kill lawn weeds but not the lawn grass. This seems amazing, to me. How does this work? How can a chemical be lethal to a broad range of plants, but not to grass? What’s the difference between weeds and grass?

I suggest you investigate C3 vs C4

Thanks. I see that wheat and rice are C3 plants. I’d guess that lawn grasses are similar to these?? But I also see that 95% of plants are C3, which suggests that most weeds are C3, too. Are you suggesting that lawn grasses are C4?

Those two articles are good but don't suggest any reason for selective action

From the second paper: “the underlying molecular mechanism of how auxinic herbicides selectively kill dicots and spare monocots is not understood yet”. So if dicots = weeds, and monocots = lawn grass, then I’m asking a question that didn’t have an answer in 2013.

Hmmm. To a lay-person like me, glyphosate seems like a good example of a herbicide that is NOT selective: as far as I can tell, it seems to kill everything. It certainly kills grass.


text:
When and how did the Embecovirus acquire hemagglutinin esterase?
The Embecovirus is different from the rest of Betacoronavirus by possessing an additional protein, a hemagglutinin esterase (HE).
There are known similarities between the HE's of different viruses (Coronavirus, Torovirus, and Influenza C), see e.g. this paper by de Groot (2006).
My questions are: How old is this acquisition?
Where does the hemagglutinin esterase come from?

This is not simply an answer site, but instead a site that promotes self-learning with some expert help. ——— Where have you looked for answers? Either there are papers reporting on investigation of the evolution of this virus and its acquisition of HE or there aren't; it would improve your question if you reported what you have found (with citations) and why you can't answer at least some of these questions yourself. In fact, if you look at the abstract of the first reference for the wikipedia article you linked to you will find at least one answer.

Did you look at embecovirus NS2a as well "putative cyclic phosphodiesterase" it is interesting because (at the same location just after ORF1b) there is a 40% similar ORF in Lucheng rat alphacov NC_032730

@reuns No, not beyond just noticing its existence in the embecovirus. And I noticed that the placement of HE in the Torovirus genome is different from the one in Embecovirus genome.


text:
Which single substance among Potassium and Phosphate has the greatest osmotic activity in the Intracellular fluid?
My physiology textbook mentions that potassium has the greatest concentration ( 155 mEq/L ) in the Intracellular fluid and that I thought would make it the most osmotically active but the answer given is phosphate and I can't understand how this is the case. Is it because a compound of phosphorus would contribute more osmoles than potassium?

I don't have an answer, though I have a suspicion it may have something to do with the charge of their ionic forms. Potassium ions have +1 charge. Phosphate ions (the most common form of phosphorus in cells) have a -3 charge.

Can you provide a short quote from your actual textbook?

@BryanKrause actually this is a review question given at the end of the chapter. In the chapter they have given the respective concentrations of potassium, phosphate and other ions only and explained about osmosis and other transport mechanisms in a cell.

@acvill I've thought of a solution but I am not sure.Osmosis is defined as the movement of water from the region of its higher concentration to lower concentration through a semipermeable membrane which is impermeable to the solute. Although potassium is more concentrated in ICF(155 mEq/L) it can pass through the membrane whereas phosphate which is less concentrated (90 mEq/L) cannot pass the membrane and hence is more osmotically active. Can this be the reason ?

I'm guessing if you go to the textbook section that the question pertains to you'll find what specifically the author is wanting you to take away.

@Bryan In the chapter there is actually no reference to anything called osmotic activity which is the reason I cannot understand on what factors osmotic activity might depend on.I think this a inference based question in which we ourselves have to find the cause based on the facts given within the chapter.Can you please check out the comment I made earlier and if that might be the possible explanation of the question.


text:
How does genetic feedback shape the evolution of whole ecosystems?
While looking into the organization of ecosystems and how evolution shapes it, I've been reading "Ecology" (1975) by Eugene Odum. In chapter 6, p. 167, Odum speaks about the mutualistic relationship between bullhorn acacia and acacia ant, and writes:

As one species evolves to take a selective advantage of the
association, the other species comes under selective pressure to
strengthen the interdependence. We can see how a genetic feedback
process of this sort could shape the evolution of a whole ecosystem.

I don't understand the first sentence. So, the acacia increases its fitness through the association with the ant, and the ant would come "under selective pressure to strengthen the interdependence" with the acacia? What is Odum trying to say here?

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, your title question is much too broad and doesn't reflect the body. It would also strengthen your question if you referenced more current material (or at least sources available online) that you had used to try to work this out yourself.

Thank you for your welcome. I read what you recommended and I edited my question, making the title and the question more specific, with the detailed question about Odum's own answer being better integrated with the question. I also explained why I read this old source.

Can you add the page number for your quote of Odum?

Sure, it's page 167. I see you also suggested an edit of my question. Thanks, however the phrasing is too specific and doesn't match my real interest. That being said I would welcome someone simply explaining the Odum quote. Odum does reply to the question I'm asking, so explaining his reply is a way of replying to my question. (Reposted for more concision and clarity.)

I have approved the edit (with minor adjustments). I think that the edit at the least clarifies an answerable question. It is not obvious what else beyond this was of interest (except perhaps that you are looking for more general principles of the phenomenon). I encourage you to a) further edit or b) ask a new question building on the specifics in this one if you are not satisfied with the edit.

@MaximilianPress I don't see how my original question was unanswerable. It is in fact the question Odum is answering in this quote. Had you written an answer to explain why you think it was unanswerable, that might have been helpful. On the other hand I can see how asking both a general question and a specific one about a quote may have seen undesirable. As it stands the question is a bit strange but it's at least restricted to the quote; let's see if someone will be able to explain it.

Not that it was unanswerable. Simply that the answerable part of it has been clarified and made much more obvious by the edit. (I upvoted the question, contingent on the edit!)

I don't claim that this is a fully fleshed out answer, but it's too long for a comment.
I suggest taking a look at some of the classic models for the evolution of cooperation. One example would be Axelrod and Hamilton (1981) in Science, who formulate a series of theoretical conditions under which cooperation 1) arises, 2) is a robust strategy, and 3) stabilizes. The paper was then treated at book length by Axelrod.
Briefly, they argue that cooperative strategies are more successful when the frequency of cooperating partners is higher (and obviously, when the benefit of cooperation is higher).
In a very simple example, cooperation in the Prisoner's Dilemma becomes a better strategy as the game is iterated, and you learn whether your partner is trustworthy or not.
Extended to the evolution of associations like ant-acacia, if one species (say acacia) "takes selective advantage of the association", then necessarily the frequency of acacia individuals willing and able to cooperate will increase. This could be either because there are more acacias or because more of a stable population of acacias will cooperate with ants.
Therefore, the benefits of cooperation will increase for ants, because the frequency of cooperating acacias is higher. This would then be the "selective pressure" for cooperation that Odum writes about.
Increased fitness of cooperators relative to non-cooperators is "selective pressure" to cooperate, meaning more cooperation in the long term under assumptions of a stable environment.
The paper itself is light on equations, using instead mostly simulations. Others have gone so far as to build more modern simulation packages implementing a variety of strategies, in case that is helpful.

I read the article you suggested (Axelrod 1981). They do show how, within their game-theoretic model, constant defection is evolutionarily stable relative to any kind of cooperation, and therefore cooperation can only prosper in an environment with some cooperators -- which I guess is what you are alluding to. Still I'm not convinced that you are explaining the quote satisfactorily. I think Odum is making (in 1975) a general statement about how mutualistic relationships arise from coevolution and end up shaping whole ecosystems. But I don't understand his sentence. It may be a phrasing issue.

@MartinP. I guess I have a very different reading of that paper. I see the paper as making a series of arguments about why cooperation evolves even in the presence of incentives for defection (title: "The Evolution of Cooperation"). To me, all that Odum seems to be saying is that cooperation is a comparatively better bet when there are lots of cooperators, relative to when there are few cooperators. In other words, it only makes sense to have a credit card when the stores you shop at mostly accept credit cards.

I was not making a summary of the paper, but of the part that seemed to justify your reference to it in your answer. My impression is that the paper's model has very specific assumptions and is not much help for ants and acacias. One such assumption is that all individuals can cooperate with each other. Acacias can't cooperate with each other.

In your bank and credit card example, how are the credit cards holders pressured "to strengthen the interdependence", as Odum writes? I'm thinking more of an employee-company analogy. The employee is happy with their job, so they go the extra mile to make sure the company is happy with them and keeps them. That is "strengthening the interdependence". See my own answer.

@MartinP. Imagine that I sell tacos out of a truck in 1970. 0% of my customers want to use a credit card to buy tacos, I have no reason to accept cards. However in 2022, probably 80-90% of my customers will want to use a card. Likewise, over those years those customers went through a change where more and more businesses accepted cards (and now some don't accept cash). Both agents adapted to each others' behavior to strengthen the interdependent behavior (where behavior == "credit card transactions"), driven by increasing frequency of cooperating behavior.

My guess is that Odum is trying, and possibly failing, to provide a general reasoning about how stable mutualistic relationships might naturally evolve and shape ecosystems. Consider ants and acacias.
At first, a particular mutually beneficial exchange happens by happy coincidence between some ants and some acacias: the ants find shelter in the acacia's thorns, and their natural reaction to intruders serves as a defence for the acacia. The acacias figure out through evolution that if they can thus count on the ants then they can stop the costly production of the bitter alkaloids that acacias usually have for their defense, which gives them an edge relative to other acacias that bear that cost. To make sure the ants do keep coming and the happy coincidence becomes a way of life, they also evolve to produce (less costly) Beltian bodies on which ants can feed.
The ants are glad to have have found a provider of free food and shelter (free, because it was a happy coincidence at first and by hypothesis the ant hasn't yet evolved to specially adapt to it). However, now that they have found such a worthwhile partner, they don't want to lose it and therefore evolve to "strengthen the interdependence" (as Odum writes). Perhaps they become even better defenders of the acacia by making their pheromones even more repellent to the acacias' ennemies. And that is how what was a happy coincidence becomes a stable mutualistic relationship.
I'm not sure this second part makes sense as it is (we'd probably need a more precise explanation of why the ant needs to do anything more), but it may be the logic Odum was suggesting in 1975.
It may be that, contrary to what Odum suggests (and to what I assumed as well), there is in fact no generally accepted evolutionary mechanism that explains mutualism, only particular stories for particular cases. Someone in fact writes, in an article that I should probably read, "Simple, general principles governing the evolution of mutualism have proved elusive" (The evolution of mutualism, 2012).


text:
I am conducting an experiment with oil eating bacteria. However, I am struggling to find a method to check how much oil they cleaned?
I am experimenting to determine the optimum conditions for microbes to break down motor oil. The conditions I am going to test are different pH levels to resemble freshwater pH and saltwater pH. I will be using the chemical NaCl to adjust the salinity of the solution.
I have researched and found that one method is using a standard plate count. To just count the bacteria after incubating them for a few hours with the oil and pH concentration. The greater the number of bacteria, the more oil was degraded.
But my professor wants me to measure exactly how much oil is degraded by the bacteria to make a distinction from how much oil was at the beginning to how much is left at the end of the experiment.

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, it appears that you are looking for methods to quantitate how much oil is present in a solution? If so, that isn't really a biology question. In addition, it is generally true on SE sites that you are expected to show evidence of prior research. For both of these reasons your question is may be closed or downvoted.

You could measure and test just one component of the oil. Perhaps make sure that the oil is the only energy source for the bacteria. Measuring oil degradation or actual consumption?

Centrifuge out the oil and weigh it?

is the oil a purified hydrocarbon, or a commercial motor oil which can consist of up to 30% additives including various detergents, surfactants, friction modifiers, corrosion inhibitors, etc. In either case, a hexane wash (or two) of the spent media (after harvesting cells) would likely removed most of the residual oil, but it's hard to say how much of the additive package might be left behind. Make sure to use an appropriately sized separation funnel. Probably also want to work with an analytical chemist to quantify residual hydrocarbons compared to the inputs.


text:
How to choose which animals to study when designing evolutionary neuroscience research project
I am currently writing a reseach project for a scientific initiation and my idea would be a literature review identifying all empirical physiological and anatomical evidence for the presence and characteristics of a specific neural circuit in different animals, and possibly come up with insights about the development of said neural circuit during evolutionary history. My problem would be: which criteria should I use for choosing the animals to research? My focus would be to find the highest ammount of evidence possible for the presence or absence and development of this neural network across the evolutionary tree, so I was thinking about choosing animals that could represent certain taxons and also ones that have been extensively studied before; I wish to include both vertebrates and invertebrates such as mollusks to investigate the possibility of convergent evolution. My main problem is that I am a medicine student and although having some prior experience in neuroscience research, I have no formal experience in evolutionary biology. So I accept book recommendations as well as scientific papers on the topic that would help me. I also accept feedback on my idea, what do you guys think, is it too broad of a topic, too ambitious? I would have a year to complete the research and try to publish it as a paper, and the advisor I wish will help me is specialized in comparative animal neurobiology. But first I need to write a good project.
Thanks in advance.

What "specific neural circuit" do you have in mind?

I would suggest starting with a relatively simple neural system that is very well characterized; the obvious suggestion would be C. elegans. It's not clear to me why you would need invert/vert both, you will probably see significant relatively interpretable variation (including convergence) even in related worms. One might consult e.g. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6748829/. How workable all of this is depends heavily on your answer to Bryan's question.


text:
What are the definition of pecking order?
Pecking order is the phenomenon that dominating individual usually eat first. It is commonly observed in animals. In animals, it is often due to the fact that the strong individual won the fights for eating first, or is able to win those fights in future.
This is what I used to learn: "a pecking order is about access to resources decided before the access as the result of a competition, not just straight competition". For example, the order of food-feeding in bird is sometimes decided by brightness of feathers, without any direct competition (fight) for the food.
However, many other sources equate pecking order with dominance hierarchy, or the metabolic evolutionary pressure, namingly some individuals have an evolutionary advantage over others, making them more fit to survive .
For example, bacteria can has dominance hierarchy (a.k.a pecking order). Supporting literature include this.
See also history of "pecking order", pecking order of plants, and another article on dominance hierarchy.
I am not sure if my understanding is correct and if this viewpoint is universally accepted -- is there a consensus on the definition of pecking order?

I think you have it wrong - a pecking order is about access to resources decided before the access as the result of a competition (usually strength, but not always, brighter feathers, bigger antennae can work for this), not just straight competition (being able to move faster). Voting to close for homework.

@bob1 How does this look like a homework? I get your point. I used to have the same viewpoint as yours but later I found that "pecking order" is equivalent to "dominance hierarchy" according to Wikipedia. I don't know who to trust. If you have one or two reliable reference I'll be appreciated!

It looks like homework because of these sections of the homework part in the help: "A question that addresses a basic biology concept that may seem trivial to biology professionals" and "Include details of how you have attempted to form a solution. We will not do your homework assignments for you but we will point you in the right direction if you have made the effort to research the topic first."

@bob1 "Include details of how you have attempted to form a solution" makes a question good, not bad (or close-worthy). All questions are encouraged to include the attempts to solve the question.

But you don't show how you have attempted a solution - you've found a paper on bacterial competition, but you don't provide why you think this is appropriate to support your postulate, or any other evidence that you actually know what a pecking order is. Also your "pecking order" (1st) link is literally on peck strength in birds - nothing to do with pecking order at all. These together mean this is a low-effort homework post.

@bob1 I don't get your statement. First you said this question "looks like homework because the question include details of how I have attempted to form a solution"; then you said I did not attempt anything.

@bob1 Anyways, I must restate that this is clearly not a homework question. So it seems like that you have a different definition for "pecking order". May I again kindly ask your reference or sources? Most sources I found uses a similar definition to Wikipedia

No, what I said was that you need to provide details of how you have attempted to find a solution - read the link in my second comment. You haven't provided details. A pecking order is an informal hierarchical social dominance order where individuals higher in the order have more dominance or authority over those lower in the order. An example might be a family - Parents -> elder child -> younger child. A basic ecology or biology text will have a similar definition. This means again, homework as based on the "trivial for expert" part I quoted from the help page.

@bob1 You said that my first link is irrelevant to "pecking order". Could you please again provide reliable reference that Ebbe 1913 paper is irrelevant to pecking order?

My apologies I mis-read and looked at the citing paper, my Norwegian being somewhat lacking. However, I believe that the publication should be this one from 1921: Beiträge zur Biologie und Sozial- und Individualpsychologie bei Gallus domesticus (Contributions to the biology and social and individual psychology in Gallus domesticus) . Hønsenes stemme. Bidrag til hønsenes psykologi translates to "The voice of the chickens. Contribution to the psychology of chickens", which doesn't quite look right. However, I haven't been able to view the originals.

"Earliest" is a bit problematic; all species on Earth have been evolving for the exact same amount of time. In terms of generations, complex eukaryotes with long life spans have been evolving for a shorter time than many single-celled organisms.

@BryanKrause For example, the "earliest" language is created by Sumerian, according to many of the main stream anthropologists. In this question, the word “earliest” means the same thing. Maybe for biologists this word is a bit ambiguous. Of course, you are very welcome to suggest an alternative word or expression.

@HighGPA Well unless you expect to find this from the fossil record, the issue is that "earlier" things like Sumerian don't exist any more to be observed.

@BryanKrause Probably I should change the question to "approximately when did organisms evolved the property of pecking order?" Sometimes scientists and theoretically deduce an approximate time even before the actual evidence is discovered. Does this sounds better?


text:
How are PCR tests for detecting COVID-19 performed on hamsters?
This is something I've been wondering about ever since the stories of people finding hamsters with a COVID infection in Hong Kong. Apparently those animals were tested using a PCR test, but I'm struggling to understand the logistics. In humans, PCR tests are nasal swabs, but it feels like it would be a REALLY inhumane thing to stick a nasal swab into the nostril of an animal the size of a hamster.
How are PCR tests performed on these animals?

This is probably quite different from the example you're thinking of, but here's an example where they were using a hamster as a model organism for testing possible COVID-19 treatments for humans:
Kreye, J., Reincke, S. M., Kornau, H. C., Sánchez-Sendin, E., Corman, V. M., Liu, H., ... & Prüss, H. (2020). A therapeutic non-self-reactive SARS-CoV-2 antibody protects from lung pathology in a COVID-19 hamster model. Cell, 183(4), 1058-1069.
Their method for obtaining samples for PCR:

RNA was extracted from homogenized lungs, nasal washes and tracheal swabs

They don't go into detail about the nasal washes and tracheal swabs, but I would presume that the tracheal swabs are performed much like a human nasal swab, except into the mouth, and using a size of swab appropriate for a hamster. Again, they don't provide much information about the nasal wash and I haven't done this myself in a rodent, but I'd suspect it's done a lot like the nasal irrigation some people use for treatment of sinus complaints, they're just collecting the fluid that comes out.
For the lung homogenates, you can assume that they've euthanized or anesthetized the animals first, then removed the lungs.
If your source is referring to pet hamsters I'm guessing they've used something like the tracheal swab or possibly nasal irrigation.

I'll add that animals are typically anesthetized for a nasal wash. Not sure about tracheal swabs, but it would be pretty hard to tell whether the swab was in the trachea or the esophagus in a hamster. I bet it was closer to an oropharyngeal swab.


text:
What is the best way to stack parafilm wrapped petri dishes?
I have several petri dishes that are individually wrapped with bemis parafilm.  As space is somewhat limited, I've begun stacking them on top of each other, however in doing this the wrapping for each plate will sometimes get stuck to the wrapping on the other plates.  Is there a good technique or separator or tool or something I can use to both efficiently store my plates and not jeopardize their parafilm seal?

Thinner strips of parafilm.

Is a sheet pan rack/"speed rack" a possible option? Or would that take up too much space for the number you need?

Yea that would take up too much room.  If I had plenty of space, I would just have them all laid out.  Considering trying to use 6"x6" wax paper for hamburger meat to separate them.  Kind of need to vertically store them and access them daily to track growth progress.

Do you need to individually wrap them? We used to just store a stack of them in the plastic bag the stack came in, resealed with tape at the end.

Our lab uses food-wrapping-foil to seal agar petri dishes instead of parafin. We buy a rool at grocery store an cut the rool with sharp knife into cca 1.3cm wide minirools which we than use. It is cheaper than parafin and food-wrap comes sterile from production. Never had problem with plates sticking to each other when stacked.

Guess it depends on how long you need to store them. Sometimes I've put them in a refrigerator-sized plastic tupperware container with a sealing lid. Didn't last quite as long as parafilm, but kept them from drying out long enough for my needs.

I ended up getting the 6"x6" wax paper for hamburger meat and putting a sheet between stacked and wrapped petri dishes which prevented them from sticking to each other.  Their footprint is now bigger but it works.  I could cut the sheets down or probably get smaller ones if I really wanted though.
Above there are some interesting other solution suggested like saran wrap and other methods of storing them that may work for some other use case.  As I need to document my dishes progress regularly they get handled at least daily so 'extra' or a thick application parafilm is used to make sure they stay tightly sealed.


text:
What is the modern experiment in which a frog was heated at the slowest rate?
I did a bit of research on the boiling frog phenomenon. It turned out that:

In the 19th century, there have been done three experiments in which a frog in water was heated very slowly. It didn't jump out and then it died.
Modern experiments did also heat frogs, and they did jump out.
Actually, a frog dies in water of $40^{\circ}$ C. Therefore, to properly conduct the experiment the water should be heated from a normal temperature to 40 degrees.

In order to prove that the 19th century experiments were wrong, there should be a modern experiment where the frog is heated just as slowly as in the 19th century. According to Edward Wheeler Scripture (see Wikipedia), he performed the experiment with a rate of 0.002 degrees per second.
Are there modern experiments which also have such a slow rate? What is the slowest rate of a modern experiment?
EDIT
The following article claims that the modern experiment with the slowest rate is still 9 times as fast as that of Scripture. Is this really true?

If the current climate science stats are accurate, all frogs on earth are being heated at a rate of 0.2° C per decade, on average. Sure, there may be a few covariates to account for, but the sample size is huge.

As noted in one of your links: "they don't sit still for you" seems to be the problem. If you put a frog in a pot, it doesn't matter if you heat it at all, if you allow them to escape they will escape. I kind of doubt anyone has actually published on that, though; people don't usually publish such trivialities.

@acvill, unfortunately frogs won't be able to jump out of the earth when it becomes too hot

@Bryan Krause, if the frog did escape, then it would indeed be too trivial to publish. Exactly the fact that the frog didn't escape, made it memorable.

@Riemann It seems the modern commentators are saying that the frog doesn't need any temperature increase to escape. If you put a frog in a pot it will jump out if it can, heat or no heat, so they don't see the point to do the experiment with a gradual temperature change. Presumably in the original experiment (which I haven't read) the frog was not actually able to escape, otherwise it would have (again, not because of heat, but because of frogs doing frog things, like moving around freely when they can).

@Bryan Krause, wouldn't it be possible to wait until the frog is sleeping or something like that?

@Riemann It seems like that would be a separate experiment, but not necessarily; how do you plan to put a sleeping frog in a pot without waking it up? Behavior under sleep is also different from waking behavior - reduced response to stimulus is a hallmark of sleep. Also, your question implies Scripture did this experiment; I can't see any source that suggests that he did. Wikipedia says he "recounted" aka told a story about; in the cited source he refers to experiments by Heinzmann and Fratscher.

OP: The most amazing of all your statements is that a dead frog jumped out of hot water! No wonder the experiment could not be reproduced! ("...a frog in water was heated very slowly. It didn't jump out until it died.") Like I said, that is one for the books. Or if one prefers journals, The Journal of Irreproducible Results.

I don't really read enough German to read Heinzmann, but it seems that most, if not all, of his experiments were done in decerebrate frogs. It's a study of the reflex arc of the frog's leg and spine, rather than the behavior of the frog, from what I can tell.

"a frog dies at 40 C" - citation needed I think.

@Anongoodnurse: very good point! I corrected it

@bob1 I added citation

@Riemann - thanks, but that isn't a citation for fact it literally says "The facts go roughly like this: ...   ...The fatal temperature for a frog is below boiling point, more like up to 40 °C." without citation. The link for a supposed citation (provided at the end of the article, not referenced) is to zeit.de and is paywalled, so unverifiable.

To clear up some things, I have made a partial answer here.
While it is old, you shouldn't discount the observations made by scientists from the 1800's. Many great scientists from this period laid the foundations for science as we know it now. These include names such as Charles Darwin, Alfred Wallace, Robert Koch, Gregor Mendel, and Louis Pasteur, to name a few well known biologists, whom no-one would think to doubt. Scientists in the 1800s were certainly exact in their measurements, observations and records, and I don't doubt that the observations that they made were exactly what they claimed they were.
To this end, I had a look at Goltz's 1869 book1 (PDF here) in the original German, and put it through Google translate ('cause I don't read German well enough to follow at this level) at the relevant point. Fortunately the PDF linked is text-selectable, so I was able to copy this directly and edit some minor misinterpretations from the paste. Google translate is pretty good for German and German has not changed significantly since the 1800's I believe.
Here's the bits I copied from pages 127 and 128 (you can see the errors at line-ends and in special characters, and where some bits can't be recognized as they are in the spine end of the text):

Von drei gleichzeitig gefangenen, gleich grossen und reiz-
:en Fröschen schneide ich zweien mit der glühenden Platin-
linge des galvanokaustischen Apparats die Köpfe ab. Dem
tten sonst unversehrten blende ich die Augen, um unnütze will-
1 liehe Bewegungen desselben möglichst auszuschliessen. Darauf
ce ich den zuletzt geköpften Frosch in ein weites blechernes
iäss, dessen Boden mit mehreren Schichten Leinwand bekleidet
und bringe ihn sogleich in die hockende Stellung, welche
hirnte Frösche immer annehmen und dann nicht wieder von
')St verlassen. Das Gefäss fülle ich jetzt so weit mit Wasser,
'S nur ein kleiner Theil des Thieres daraus hervorragt. Zu
1 Enthaupteten setze ich dann den geblendeten Frosch, wel-
r sich alsbald ebenfalls in hockender Stellung niederlässt und
iangslos verharrt. Den zweiten Geköpften behalte ich in der
le des Gefässes unter Augen. Jetzt fange ich an das Gefäss 128 Ueber den Sitz der Seele dea Frosches und
zu erhitzen, die steigende Temperatur des Wassers an einem :
dasselbe eingesenkten Thermometer ablesend. Die Zimmertempi
ratur beträgt 17i”C.
Hat das Wasser aber erst die Temperatur von 25“ erlangt, li
verändert sich die Scene. Dem behirnten Frosch beginnt es uj
behaglich zu werden. Er verändert den Ort, steckt den Kot
weit zum Wasser hinaus, und fängt an, schneller zu athmen. j
höher die Temperatur steigt, desto ängstlicher werden seine B<
wegungen. Verzweiflungsvoll schwimmt das gequälte Thier ij
Behälter umher, bald den Kopf weit hinausstreckend und imm<
geschwinder nach Kühlung jappend, bald auf den Grund d<
Gefässes tauchend, um dort der Pein zu entrinnen. Die Hita
nähert sich gegen 38“. Das Thier macht verzweifelte Sprüng«
um aus dem Behälter zu entkommen. Es klimmt an den glatte
Wänden empor und muss in das heisse Wasser zurück gestosse
werden. Die immer geschwinder auf- und niederfliegenden Atb
mungsmuskeln erlahmen, die Athmung setzt aus. Immer wild^
werden die Schmerzensäusserungen, und endlich bei einer Teib
peratur von etwa 42“ verendet das gequälte Thier unter tetan^
sehen Krämpfen.

And the translation:

I cut off the heads of two of three frogs of the same size and attractiveness that were caught at the same time with the glowing platinum pieces of the galvanocaustic apparatus. To the
I blind the eyes of those who are otherwise undamaged in order to exclude useless voluntary movements as far as possible. Then I put the last decapitated frog in a wide tin vase, the floor of which was covered with several layers of canvas
and immediately bring him into the squatting position, which
brain frogs always accept and then not from again
')St leave. I fill the vessel with water now,
'S only a small part of the animal protrudes from it. to
I then place the blinded frog on the decapitated one, which soon also settles down in a crouching position and
fearless. I'll keep the second decapitated man in the
le of the vessel under the eyes. Now I start the container, the water has reached a temperature of about 25", both frogs sit still in the warm bath. On the decapitated one sees the movements of the thighs, so common in decapitated people: he might pull one thigh up a little more or straighten a zoe, movements such as those used outside of the bath
Lingering second decapitated also shows, which are therefore not dependent on the increasing temperature, and which incidentally will soon stopBut once the water has reached the temperature of 25", the scene changes. The brained frog begins to get uncomfortable. He changes the place, sticks the feces
far out to the water, and begins to breathe faster. j
the higher the temperature rises, the more anxious his movements become. The tormented animal ij swims in despair
container around, soon stretching out the head far and imm
Quickly yapping for coolness, soon to the bottom d
vessel to escape from the torment there. the hita
approaching around 38". The animal makes desperate leaps
to escape from the container. It climbs to the smooth
walls and has to be thrown back into the hot water
will. The respiratory muscles, which fly up and down faster and faster, become slack and breathing stops. Always wild
the expressions of pain become manifest, and finally at a body temperature of about 42" the tormented animal dies with tetanic convulsions.

You can see the bits, which the translator can't cope with - these are bits which didn't transcribe well, due to being in the spine of the book and not scanned properly. I also can't read these or even make a guess at what the proper word would be in many cases, though I have fixed those that I could. However, I think that the general text is largely fine to read and easy to interpret.
Basically, what Goltz did was attempt to study the nervous system and physiology of frogs. He did this by comparing decapitated or decerebrated frogs with intact ones (apart from blinded eyes, to exclude visual stimuli). He placed both of these in room temperature water and then heated it. When heated, the decapitated frogs did not show any reflex action and would sit still until dead unless stimulated by a different stimulus, which was some mild acetic acid applied to the back of the frog (bottom of page 128, not translated here). On the other hand, intact frogs would violently try to escape and would have to be placed back into the heated container, up to about 42 C, at which point they died.
Edited to add:
On page 130, there is a passage:

Behälter einen solchen, welchem ich das Gehirn mit einem qu
Schnitt dicht vor den Sehhügeln abgetrennt hatte. Zu ihm s*
ich einen geköpften Frosch, welchem ich die Hinterbeine i
oben geschilderten Weise verschränkt hatte. Beide Frösche bli!
ganz regungslos sitzen, bis die Temperatur des Wassers 32|'*
reicht hatte. Da machte der hirnbesitzende Frosch mit dem
eine Bewegung nach oben und fing an schneller zu athmen.
35“ machte er mit dem Körper eine kleine Wendung und sp
dann plötzlich mit einem kräftigen Satz aus dem Behälter hii
In’s Wasser zurückgebracht, machte er alsbald einen zweiten Sp>
aus dem Geföss. Ausserhalb desselben wiederholte er die Hi
bewegungen nie, sondern verharrte nach dem einen Satz, mit
ehern er das Bad verlassen hatte, in Ruhe. Nachdem er, i:
wieder in’s Bad zurückgebracht, im Ganzen sechs Sprünge g'
hatte, und das Wasser inzwischen allmälig eine Hitze von
erlangt hatte, starb er unter tetanischen Krämpfen. Während
ser Scenen hatte der Geköpfte mit verschränkten Füssen ruhi
gesessen. Bei 37?“ machte er die zuckenden Bewegungen, dij
aussahen, als wenn er die verschränkten Füsse auseinander bri
wollte. Bald wieder beruhigt, blieb er regungslos sitzen. Ui
Zeit, als der Behirnte in Krämpfe verfiel, begann bei dem ^
köpften die Wärmestarre der Muskeln. Ohne dass die v
schränkten Füsse sich lösten, wurden die Schenkel |
allmälig etwas nach hinten gestreckt, und das ganze Thier
hart und steif.

Translated:

Lately I have completed this experiment in the following way-
changes; Instead of the blinded frog, I put one in the container, which I pierced the brain with a qu
cut just before the brow mounds. To him a decapitated frog, whose hind legs i
entangled in the manner described above. Both frogs bli!
sit completely motionless until the temperature of the water is 32
had enough. Then the brain-possessing frog did that
a movement upwards and began to breathe faster.
35” he made a small turn with his body and sp
then suddenly with a powerful leap out of the container
Brought back into the water, he immediately made a second spat from the vessel. Outside of this he never repeated the hi movements, but after one set he stayed with
as soon as he had left the bath, in peace. After he had had six jumps in all when he was brought back into the bath, and the water was gradually getting hotter
he died from tetanic convulsions. While
The decapitated man had these scenes with crossed feet
sat. At 37?” he made the twitching movements that looked like he was breaking his crossed feet apart
wanted to. Soon calmed down, he sat motionless. wow
Time when the crippled went into convulsions began at the
beheaded the thermal rigidity of the muscles. Without the v
when feet broke loose, the thighs were gradually stretched back a little, and the whole animal
hard and stiff.

This is using frogs with their hind limbs crossed (and pinned?; see image page 103), so that they can no-longer swim properly and jump.  The frog still gets out and is returned to water that is gradually getting hotter. Eventually it does not attempt to escape again. Note that the intact frog still tries to make movements and escape, just can't in the long run. I can only speculate on why it doesn't continue to try to escape, perhaps the water is too hot for proper function at this point, or perhaps it has learned that it can't escape, so gives up, which is a pretty sad conclusion to come to.
So, TL:DR - frogs try to escape when the water is too hot for them!

Goltz F. 1869. Beitrāge zur lehre von de function der nervencentrum des frosches. Berlin.

Thanks for the elaborate answer! This corresponds to what Wikipedia says about Friedrich Goltz's experiment. See https://en.wikipedia.org/wiki/Boiling_frog#Experiments_and_analysis

However, according to Wikipedia, Heinzmann and Fratscher got results in which a normal frog did not jump out

@Riemann - you can track those publications down and have a look at them yourself. The author of the Wikipedia page obviously only looked at Sedgewick 1888, as they don't provide a reference for Fratscher. Heinzmann is in German, but translatable. Numerous experiments performed, but my German isn't good enough to read it, and I don't have the time to put in to translate it all.

I also haven't been able to track down Fratscher. All references come back to Sedgewick.