text:
How much air does a square meter of sugar beet consume per hour?
I've come across a person who tried to disprove photosynthesis (yeah, I know). The basically took numbers of record sugar beet crop in Chile (192 tonnes per hectare), and tried to calculate how much air the plant would consume in order to grow. They've ended up calculating that a square meter of sugar beet field needs 7.32 cubic meters of air per hour, and they decided that this is too much, as it is amount 14 people breath in, hence their conclusion is the photosynthesis isn't real.
Where's the error?
The numbers they ended up with were:

125 days to harvest.
That is 127 kg per hour per hectare, or 12.7 gramms per hour per square meter.
Dry mass of beet is 15% hence 1.9 grams per square meters per hour.
45% of that is carbon which is 0.86.
Carbon is 27% of mass of CO2 (12/44), since one cubic meter of air weighs 1.22 kg and that is 0.117 grams of carbon.

At this point they assumed that a square meter of sugar beet should "pump" 7.37 cubic meters of air through their leaves in order to produce this kind of harvest.
Where is the error (or more than one)?

Welcome to Biology.SE. Please take the [tour] and consult the [help] starting with [ask]. In particular, this is a site for clear, focused, well-researched biological questions — it is not a site for debunking crackpot "theories". Among other things, air is not "consumed" by plants (or animals) — you seem to be talking about carbon dioxide? Most importantly show us that you have tried to answer this yourself and how — start by providing references (to reliable sources) for your numbers.
This is not simply an answer site, but instead a site that promotes self-learning with some expert help.

Oh my gosh... I would just totally file that person's belief under "useless to bother arguing with". My own father believed in spontaneous generation. I never argued with him about it. (He was not highly educated, and it would have seemed I was lording my education over him.) Pick your battles to preserve your sanity.

@tyersome, I would honestly prefer if you've answered this question instead. I've participated on se before and know the drill. Regarding the question I've checked his numbers and tried to calculate amount of carbon plant is supposed to generate myself. The thing is resulting numbers ended up close to his results, and I was unable to find an obvious error in calculations. Which means I'm lacking domain knowledge and that's why I asked it here. It is not debunking. It is looking for a missing knowledge. His conclusion is wrong, but I can't tell why. Hence I ask.

@anongoodnurse I asked because I'm unable to locate the error in their logic by myself. I don't care about battles, but I'd like to know what the error is.

Taking it slowly;
192 tonnes per hectare is
0.0192 tonnes per square metre (div 10,000)
19.2 kg per square metre over the year
0.1536 kg per day per square metre (div 125 days)
153.6 grams per day per square metre
6.4 grams per hour per square metre. (Div 24)
0.96 grams of dry matter per hour per square metre (x 0.15)
0.432 grams of carbon per ... ( x 0.45)
Derived from 1.584 grams of CO2 (div 12/44)
Using CO2 level of 410 ppm,
A cubic metre of air weighing 1.22 kg contains 0.7588 grams of CO2
The averages work out to:
the square metre of beet, per hour uses the CO2 from 2.08 cubic metres of air. (1.584 / 0.7588)
The enzyme RuBisCO captures this CO2.
The amount people breathe isn’t strictly relevant. But....
A common claim is that sedentary people exhale about 1.1 kg of CO2 per day. That’s enough to supply 28 square metres of these beets. (1100/(1.584 x 24))
This sort of maths is sometimes done for hypothetical “how much do I have to grow in my spacecraft” questions

Thank you very much. Few minor details, however:  The original poster I ran into also took day time into account (different from spacecraft, as spacecraft can have continuous light).... and I recall that sugar beet is 20% sugar and 5% pulp. Does the dry matter calculation take that into account?

I haven’t investigated the dry matter calculation; but I feel that carbon content of dry matter will be fairly constant, by a factor of two anyway. That’s a huge crop - but I regard it as referring to whole plant. Carbon content in sugar similar to carbon content in cellulose or lignin.


text:
What is this tooth or tusk that was found with several others in a scrimshaw kit from Nantucket?
This was in a scrimshaw kit that was purchased at a yard sale about 20 years ago. Kit was sold by a company on Nantucket, and was old at the time of the yard sale. It is not known if this and the three other similar pieces were original to the kit or were added later on. What animal did this come from?

From the location of purchase, conical shape, color, and size, the tooth is that of a sperm whale (Physeter macrocephalus). Sperm whales have 17-29 teeth in the lower jaw that range 3-8 inches (see Perrin et al., 2009). Their teeth were most often used as scrimshaw, and many can be seen at the Nantucket Whaling Museum.
Just as an FYI, under the Endangered Species Act, it is illegal to buy or sell sperm whale ivory harvested after 1973. So you may want to have the tooth aged.

Thank you. These aren't going to be sold. And based on the age of the kit it seems probable that it predates '73 anyway.

source: Stack Exchange

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text:
Population numbers in the presence of restricted resources
I wonder if the following simple system is considered in population dynamics, under which name, and in which textbooks.
Consider a population $X$ (also indicating its number of individuals) with a default birth rate $\beta_0$ and a default death rate $\delta_0$. Let the effective birth rate be given by
$$\beta = \beta_0\,\frac{\alpha}{\rho}$$
where $\alpha$ is the amount of resources available to each individual, and $\rho$ is the amount of resources needed by each indiv idual. We have $\beta > \beta_0$ when there are more resources available than needed, and $\beta < \beta_0$ when there are less resources available than needed.
For the sake of simplicity let's assume that the effective death rate is given by
$$\delta = \delta_0\,\frac{\rho}{\alpha},$$
i.e. the effective death rate decreases with increasing $\alpha/\rho$ and increases otherwise.
The equilibrium condition $\dot{X} = 0$ of the system $\dot{X} = \beta\,X - \delta\,X$ is given by
$$\frac{\beta_0}{\delta_0} = \frac{\rho^2}{\alpha^2}$$
With the final assumption of restricted but fully exploited resources, specified by
$$X\,\alpha = R = \text{const.}$$
we get the equilibrium condition
$$\frac{\beta_0}{\delta_0} = \frac{\rho^2}{R^2}X^2$$
Resolved with respect to $X$ we have the equilibrium population
\begin{equation}
X_0 = \frac{R}{\rho} \, \sqrt{\frac{\beta_0}{\delta_0}}
\end{equation}
The next step would be to consider systems of populations $X_i$ competing for the same resources $R$, especially with different values of $\alpha_i$ (indicating different fitnesses in the struggle for resources), but also with different values of $\rho_i$ (indicating different efficiencies in utilizing the resources). But I'd like to take the first step first. Is it a sensible approach?

Birth rate cannot increase exponentially with the number of avaliable resourses. Each birth requires some amount of resources, so it increases at best linearly. In reality, there is some limit on how much resources each specie can process, so the birth rate is limited.

There are still some aspects of this that are unclear to me. Is $\alpha$ meant to be a constant valuable rather than a dynamical variable? That wouldn't make sense because then we'd just have exponential growth (and your constraint wouldn't make sense). If $\alpha$ is meant to be a dynamic variable then we have $\alpha \propto 1/X$ and we get something of the form (I think) $\dot X = c_1 - c_2 X^2$, or $d(\log X)/dt = c_1/X - c_2 X$. As @user31264 points out, the per capita birth rate diverges at $X=0$, which is weird.

This is somewhat similar to a single-species version of ratio-dependent predator-prey dynamics (e.g. https://pubmed.ncbi.nlm.nih.gov/19083063/ ), which has been argued about a lot "Since the ratio-dependent model always has difficult dynamics in the vicinity of the origin ..."

@BenBolker: I consider the total amount of resources $R$ to be a constant, the amount of resources available to a single individual (of which there are $X(t)$ at time $t$) is $\alpha(t) = R/X(t)$.

If we express your equations in their simplest form (by substituting $R/X(t)$ for $\alpha(t)$) we get
$$
\dot X = (\beta_0 R/\rho) - (\delta_0 \rho/R) X^2
$$
or
$$
(\dot X)/X = \dot{(\log X)} = \frac{(\beta_0 R/\rho)}{X} - (\delta_0 \rho/R) X
$$
(assuming I didn't screw up the algebra — however, the important point here is the form of the dependence on $X$).
This means that the per capita reproductive rate diverges as $X \to 0$, which is weird/unbiological. That's not necessarily a deal-breaker — there are plenty of models that are pedagogically or practically useful (e.g. see Lehman et al 2020 for models where the population density diverges in finite time) — but it does ring an alarm bell.
An initially linear growth rate (i.e. constant absolute growth rate near 0) is more typical of abiotic resources that are being considered to be added to a system at a constant rate, as in a chemostat model.
This model reminds me of ratio-dependent predator-prey models, which have been extensively analyzed in the math-bio world (see this Google Scholar search), but much less used by ecologists. Abrams and Ginzburg (2000), whose co-authors are respectively a strong opponent and a strong proponent of ratio-dependent models, might be a good starting point in the ecological side of the literature.

Abrams, Peter A., and Lev R. Ginzburg. “The Nature of Predation: Prey Dependent, Ratio Dependent or Neither?” Trends in Ecology & Evolution 15, no. 8 (August 1, 2000): 337–41. https://doi.org/10.1016/S0169-5347(00)01908-X.
Lehman, Clarence, Shelby Loberg, Adam T. Clark, and Daniel Schmitter. “Unifying the Basic Models of Ecology to Be More Complete and Easier to Teach.” BioScience 70, no. 5 (May 1, 2020): 415–26. https://doi.org/10.1093/biosci/biaa013.

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text:
Does an "empty stomach" have acid in it?
I know that the pH of the acid in an empty stomach is higher than a stomach with food.
I was trying to understand how water passes through stomach to intestines with the absence of food.
But this webpage : Acid reflux mythbusters has this bizarre claim :

Drinking water on an empty stomach does not dilute stomach acid because it was never released in the first place.

How is this possible? Ok sure, not "more" acid is released because it's just water. But there is still acid already present in the stomach, right?
Note : I'm not concerned about diluting the acid or not. I just want to know if there is acid in the empty stomach or not. Or if there is any possible scenario where the stomach is actually completely empty.

When an individual is fasting, acid secretion is inhibited by somatostatin from gastric D cells (some helpful stomach acid secretion scientific papers, and an article on stomach acid regulation). This causes there to be a minimal amount of stomach fluid (aka stomach acid) around, but due to the nature of the stomach a pH of 1.5-3.5 must be maintained and so there is always going to be some amount of stomach acid even if it is not the 1L pool of acid some people imagine there to be. In order for more stomach fluid/acid to be produced, neurological stimulus must occur that somehow relates to food or drinks (such as smelling food or thinking of food or obviously, consuming food/drinks).
Hope that helped!


text:
How do I calculate a "full-life" from a half-life of substance elimination?

The half-time of carbon monoxide disappearance from blood under normal recovery conditions while breathing air showed considerable between-individual variance. For carboxyhaemoglobin concentrations of 2–10%, the half-time ranged from 3 to 5 h (Landaw, 1973); others reported the range to be 2–6.5 h for slightly higher initial concentrations of carboxyhaemoglobin (Peterson & Stewart, 1970).

(from here)
To get a "full-life" (or the best approximation of it), should I multiple it by 2 or 6.64 (99%)? Is carboxyhaemoglobin's "full-life" in bloodstream 4-13 or 13-86 hours? That's a huge difference

There is no such thing as a "full-life", because in most relevant mathematical models (the simplest and most common being first-order exponential decay), the time required for all the the substance to be gone is infinite.
For example, the half-life is marked on the following graph as $t_{1/2}$. Is two times the half life a "full-life"? What must $t$ be for the quantity (concentration, number of particles, whatever) to become zero? Based on my first paragraph you should be able to answer these questions.

What you can do, given data or an equation, is calculate the amount of time required for the quantity to drop to a specified amount. For instance, you could decide that you'd like to know the time it takes for the CO concentration to drop by 90% or 99% or 99.9% from the initial level. A rule of thumb (which can be derived from the exponential decay equation) is that the quantity will be depleted by around 99% in approximately seven half-lives. You could derive a similar relations for any desired percent. Which percent to choose for the cutoff of interest is at the discretion of the person doing the analysis, and different fields and contexts have different standards. The substance will never be "completely" gone, but there may be a meaningful threshold beyond which it becomes negligible.


text:
effect of pH, temperature and enzyme concentration on Km
I understand that enzyme concentration does'nt affect Km since the Micaelis Menten equation is based on the steady state approximation wich requires high levels of substrate compared to enzyme (that's why changing enzyme concentration is negligible compared to substrate concentration and therfore there is no apparent change in Km). but what about change of temperature or pH? it's known that change in those parameters can change enzyme activity, but does this actually can change kinetic parameters like Km?
Why should i think not? because the same explanation that says that change in enzyme concentration does'nt affect Km sould be applied here. there is a lot of substarate anyway and therefore there should not be apparent change in the Km? or am I wrong?
another issue which makes me think so: In all the biochemistry literature that I have encounterd Km and Kcat appears for each enzyme with no indication of the temperature or pH for wich thouse values were observed (not in Leninger, nor Wikipedia or other textbooks).
I couldn't find any orderd explanation about this issue.

Wikipedia: “The value of Km is dependent on both the identity of enzyme and that of the substrate, as well as conditions such as temperature and pH.”

Michaelis constant is defined as $$K_\textrm{M} = \frac{k_{-1}+k_2}{k_1},$$ where $k$s represent the rate constants for the reactions $$\mathrm{E+S} \;\;\underset{k_{-1}}{\overset{k_1}{\longrightleftharpoons}} \;\;\mathrm{ES}\; \overset{k_2}{\longrightarrow}\;\mathrm{E+P}.$$ Rate constants can generally be expressed by the Arrhenius equation: $$k(T) = A(T)\exp\left(-\frac{E_a}{RT}\right).$$ Because the parameters $A(T)$ (pre-exponential factor) and $E_a$ (activation energy) are generally not equal for all three reactions, the change in temperature does change the value of $K_\rm{M}$.
When measuring the enzyme kinetics and calculating $K_\rm{M}$, one has to explicitly state at which temperature the experiments were performed. This is probably not mentioned afterwards in the textbook because it is not of significant importance to the surrounding text and concepts.
Here you can find an article example with the measurements of enzyme kinetics at different temperatures. You can clearly see the change in $K_\rm{M}$.


text:
Does cancer really remain undetected about 80% of its life?
I was reading Atomic Habits by James Clear, who mentioned this and decided to google it. The only mention of this at least in the first search page was from this source from February, 2012. Is there any new resource that mentions this that isn't a decade old?

A study conducted by researchers at Stanford University School of Medicine provides strong new evidence that malignant tumors may grow undetected in the body for a decade or more before they can be sniffed out by the most sophisticated blood tests currently available.

There is undetected and there is unidentified; I detected my cancer symptoms for about a year before I found a doctor that could identify it as cancer.

I'd suggest finding that Stanford study on PubMed or google scholar and looking for studies that cite it.

@blacksmith37 - The question is, I believe, about size, not symptoms.

Your source bases "undected" on a blood test indicating the presence of a cancerous lesion. This says more about the lack of tumor-specific biomarkers than anything else. Many cancers present with symptoms. If you want to know about advances in tumor-specific biomarkers in the past decade, I'd look for that.

The size was stage 4 , the largest size category, I understand.

Once the Dr decided to do a blood test , it required only a couple days to identify it as HPV 16 induced cancer.


text:
How does natural selection interacts with sustained mask use?
At leasts in some European countries, the number of respiratory (non-covid) infectious diseases on children this term is higher than last year and similar to pre-pandemic years in spite of social distance and use of masks. On the other hand, we are seeing how covid variants more infectious are appearing. So my question is: is the use of masks (or social distancing) increasing (from the point of view of natural selection) the (already) higher advantage of more infectious respiratory viruses? At a first sight, it seems to me that the answer is no, but I'm not an expert, and I wonder if this has been studied. In other terms: are we sure that we are not making (with social distance measures) current respiratory viruses (such as influenza) more infectious?

can you link to the sources indicating the general increase in respiratory illnesses? For influenza in the USA at least this appears to be the opposite of the case (I know that you mentioned Europe, but it's hard to imagine that it's so decoupled): https://www.cdc.gov/flu/weekly/weeklyarchives2020-2021/week53.htm (ILINet chart comparing flu seasons). Some flu strains are thought to have effectively gone extinct due to COVID safety measures: https://www.webmd.com/lung/news/20211025/covid-pandemic-may-have-driven-a-flu-strain-into-extinction#1

It's an interesting idea. I suspect the figures for an increase might be as much to do with alert parents being liable to report trivial sniffles more than before - that being said - if you can provide a bit more info to say where you got the figure and how it was worked out (if available) then we'll be in a better position to judge.


text:
Can Covid-19 virus be simply filtered out from infected patient’s blood?
Can Covid-19 virus be simply filtered out from infected patient’s blood?
If a Covid+ patient’s blood is passed through a filter, say 100 nm or a system of filters, 100 nm and 500 nm can we isolate the virus from serum including small and large blood particles? This is somewhat like a dialysis of the blood. I am particularly interested to know if graphene filters will be of help here. Has somebody worked on that? I am thinking if size can be exploited to isolate the virus (irrespective of mutants) and aid the primary treatment of the patient. I am not a virologist and new to the subject.

No, this wouldn't work, and if you think about it for a bit you'll see why. First and foremost, your 100nm filter would catch all the cells that are in the blood. Therefore, all you'd end up with is plasma, and the patient would die within several minutes of beginning "therapy" due to not being able to transport oxygen with red blood cells. On a practical note, all those cells would clog your filters, of any size, immediately.
Another reason: SARS-CoV-2 primarily infects epithelial cells in the respiratory system, and can easily transfer from cell to cell without having to use the bloodstream. In fact, it's my understanding that the serum load of virus is actually rather low. Filtering the blood wouldn't prevent any of that cell->cell transfer.
Final reason (for now): there are other things in the blood that are in the vicinity of the same size as virus particles - cholesterol/lipoprotein aggregates, larger protein complexes, platelets, etc. You'd lose all these vital components of your body with any kind of filtering scheme.

Thank you.
I was suggesting a system of three filters, 800 nm, 200 nm and 100 nm in that order. Infected blood passing through this system will isolate the virus while retaining the useful constituents of the blood. I agree that there may be blood constituents in the same size range as the virus which should be identified and replenished back. I also agree that the larger problem is in the epithelial cells which should be addressed by standard vaccination. To avoid filter clogging, if filtering is done in small quantities of blood at a time then it may not be a problem. Let me refine this.

Feel free to revise your design, but trust me - there are reasons why this is not a clinical therapy, for viral infections or anything else. I've laid out some above, but there are others. Filtering small amounts of blood at a time won't work, b/c you're always going to lose something important when you filter. Even if you can get 95% of the RBCs back, there's still that 5% gone each time, and there'd have to be many, many rounds if you want to reduce the whole viral load appreciably. It's just not a good idea.


text:
Why do immunoglobulin heavy chain genes sit next to the telomere?
I just noticed that IGH genes are the last group of genes at the end of Chromosome 14.
Is there a reason / selection pressure to explain why that is?
Below is a snapshot of the UCSC genome browser. As indicated by the red box at top right, there are no more genes further towards the telomere.
Regarding the fact that IGH genes have to go through DNA recombination, it superficially counteracts the telomere's mission to safeguard chromosome stability. Then is it merely a coincidence or reflecting selection pressure?
And why aren't light chain genes sitting at the end of a chromosome?


text:
Recommendations for good books on bacterial genetics & molecular biology?
I'm starting a new phase of my PhD soon, and am feeling very under-prepared with respect to my general bacteriology knowledge. I was recommended to read up on basic bacterial genetics and molecular biology.
All the textbooks which I am familiar with from my past (Molecular Biology of the Cell etc,) rarely go in depth on the bacteria side of things. I really want a text which focusses solely on bacteria, and nothing else - this seems relatively hard to find recommendations for. I have Googled and found a few, but it would be nice to hear some first hand accounts on what books people recommend.

Why not start with a microbiology text? They tend to be very strong on those subjects, by my fuzzy recollection.

@MaximilianPress thank you. Do you have any favourites?

Afraid I'm quite out of date on these texts. You can find some material online via searches (e.g. https://bio.libretexts.org/Bookshelves/Microbiology/Book%3A_Microbiology_(Boundless)/7%3A_Microbial_Genetics), possibly some combo of "microbiology", "microbial genetics", "bacterial genetics" etc. will get you there.


text:
Why is Fst/1-Fst used when calculating isolation by distance?
In population genetics a common analysis when considering the genetic structure of a population is to examine isolation by distance - the relationship between the genetic difference and the geographic distance between populations. Commonly Fst (the P of variation attributable to differences between rather than within populations) is used as a measure of genetic distance and the analysis is usually some form of regression, however actual variable used for genetic distance is often Fst/1-Fst rather than the raw Fst estimate.
This practice I can generally trace back to Rousset 1997 (doi: 10.1093/genetics/145.4.1219) who appears to have set this standard, however I can find no satisfactory explanation as to why this is - the explanation provided in Rousset's paper uses a far higher level of math than I can interpret.
I assume that somewhere it has to do with a non-linear, more logarithmic relationship between Fst and geographic distance but I am hoping someone can provide a bit more detail on this (or correct me entirely!)

Hi, rainbird. Did you happen to see this and does it help? I'd try to help, but I really stink at math.

Hi, @anongoodnurse, yes I have had a look at the wiki but this entry really only discusses the calculation of Fst itself, not the relationship with distance. There is actually a separate wiki on isolation by distance but all of the Fst examples there use raw Fst. Actually so do quite a few of the recent papers it references, so perhaps this use of a modified Fst isn't quite ubiquitous, but it's still common enough to make me curious.

I do wish I could help. It's a valid question.


text:
Should Secondary Antibody Bind better through adsorption than using an EDC Linker?
Recently, I conducted an experiment to compare the use of EDC versus passive adsorption.

I attempted to immobilize goat anti-rabbit HRP secondary antibody to Carboxylated polystyrene beads via EDC and NHS linking protocol.
As the beads were polystyrene, we used centrifugation to clean the beads in between each step. Otherwise, we followed ThermoFisher's DynaBeads protocol. After immobilizing the ligands we added 100ul of HRP substrate to each sample and measured the luminance using Molecular Device's ID3.
The Materials used are as follows:

3um Carboxylated Beads (dyed red) from Polyscience
2%BSA
ThermoFisher's Pierce Premium EDC
25mM MES Buffer (6.33 pH)
50mg/ml EDC
50mg/ml NHS

Antibody and Detection

Goat Anti-Rabbit HRP Secondary Antibody
HRP substrate

However, when measuring the luminance of the HRP substrate the passive adsorption seemed to consistently provide significantly brighter results, suggesting that the EDC linker is not as effective as I thought.

Further, when testing different concentrations of EDC I noticed that luminance decreased as the concentration of EDC increased.

These results seem consistently odd and I'm not sure what to make of them. Looking for advice, as I am completely new to this procedure.


text:
What is bacterial (prokaryotic) cell division called?
Eukaryotic asexual cell division is sometimes referred to as mitosis, although this is more strictly used to refer to the specific stage at which “the replicated chromosomes separate into two new nuclei”.
The term is specific to eukaryotic cells, as prokaryotic cells have no nucleus. Is there a corresponding more specific term technical term that applies to prokaryotic cell division?
I thought this might be related to “binary fission”, but an internet search indicates this can be applied to eukaryotic organisms, such as starfish and other echinoderms.

Comments are not for extended discussion; this conversation has been moved to chat.

Fission, binary fission, cell division: these are all used more or less as synonyms for prokaryotes. "Fission" and "cell division" are more general, because they include mechanisms resulting in more than two resulting cells or an asymmetric division. As a supporting example from the literature, consider this paper:
Angert, E. R. (2005). Alternatives to binary fission in bacteria. Nature Reviews Microbiology, 3(3), 214-224.
Right in the title: "alternatives to binary fission", where binary fission is taken to be the standard prokaryotic division strategy, and in the abstract:

Whereas most prokaryotes rely on binary fission for propagation, many species use alternative mechanisms, which include multiple offspring formation and budding, to reproduce

The same terminology is used for organelles in eukaryotes.
Mitosis itself also involves "fission", and though the term isn't used as often with eukaryotes it does come up in some cases, like in contrasting "fission yeast" (Schizosaccharomyces pombe) from "budding yeast" (Saccharomyces cerevisiae).
Terminology in biology isn't always strictly standardized. Standards tend to proliferate and language itself is not strict. In biology there is a tendency to conform with the terminology others have used in order to keep consistent in the scientific record in which publications build on previous work; there's little motivation to generate a new term to refer specifically to prokaryotic division if existing language used to describe it is sufficient. It's rare that there would be confusion between fission of multicellular organisms like echinoderms and fission in single cells, so there's no need for a separate term. If you're having trouble with your search results, you could try adding other keywords like "bacteria" or "prokaryote" to focus your results, or using excluded keywords with the minus sign, like:

"binary fission" -echinoderm

which on a search engine like Google to only return results without the word "echinoderm" in the result; testing that myself in a Google search only excludes about 10% of the total, though. If you're using Google, I wonder if you've also recently searched things about echinoderms and that's influencing your search results. You can try using another search engine that doesn't track your past like duckduckgo, or using Google's incognito mode to not use your history in your results.

I'm not sure that a discussion of search engines is relevant to your answer, and the specific context from the comments suggests the poster needs different advice. If he wishes to find English terms when his computer defaults to German he would be advised to use Firefox as a secondary web browser and set its primary language to English (while retaining German in a different primary browser). Then he is likely to see English terms. 2. He can search Wikipedia in German and then switch to the English version in the left column. I use these techniques with the various languages I work in.

I think your answer would be improved by a linguistic explanation of the meaning of the basic terms, "fission" and "binary fission", neither of which are Anglo-Saxon in origin. The Wikipedia article on the subject states "Binary fission means 'division into two'", and reference to dictionaries hardly extends the meaning of "fission" beyond "division".


text:
Is this a Enoki aka. velvet shank aka. Flammulina velutipes?
In December in southern Germany I found the following mushroom on a some remains of a tree. From what I read, saw and felt (sticky cap when wet), I am very sure it is a velvet shank, especially because in winter there are not many other types of mushrooms around to be confused with. However I would like to know if someone can confirm/debunk my assumption?

Please don't rely on any identification help given here to decide whether you should eat a mushroom you found.

I would agree with your identification of Flammulina velutipes based on the description in Mushrooms Demystified (David Arora, 1986) and the page on MushroomExpert.Com (Michael Kuo, 2013). Arora emphasizes the viscid yellow-orange to brownish cap, velvety dark-brown stalk, lack of a veil, white spores, and growth habit as diagnostic characteristics. Take a spore print and note the texture of the stem next time you come across them as additional tests. If the substrate is not too decomposed, also note if it is growing on a hardwood or softwood (F. velutipes only grows on hardwoods).

Fig. 1. Flammulina velutipes. source: MushroomExpert
I'm not familiar with European mushrooms, so I don't know if there are look-alikes where you are, but this mushroom does grow in Germany (see map at MushroomExpert).
And of course, heed Bryan Krause's advice.


text:
The evolutionary advantage of sending the most fearless to the front
Let species A be prey to another species B. Assume that predators B only attack isolated individuals A (because they are afraid of larger groups of A's). So it is good for species A to be on the way in rather dense herds, flocks, or swarms. But individuals A which find themselves isolated (which happens every now and then) are well adviced to flee when a predator is in sight. So there are two antagonstic tendencies in individuals A: to flee or not to flee when a predator comes into sight. To flee as a herd, flock, or swarm should keep it together, so it's best to flee into the same direction as one's neighbours. Nevertheless single individuals will become isolated and be easier catch for the predator, so for the species (herd, flock, or swarm) it is best not to flee at all.
This can be advanced when the individuals with the least tendency to flee (the most fearless ones) are at the outside border of the herd. So it would be an evolutionary advantage of the species when the most fearless individuals come to be at the border of the herd - by own initiative or being pushed by the others.
I wonder if there have been investigations of this: Are there species of which it is known that (and how) the most fearless individuals are at the border of their herds, flocks, or swarms?

This is how the investigation could go:

Are there the same individuals at the border of the herd more often than not?
Do they start fleeing at a smaller rate than other indivuduals which happen to be at the border?
Why are they at the border? Is it because the others tend to go away from the border, into the center of the herd?

Note that my question is not for the strongest individuals but for the most fearless. (I know the case of the muskox and its typical defense formation.) There may be species with no extraordinally strong, but with extraordinally fearless individuals - which is another case.

Species evolve, but individuals are selected. Simplifying a bit, a species evolves as relative allele frequencies change in the population. When natural selection is at play, these changes in allele frequencies come about because individuals are more effective at transmitting their genes to offspring compared to others of the species. If individuals with a particular allele P reproduce more than individuals with a different allele Q, there will be a bigger ratio of P:Q alleles in subsequent generations.

So it would be an evolutionary advantage of the species

is not the sort of question you should ask, because advantages of the species don't affect allele ratios within the species. If there is a "fearless allele" F that causes individuals with that allele to occupy the outside of the herd, and a fearful allele G that causes individuals with the allele to group up and occupy the inside of the herd, and this reduces predation of the herd equally, then the ratio of F:G stays the same. If, on the other hand, those fearless animals on the outside of the herd are at higher risk for being on the outside (remember that fighting in nature is very dangerous; you don't have to lose the fight to die, as an injury that makes you slower, more susceptible to infection, interferes with eating, etc, still prevents you from reproducing in the future, even if you kill the predator and save the day), you can expect that the ratio of F:G will decrease: there will be more G alleles in the future generations. This is the basis of selfish herd theory
Herd behavior is fairly well-studied and doesn't really result from the antagonism you mention (flee vs not flee/stay as a group) but rather from aggregating sets of individual selfish rules like trying to be at the center of a group of conspecifics.
The exception to this is group selection, which is when selection acts on whole groups. In this case, instead of thinking of selection by individuals you might think of different herds. If herds with a higher percentage of F alleles reproduce better than herds with a higher percentage of G alleles, then there could be selection in favor of F across herds. However, the features that promote selection of this type can still be thought of at an individual level and this helps to reveal the features of groups that promote selection. For example, if the F allele promotes aggression against predators specifically in adults, or perhaps specifically in adult males, and the animals live in small groups of related individuals, then individuals with the F allele may have better reproductive success due to improved survival of their offspring, and those offspring are also more likely to have the F allele than offspring of parents without F, so the frequency of F increases.
In summary, think of the advantages that a trait like this provides the individuals with the trait, rather than the group as a whole. If you're looking for species where certain individuals defend the borders of their groups, you want to look for species that live in familial groups, where related individuals benefit the most from this behavior. Examples where you might find this would be in species like elephants (smaller family groups) rather than species like wildebeest (very large groups of only distantly related individuals).

Thanks a lot for this instructive answer! But what about alleles that allow individuals to become or better: to learn to become more fearless? Not all individuals that have them will necessarily become fearless, but due to circumstances some of them do. (The predecessor species without the allel may have had only fearful individuals.)

@Hans-PeterStricker You'd think about it exactly the same way: if an allele "allowing an individual to become more fearless" causes there to be more instances of that allele in the next generation relative to other alleles, it is being selected for and you can expect its frequency to increase in the population. If that allele causes some individuals possessing it to behave in riskier ways for that individual and therefore not reproduce as well on average (for example, because they are more likely to die of injury) you'd expect it to be selected against.

The only difference is that you'd expect the rate of change in the population (in either direction) to be slower if only some individuals with the gene express the trait.


text:
Looking for literature on hand-head movement coordination (not hand-eye)
sports scientists and kinesiologists, I'm a linguist working on sign languages and I'm looking for papers that discuss motor coordination of hand and head movements and potential constraints on such parallel movements (not hand-eye coordination, there's plenty of papers out there on that topic). In particular, I care about combinations of a repeated headshake and small, repeated twisting movements of wrist, as they occur in this sign in German Sign Language: https://www.sign-lang.uni-hamburg.de/.../type18133_de.html. Or head nods combined with a 'no' side-to side gesture of the dominant hand. Does anybody have clues as to why such movements might be difficult to combine? I'd be so grateful for any pointers!

consider also SE Medical Sciences, https://medicalsciences.stackexchange.com/, and maybe also fitness https://fitness.stackexchange.com/. If you do cross-post, make sure that you link each question to each other post to make it clear that you've posted in multiple places.

@MaximilianPress The guidance on cross-posting is that unless each post can be specifically tailored for the target site such that they aren't quite the same question anymore, the poster should choose one site for their question to live on, rather than posting in multiple places. It's fine to delete a question on one site to post it on another if OP changes their mind about the most appropriate venue.


text:
Is the nervous message sent by an eyelash being flexed sent all the way to the brain?
Since the reflex to close the eyelid once an eyelash is touched seems very fast, does the signal from the neuron detecting the touching travel all the way to the brain, get processed then back to the eyelid muscle?
Or does it have some kind of bypass that activates the eyelid muscle right away as some sort of reflex mechanism?

I don't think any reflex is controlled by the brain. Then again, I guess it might not be the case for something near the eyes since other reflexes tend to go through the spine's grey matter and the eyelashes obviously don't.

Welcome to Biology.SE. This is not simply an answer site, but instead a site that promotes self-learning with some expert help. Consequently, questions that show little or no prior research effort are off-topic on this site. 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. Please take the [tour] and consult the [help] starting with [ask] for details.


text:
Can SARS-COV2 strain competition be modelled by inter-species lotka volterra equations?
Currently studying infectious diseases epidemiology and never studied ecology. But I was wondering if the interspecies Lotka Volterra equations could model and explain strain dominance.
r = could be the effective reproductive number of the virus;
x = prevalence of people currently infected with a certain strain;
alpha = formally is the inhibitive effect of species one on species two; Here I think they'd be equal to each other. if a strain infects someone, he or she cannot be infected by the other competing strain.
Finally K, which is in the ecological context, the carrying capacity defined as the maximum number of individuals of that species the ecosystem is able to accommodate, where the number of births is equal to that of deaths so for this case it may be defined as the prevalence of the strain where the number of infected individuals remain at an equilibrium i.e. every infected person infects, on average, one other person so the effective reproductive number = 1.
So for instance Omicron and Delta in the UK.
where it took omicron only one month to supplant delta as the dominant strain.

https://www.frontiersin.org/articles/10.3389/fmicb.2020.572487/full

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In addition, note that "if a strain infects someone, he or she cannot be infected by the other competing strain" is unlikely to be true — one of the ways that viruses change occurs when different viruses infect the same cell. If you have evidence that this can't happen for coronaviruses, please add that to your question.

@tyersome its more parsimonious to assume that active infection with a particular strain will constrain another strain from establishing infection when exposed, given that the innate immune response is heightened making the respiratory tract inhospitable. And besides as far as we know human coronaviruses do not undergo antigenic drift. So what i really meant was once a person is infected and becomes symptomatic, they will not be able to be infected with the competing strain until the person becomes susceptible to the competing strain again (because of cross protection)

From everything I’ve read about SARS-CoV-2, it absolutely has experienced antigenic drift throughout the pandemic. Of course, the sensitivity of an existing immune response (or priming due to vaccine or a prior infection) to that drift is still an area of research. That said, the degree of vaccine escape by omicron (along with the many mutations relative to past variants) implies some amount of antigenic drift.

@Greenstick sorry I meant to say antigenic SHIFT not drift. Because tyersome was implying that coinfection of the same cell could produce genetically distinct strains, which is the definitely the case with flu but not so with human coronaviruses.

FWIW, coronaviruses can recombine too, just not in the same way as influenza.

Presumably by "interspecies Lotka-Volterra equations" you mean the L-V competition equations (the predator-prey version is much better known).
Let's start with a two-strain epidemiological model without coinfection, i.e. a host can only be infected by one strain at a time:
$$
\begin{split}
S' & = S (-\beta_1 I_1 + \beta_2 I_2) \\
I_1' & = \beta_1 S I_1 - \gamma_1 I_1 \\
I_2' & = \beta_2 S I_2 - \gamma_2 I_2 \\
R' & = \gamma_1 I_1 + \gamma_2 I_2
\end{split}
$$
This doesn't look like the L-V competition equations, which reach some sort of competitive equilibrium, because there is no renewal of the "resource" (in this case, susceptible people); the epidemic runs its course and dies out. However, we could allow waning immunity and make an SIRS model so that the recovered people eventually become susceptible again:
$$
\begin{split}
S' & = S (-\beta_1 I_1 + \beta_2 I_2) + \phi R \\
R' & = \gamma_1 I_1 + \gamma_2 I_2 - \phi R
\end{split}
$$
(the $I$ equations stay the same). This is getting closer, but still doesn't quite match the LV equations. We have to take one more step (which is actually away from the direction of a realistic COVID-19 model) and allow recovering people to become susceptible immediately (i.e. no immunity, as in a disease like gonorrhea), so that we get:
$$
\begin{split}
S' & = S (-\beta_1 I_1 + \beta_2 I_2) + \gamma_1 I1 + \gamma_2 I_2 \\
I_1' & = \beta_1 S I_1 - \gamma_1 I_1 \\
I_2' & = \beta_2 S I_2 - \gamma_2 I_2 \\
\end{split}
$$
This is an "SIS" model. In the SIS and SIRS models the population size is constant, so in particular for the SIS model we can write $S = N -  I_1 - I_2$ and drop the redundant $S$ equation so we get
$$
\begin{split}
I_1' & = \beta_1 (N - I_1 - I_2) I_1 - \gamma_1 I_1 \\
I_2' & = \beta_2 (N - I_1 - I_2) I_2 - \gamma_2 I_2 \\
\end{split}
$$
which we can rearrange to
$$
I_1' = (\beta_1 N - \gamma_1) I_1  - \beta_1 I_1^2 - \beta_1 I_1 I_2
$$
and a symmetric equation (exchanging $_1$ and $_2$ subscripts) for $I_2$. We can rewrite this as
$$
I_1' = (\beta_1N-\gamma_1) I_1 \left( 1 - \frac{I_1 + I_2}{N-\gamma_1/\beta_1}\right)
$$
Comparing this with  (one particular parameterization of) the L-V competition equations,
$$
N_1' = r_1 \left( 1 - \frac{N_1 + \alpha_{21} N_2}{K_1} \right)
$$
We see that these are equivalent with $r_1 \equiv \beta_1 N - \gamma_1$, $K_1 = N-\gamma_1/\beta_1$, $\alpha_{21} = 1$.
A few general comments:

a lot of your guesses are right. For this case the two strains are equivalent (each occupies one unit of "resource", i.e. one susceptible host), so $\alpha_{12} = \alpha_{21} = 1$.
the r in the L-V equations is a growth rate (i.e. rate of exponential increase when rare), not a growth multiplier per generation ($R$ or ${\cal R}$), so it's $\beta N - \gamma$ (with units of 1/time) rather than $\beta N/\gamma$ (unitless)
The carrying capacity is indeed the number of hosts infected by $I_1$ at a monoculture equilibrium, i.e. $N ( 1- 1/{\cal R}_{0,1})$
in order to have a usefully realistic model of COVID-19 competition, you would probably need some of the following:

go back to a short time scale and forget about the detailed equivalence with the L-V model
allow for imperfect cross-immunity, i.e. one of omicron's big advantages is that it appears to be able to reinfect people who have recovered from delta while the converse seems less likely (although that is much less well known)

the assumption of no co-infection seems like a reasonable simplification, given that the prevalence (fraction of the population infected) is low relative to the population size even at the peak of a COVID-19 spike (i.e., a small percentage of the population has an active infection)

Wow, thank you! I wonder if there is an established field devoted to modelling infectious diseases epidemiology as ecological phenomena, I am defnintely interested to dig deeper! Thank you again for the answer!

There are very close connections between ecological and epidemiological modeling. For example, Robert May https://en.wikipedia.org/wiki/Robert_May,_Baron_May_of_Oxford was both a theoretical ecologist and an  eminent epidemiological modeler. One other example: Martcheva, Maia, Benjamin M Bolker, and Robert D Holt. “Vaccine-Induced Pathogen Strain Replacement: What Are the Mechanisms?” Journal of the Royal Society Interface 5, no. 18 (January 6, 2008): 3–13. https://doi.org/10.1098/rsif.2007.0236.

I'm wondering now why strictly adhering to the L-V model would not result in a useful/realistic COVID-19 model for predicting strain competition. Is it because of practical factors such as vaccination and lockdowns (and other interventions) or is it inherent to the model itself?

The most unrealistic aspect is that it assumes there is no natural immunity after recovery.


text:
mRNA vaccines: Can a spike protein by itself have different side-effects than the virus itself?
I was wondering, is it possible for the isolated spike protein, as resulting from an mRNA vaccine, to cause harmful side effects in an individual, that would not have developed in that individual if it had been exposed to the actual virus? I am wondering about the spike protein in particular, i.e. I am specifically excluding any other compounds contained in a vaccine, but I would include "side-effects" caused by the spike protein of the actual virus.
The only way I could imagine this to be the case, if by being isolated and this being quite a lot smaller compared to a whole virus, the protein could find its way into areas of the body where it could "fit" otherwise.
Am I correct in assuming that the side effects that had been observed so far for these vaccines could be explained by an individuals immune reaction, rather than the spike protein itself?

In both infection by the virus and mRNA-mediated expression of the spike protein, spike proteins are produced in the host cell as membrane-bound proteins; they're not just separate particles floating around. Whether or not the rest of the viral machinery is present, these will end up displayed in the membrane of the infected cells. Here's a diagram showing that process in infection (note the little "blue spikes" in the cell membrane at the far right):

Figure from Duan, L., Zheng, Q., Zhang, H., Niu, Y., Lou, Y., & Wang, H. (2020). The SARS-CoV-2 spike glycoprotein biosynthesis, structure, function, and antigenicity: Implications for the design of spike-based vaccine immunogens. Frontiers in immunology, 11, 2593.
B-cells will recognize these foreign antigens, again whether their production was initiated by the virus or by a vaccine (here the equivalent of the "blue spikes" in the first figure are the "green S protein"):

Figure from Teijaro, J. R., & Farber, D. L. (2021). COVID-19 vaccines: modes of immune activation and future challenges. Nature Reviews Immunology, 21(4), 195-197.
(note: don't be fooled by the separate mRNA and AdV vaccine strategies here; the outcomes and mechanisms are the same, the diagram is just condensed to show both in one figure)
With mRNA vaccines, production of spike proteins is limited in time and space: to the cells that take up the injected mRNA, and only until that mRNA is degraded.
With normal infection, production of spike proteins is only limited by the course of the infection: as long as the virus continues to replicate, spike proteins will be produced in the membranes of affected cells, and can be produced anywhere in the body that the virus spreads (though principally in the respiratory compartments where the virus preferentially infects).


text:
Does Thymoquinone give cedar its distinctive smell?
What chemical gives cedar wood its distinctive smell? Is it the same that gives Nigella sativa its cedar-like smell?

Schreiner, Linda et al., “What Does Wood Smell like? Characterization of Odorants in Wood,” accessed January 7, 2022, DOI: 10.3217/978-3-85125-593-5-82.

mentions Thymoquinone, "known to be the major compound in black cumin seed (Nigella sativa)", which is also in incense cedar, but is Thymoquinone the primary chemical giving cedar its distinctive smell?

@tyersome I've added my research, focused the question to be about Thymoquinone.

Unfortunately, no time to write up an answer or research further. But see Odor-active constituents of Cedrus atlantica wood essential oil which attributes THE ODOUR of cedar wood to vestitenone and 4-acetyl-1-methylcyclohexene but also contains the sentence "The composition of Cedrus atlantica essential oil is generally dominated by alpha- and beta-himachalenes" (emphasis mine) which seems to agree with what is written here.  To my mind, the Phyochemistry article looks good


text:
What is the purpose of interkinetic nuclear migration during neurogenesis?
I am reading about neurogenesis and I am learning about the different types of neural stem and progenitor cells (neuroepithelial cells, radial glial cells and basal progenitors). I have read that these cells exhibit  interkinetic nuclear migration.
For example in neuroepithelial cells, the nucleus migrates to the basal side during G1 phase, is at the basal side during S phase, migrates back to the apical side during G2 phase, with mitosis occuring at the apical surface.
I am wondering if there is a clear purpose for interkinetic nuclear migration during neurogenesis? From some papers that I have read about the topic, it seems to me that the exact reason why this occurs in cells during neurogenesis is unknown, even though the molecules that are involved in the process have been identified.
Thanks.


text:
Why isn't speciation a negative feedback loop?
To rephrase my question more articulately:
Speciation begins when two groups within a species starts to become reproductively isolated, and is complete when the two groups can't interbreed (for the purposes of this discussion). But then how is this possible when any time a reproductively-isolating mutation occurs in a member of that group, the member carrying that mutation could no longer breed with the other members? Therefore, speciation is theoretically a negative feedback loop. In this context, how does speciation occur?
One of the mechanisms documented by James Patton is chromosome evolution, where changes in chromosome number and shape occurred in pocket mouse and reproductively isolated the different species-complex (https://www.jstor.org/stable/2406859). But then the question still remains that the first mouse to have a different number of chromosomes would not be able to have offsprings because there are no other members with the same number of chromosomes as it does.
unless the genetics of reproductive isolation is continuous i.e. a gentically reproductively-isolated member of a species could
A. mate and have offspring with the general population but with greater cost, for instance, hybrid offspring could be at higher risk of dying in utero or be at higher risk of becoming sterile.
B. hybrid offspring, will go on to produce more offspring, still at higher cost, unless they do so with each other AND with the general population. creating a subpopulation that mates more successfully (i.e. at lower cost) with each other than with the general population.
But I have not found any articles saying reproductive-isolation is continuous rather than binary.

Most things in biology are continuous. Sometimes they appear to be binary due to thresholds, but it's rarely true. I would suggest reading some more about the genetics of speciation, e.g. https://www.sciencedirect.com/science/article/pii/S0960982206026649. Incomplete reproductive isolation is quite common; for example, there are various examples where offspring are sterile when male but fertile when female (e.g. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2776091/). Also remember that genetics can act indirectly through behavior, which is notoriously sloppy. Or simple geographic isolation!

Concerning the continuous vs. binary question with regards to speciation, I think the concept of Ring Species may be enlightening

This is getting clearer, but is still very awkwardly worded. ——— In addition, there is an expectation that users will do research before posting, so I encourage you to check out some of the online resources available for learning more about evolution. For example, this a useful introduction to evolutionary theory from UC Berkeley.

I'd suggest looking at this article, which contains an intuitive model for how hybrid incompatibilities can arise between isolated sister taxa (i.e. populations). This criterion of pre-existing isolation is an important factor in most models.
I think that one thing that is missing from your representation of speciation is that you are assuming that every organism in a species is in one big population. This is not true. Isolation by distance is one of the simplest ways that isolation can happen.
For example, Bateson-Dobzhansky-Muller incompatibilities arise when two isolated populations of the same species each have diverged in two genes. Each change is harmless on its own, but when you put divergent allele from gene 1 from population 1 together with divergent allele from gene 2 from population 2 together, suddenly you get hybrid sterility or lethality.
Of course, the divergent alleles of gene 1 and gene 2 can't arise in the same population, for reasons you point out. Incompatibility can only evolve when these two divergent alleles arise in different populations of the same species.
For a simple isolation by distance model, imagine a river with snails (or whatever) in it. The snails at the headwaters interbreed a little with snails just downstream. Those just-downstream snails interbreed a little with headwaters snails, and also a little with the snails just downstream from them. But by the time you get to the mouth of the river, the connection between the headwater and the mouth-of-river snails is very tenuous. Now, how much of a problem is an incompatibility between headwater and mouth-of-river snails?

Thank you! This made so much sense. Are hybrid incompatibilities the main driver of genetic isolation or are there other equally common mechanisms?

@AnethOthbo I think that part of my argument- which perhaps I should be clearer about- is that reproductive/genetic isolation can be achieved by many mechanisms. Probably the simplest mechanism is geography: if two people live on different continents all their lives, they will never meet and have children. If what you are interested in is cytological/molecular mechanisms of isolation, then yes, hybrid incompatibility is probably the big one.

This isn't a complete or exclusive answer, but inversions can contribute heavily to reproductive isolation.  A crossover within the region inverted in one homologous chromosome of a hybrid, but not the other, will typically mean one end of the chromosome is absent in the offspring, which is generally not a good idea.
Nonetheless, within the same species it is possible to have an inversion polymorphism taking up most of a chromosome.  This means that you have a species which exchanges genetic material normally within most of its genome, but is divided into somewhat isolated populations in terms of that one region.  (The barrier is not watertight, especially with such a large inversion, because a gamete produced by two crossovers within the inversion is perfectly normal)
This review discusses more about the general evolution of inversions and their role in speciation.  (I pulled it out at random; there has been quite a bit published on the topic)

While I certainly agree that inversions are an important example of an isolating molecular change, I think that the OP is asking more about how a reproductively isolating variant (such as an inversion) can arise, if it contributes to isolation- e.g. more of a theoretical and less of a cytological question. That said, your linked Kirkpatrick (2010) reference provides some helpful answers that might be worth highlighting: 1) superiority of inversion heterozygotes, 2) meiotic drive of inversions.


text:
Do bacteria duplicate the copied virus DNA to put into a Cas9 protein when fighting the virus off again?
When bacteria insert a part of invading virus DNA into its own genetic sequence, on the 2nd invasion does it duplicate that copied DNA again from wherever the bacteria placed it and put it into a Cas9 protein to search for the invading virus.

Virus invades bacteria.

Bacteria copies portion of virus DNA into its own genetic makeup. (Gains immunity)

Virus attacks attack a further point in time down the line.

So does the bacteria then copy that portion of bacteria that it had copied in the past to put into the Cas9 protein? Or does it temporarily remove the virus DNA to go fight off the virus again, to later reinsert the virus DNA back into its own genome?

Please clarify your specific problem or provide additional details to highlight exactly what you need. As it's currently written, it's hard to tell exactly what you're asking.

So does the bacteria then copy that portion of bacteria that it had copied in the past to put into the Cas9 protein?

The DNA is not copied, but rather transcribed. The captured piece of viral DNA (called a spacer) is transcribed into a guide RNA that is incorporated into the Cas9 protein to make an active Cas9 complex.


text:
What are the different factors involved in ageing?
This is a big edit of the previous question
Thanks to first comments and answers of the previous question, here is a more specific question:
An organism faces ageing. This ageing is linked with differentiated stem cells, who are not able to duplicate indefinitely. They reached an Hayflick limit. At some point, the lack of stem cells able to duplicate correctly enters the degradation of the organism.
Now, given this information, my documentation showed factors of ageing:

Loss of Telomere during replication: At each replication, the lack of telomeras enzyma in a differentiated stem cell triggers the loss of some of the telomere. At the moment all the telomere is lost (when the number of duplication reaches the Hayflick limit), the cell enters senescense.

What are other factors that involve in the ageing of an organism? I'm specifically interested in:

Factors linked to the organism behaviour

Not in:

Factors linked to agression (this part would be too important)

In Factors linked to the organisme behaviour, could be identified:

Skeleton degradation: do degradations of skeleton exist and how do the body take care of the skeleton?
Muscular degradation: musculare degradation does not seem to occur as long as minimal physical effort is done
Healing: this is not a complete repair-process, as healing often leaves marks: what is the reason of such partial achievement?

EDIT
One more question: Is the theory of gene-based ageing based on some specific genes, or only on the alteration of DNA by external causes (radiations, raidcals...)?

Please clarify your specific problem or provide additional details to highlight exactly what you need. As it's currently written, it's hard to tell exactly what you're asking.

Please only ask one question at a time, and read the Help to find out what types of questions are acceptable here. Those regarding hypothetical situations are not, and medical rather than biological questions are more suited to SE Medical Sciences.

Sort of a "catch 22" ; anyone over 90 has some compromised health condition. And tradition is to put some cause on the death certificate other than "old".

@blacksmith37 But then why do anyone over 90 has compromised health condition?
David I understand the rule but I asked one question. The side question is only there for understanding of what I am asking

It's not really possible to answer this question the way you phrased it. Nothing on this earth is immune to physical wear and tear. A tractor can't get sick, yet it won't run forever if fuel is supplied. Much of the pathology in old age is simply the result of some kind of "wear and tear" (e.g. atherosclerosis.) If there was no wear and tear  of any kind (which is impossible), sure, anything could last forever.

@anongoodnurse But how does wear and tear come? Because a tractor is worn outby friction and temperature changes, but if you change the spare parts it will be functionnal forever. And our body produces by itself its spare parts (it produces new cells all the time)

No, you can't change out worn tractor parts, that's evading the issue. The body does not make "spare parts". You can't grow a new heart or new kidneys. There is friction in blood vessels from blood rushing by. You can't escape Physics, and I don't want to argue. Reading will serve you better than arguing.

@anongoodnurse Please calm down I am not arguing, I am trying to understand the concepts and physical laws behind ageing: is it some sort of entropy?

From the [help/dont-ask], If your motivation for asking the question is “I would like to participate in a discussion about ______”, then you should not be asking here. Please familiarize yourself with how this site works by taking the [tour] and then reading through the [help] pages starting with [ask].

@tyersome Please don't put your own appreciation on my question like that: I am asking a question, I got partial answers so I ask for details. This is not a discussion.

@tyersome About your comment and to people saying it's a stupid question, I would like to highlight that Calico Labs work on that since 2013. So this is at least a plausible subject, thus a question on that subject is not stupied

I see no comments saying this is a "stupid question" — it is however poorly written. Some examples: you ramble over multiple subjects, include irrelevant details, and use made up words (e.g. elderness — that is why it was underlined in red when you typed it in). You are also expected to demonstrate that you have done some background research before posting. If you want a positive response, I suggest reading through the [help], doing some research (document this with citations to reliable sources), and then rewriting (make sure your edits address the feedback you already got).

I’m voting to close this question because it has multiple problems (documented in comments from multiple users) including multiple questions, no evidence of prior research, and being likely to generate opinion/discussion. Despite community input poster has not attempted to make improvement.

@tyersome To be honest I have only got input as "question does not apply" and that's it

@totalMongot I think the biggest issue is that it seems to be mostly an invitation for discussion, rather than a specific, answerable question. That doesn't make it a bad or stupid question, it's just that its more of a discussion/philosophical question rather than a biological one. The philosophical part is about proximate/distal causes and which to emphasize. Any level of explanation is defensible; which level is "best" is an opinion.

I voted to close this question, so it is clear that I do not condone it. However I feel that one should show a little simple kindness to posters whose first language is not English and help improve their questions and their fluency, by correcting questions. Poster: Note 1. that in English we talk about "ageing" (the process) and "old age" (the condition) — "elderliness" exists only in dictionaries. 2. Your use of pathology is incorrect. I am not an expert on medical terms, but in general speech you do not suffer from a pathology, but a disease, a broken ankle etc. 3. Try to keep it simple.

@David THank you for th input, I edited the question also for the other issues (too broad, opinion based..)

Edit added to the question to focus on the different parts of the body that suffers from degradation

Another rephrasing of the question could be :
"are humans potentially immortal?"
which we (as eukaryotes) are not, because of the end replication problem in DNA polymerase activity- due to the unidirectional nature of DNA synthesis. During semiconservative replication the end of the lagging strand  (3'-end) of the DNA is not possible to synthesise by polimerase δ (POLD1, POLD2, POLD3, POLD4), which  discontinuously synthesizes approximately 150 to 200 base pairs long okazaki fragments in 5'-3' direction (DNA-POL δ always moves in 3'-5'over the template, but the template for the lagging strand is 5'-3' itself). This causes periodic breaks in polymerisation, and the reattachment needs RNA-primers to be present.
The last RNA primer at the 3' end of the DNA sits at a distance of about 70-100 bp to the very 3' end of the DNA, therefore about 50- 100 bp of DNA length is lost every cell division. (see http://genesdev.cshlp.org/content/26/11/1167)
To not loose coding (Exons) nor regulatory (Introns,etc) DNA sequences, telomere are present at the end of the DNA. They are repeat sequences of TTAGGG in vertebrates that loop to protect the terminal regions of chromosomal DNA from progressive degradation and other false altercation.
However since these telomere get shorter in somatic cells every division cycle , you could argue humans have a natural "due date". Luckily the germline is potentially immortal due to the activity of a reverse transcriptase-enzyme Telomerase, that elongates telomere; badly its also active in most cancer cells.
Telomere where discovered by Barbara McClintock who was who was awarded the 1983 Nobel Prize in Physiology.

I think it's a mistake to overly associate telomeres with aging of organisms rather than aging of cells.

Thanks for the answer but I don't really understand : in the beginning you say "we are not immortal as eucaryote" (which means? sorry I 'm not good at biology ^^) and in the end you say that we are potentially immortal thanks to telomere?
@BryanKrause Interesting, are elderness diseases linked to organism aging or cells aging?

@totalMongot Well, by the contrast I'm making by definition elderness diseases are a part of organism aging. It's just that this answer conflates that with telomeres which have some role in limiting how many times cells divide, it's just overly simplistic to think that's the specific process behind aging of an organism.

So if I understand correctly, the problem in the process you described is cancer?

I found in some article  (I doubt of them BTW) that telomere shortening might also affect stem cells: is it true?
https://novoslabs.com/causes-of-aging-stem-cell-exhaustion/

Hello, could you please gives more hindsight about the specificity of eucaryote that makes us vulnerable to the end replication problem in DNA, compared to others? Is it because non-eucaryot organisms do not have DNA (because no nucleus in cell)?

Of course the have DNA!


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Does COVID interfere with internal respiration?
Siddiqi et al. wrote in January 2021,

Pulmonary ECs [= endothelial cells, in this paper] have an important role in immune surveillance, maintaining alveolar integrity and ensuring appropriate oxygen exchange. In COVID-19, direct viral infection and the systemic inflammatory response likely lead to severe dysfunction of these important ECs, compounding the resulting picture of severe hypoxia and acute respiratory distress syndrome frequently reported in hospitalized patients.

Question: does COVID infection of other endothelial cells interfere with internal respiration (oxygen and/or possibly CO2 exchange at the destination tissues)?

I find some of the responses confusing.  The quoted text says that pulmonary endothelial cells have a role in ensuring appropriate oxygen exchange - this is no surprise since the oxygen passes through the cells.  "Oxygen permeability" refers to how well the oxygen passes through the cells.  "Internal respiration" is the anatomical term for the exchange of gases at the systemic capillaries.  The mechanism of action, as stated in the quote, is a combination of direct viral infection and systemic inflammatory response - I expect more the latter.  Whether COVID infects the endothelial cell directly, affects a neighboring cell, or causes differences in serum cytokines that affect the endothelial cells, all I was wondering is whether as a whole, the wall of an infected person's systemic capillary would diffuse oxygen more slowly.

I just took a peek your reference. The likelihood of the answer being there in the paper is quite high. Look at Fig. 1.

I looked again ... in that figure they discuss thrombosis and vasoplegia, but not whether the permeability of the cells to oxygen changes.

I'm sorry to ask, but what does "permeability" mean to you? Or, for that matter, "respiration"? Because I'm not sure I understand your question without understanding your definitions, which seem vaguely to shift. To me, it's obvious that thrombosis (as a result of vascular epithelial cell damage) will injure cells distally, which of course is from oxygen deprivation. Whether a cell is permeable to O2 is irrelevant if there's no O2 around.

https://en.wikipedia.org/wiki/Respiration_(physiology)

Wikipedia doesn't cover internal respiration there - see https://open.oregonstate.education/aandp/chapter/22-4-gas-exchange/ .  We tend to take gas exchange across an endothelium for granted, because that's what it's for, but membrane cholesterol, glycocalyx, permeability and thickness affect how well it works.  I don't know if COVID affects it (putting any perfusion issues aside).

May I suggest you read more about the mechanism of action of the virus and how it causes cell (and organ) damage? Your questions show some inconsistencies in definitions and certainly the action of the virus.


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Meaning of "acute LSD"
I am currently reading this research paper: https://www.nature.com/articles/1395848, and I'm confused by this line: "Serotonin Receptor mRNA Levels Are Unchanged by Acute LSD".
What is the exact meaning of this sentence? I could probably understand it as "immediate", that it doesn't pertain to long-term effect instead of short-term.

In the abstract they refer to "acute LSD administration" (emphasis mine), and in the next section of the results after the one you mention in your question, they clarify it as "Acute LSD administration (1.0 mg/kg, 90 min)".
(That seems like an awful lot to me, as I understand typical recreational doses for humans are in the tens to hundreds of micrograms range.)

Thanks for the answer! Just realized it now. 1.0 mg by itself is a lot, not even talking about 1.0 mg/kg.

@TimotejLeginus Though these are rats so 1 mg/kg is probably about a 0.2-0.3 mg dose (the paper probably gives specific mass ranges for their animals but I'm just going by my memory of common sizes). Still a lot.

@TimotejLeginus Just a small addition: the term acute generally means that a phenomenon/effect lasts for a short time period, in contrast to chronic which refers to a phenomenon that continues over a long period. This doesn't mean long term responses. There can be long term effects of an acute phenomenon.

thanks for the explanation! well I wasn't so sure about that, haven't found it anywhere, so I had to ask :)


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What is the true response of human photoreceptors to different wavelengths? Why is there so much disagreement in the literature?
I can find several qualitatively different diagrams of the responsiveness of human cones and rods to different wavelengths of light.
A page referencing Bowmaker and Dartnall, 1980 has the following diagram (which indeed matches that from their paper):

Very similar plots (with the same truncation for M and L cones, and the same slight rise in sensitivity at shorter wavelengths) can be found here.
For a graph with an even sharper nonmonotonicity of the L cone at blue wavelengths, see here.
On the other hand, some diagrams show much more mountain-shaped response curves, like those derived from Stockman & Sharpe at this page (which produce for instance Wikipedia's graph):

Similar qualitative graphs can be seen in this figure, this one, or this one.
My vague impression is that the second category of graphs tends to come from more recent or reputable sources, but I'm very unsure about this, and in general I'm confused why there seems to be so much disagreement here. Are there good survey articles that discuss this discrepancy and the reasons for it?

The first one seems to indicate strong response into the ultraviolet - the discrepancy could be that the first is in-vitro, the second is with the lens in-place which blocks the ultraviolet. Can you clarify the conditions of measurement?

@ARogueAnt. It sounds like Bowmaker and Dartnall removed the lens: "The eye was dissected under dim red light (Kodak safelight no. 2). An equatorial section of the globe was made, and the anterior half lifted away. The vitreous body was then removed from the posterior half without disturbing the retina, and the remaining eye cup placed in ice-cold mammalian Ringer solution of pH 7 1." And I believe Stockman & Sharpe used live subjects, so that would seem to explain it.

That fits at least with the UV response. I'm not sure about the scaling though, I'll bow out.

It sounds like a issue with the precision of the graph. high precision graphs are not smooth curves

Welcome to Biology.SE. In the absence of units, some sort of internal standard, or any other way of meaningfully comparing these curves I would say it is impossible to make valid comparisons. Do any of these publications claim there are disagreements? If so, can you please provide a quotation and reference — if not, I think the "discrepancy" is probably illusory.

@tylersome I’m not sure of the exact units of absorbance used here, but so long as there is a consistent ordinal scale it’s still possible to meaningfully compare the two curves - for instance, the top curve shows a higher value for the L cone at 400nm than at 650nm, while the reverse is true in the bottom plot. This property is invariant under any monotonic scale for the y-axis or per-cone normalization. (Of course they could be measuring different things entirely, and not just using different scales for the same unit, which I would count as a satisfactory answer to the question.)


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vocalizations meaning for rats/mice
Rats (rattus norvegicus) vocalizations are said (in the literature) to have some positive or negative meaning, mostly 22kHz vs 50 to 80kHz. Some papers hints to nearly syllables, describing a number of different class of vocalizations depending on their spectrogram shapes.
Could we give any meaning to those "syllables" ? Couldnt find any specific answer.

What did you find during your research?

Welcome to Biology.SE. This is not simply an answer site, but instead a site that promotes self-learning with some expert help. Consequently, questions that show little or no prior research effort are off-topic on this site — saying you couldn't find an answer is not sufficient. 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. Please take the [tour] and consult the [help] starting with [ask] for details.

When searching, also try the term “DeepSqueak”. This delightfully named software is for analysing ultrasonic vocalisations.

Thanks you all for your comments. The thing is I have done a few year of academic research on the subject and where I state 'couldn't find any specific answer' I mean papers are only describing the USV but usually don't go as far as giving any meaning nor studying their occurrence in time mostly they correlate pitch with positive or negative behaviours / environement such as stress, eating ... and mostly with very young individuals


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Is there any meaningful ratio between the width of a vertebra and its height and depth?
Given the location (i.e. their entry points, but not their trajectories) of two pedicle screws, we are trying to come up with a way to approximate the sagittal distance of the vertebral foramen to the screws' entry points.
I.e. how far "down" (= towards the patient's belly) do you need to go from the screws' entry points until you're at the same height as the approximate center of the vertebral foramen?
And we're trying to do that for all vertebrae into which pedicle screws could reasonably be placed.
We don't know which screws are placed in the Traditional Trajectory (TT) and which are placed in the Cortical Bone Trajectory (CBT) but assume we can ask that, if necessary.
To further complicate the matter, we don't know anything about the patient (data protection). I.e. no age, sex, height, etc. that could help us estimate this.
We hope that we can somehow leverage the distance between the screws to get some rough estimate for the vertebra's height ("head-to-leg" direction) and depth ("belly-to-back" direction), but so far, I don't see how.
Is there any remotely useful ratio between the width of a vertebra and its height or depth?
And does it help at all if we know which vertebra it is (which we don't, but which we could ask, if necessary)?


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Are 'high-throughput' and 'large-scale' proteomics synonyms?
I wonder if 'high-throughput proteomics' and 'large-scale proteomics' are generally used synonymously? It would make sense to me to distinguish between 'high-throughput' as in a 'large number of samples' vs. 'large-scale' as in 'big samples with thousands and more of proteins'. However, I have not found any article on this so far and it seems to me that the community uses both terms interchangeably. Are there other terms commonly used to refer to these properties?

I often see the two terms used hand-in-hand, although I'd say they're not quite synonymous. Often the term high-throughput refers to the number of features being analyzed, with high-throughput methods quantifying many features in parallel. Because of the parallelization, the time needed to quantify all features is reduced, so you can process more samples in a fixed amount of time - the method has high throughput since many features/samples can be analyzed quickly. "High-throughput" typically refers to the technology being used to analyze a sample. Different proteomics technologies may be classified as high-throughput or not, regardless of how those technologies are applied.
Since a high-throughput method can process samples quickly and cheaply, it often goes hand-in-hand with large-scale analyses, which often refers to the number of samples (but sometimes the number of features) being processed. A "large-scale" analysis typically refers to the design of the experiment.
Older experiments were generally limited to small-scale by low-throughput technology, while high-throughput technology has enabled large-scale experiments. You could use a high-throughput technology to do a small-scale analysis, but it wouldn't leverage the power of high-throughput methods to run many samples in a short amount of time. Applying a high-throughput method to a single sample would be an example of such a case. You could also theoretically use a low-throughput technology to do a large-scale analysis, but it would take a very long time and be very costly, and would likely be infeasible without significant resources. Applying a low-throughput method to many samples would be an example, although this is not commonly seen in practice.
Usually you'd use a high-throughput method to achieve a large-scale analysis, which could not be feasibly achieved with a lower-throughput method. An experiment is often both high-throughput and large-scale so the terms are often seen together, but I'd say they have distinct connotations of referring to the technology and the overall experimental design, respectively.

That is a great summary of what I see in the literature as well. Most proteomics studies that I found use high-throughput to refer to numbers of features/proteins/peptides identified. Not so much regarding processing of samples in a short time.


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Is there any evidence ethylene (gas) has any detrimental impact on human health?
Is there any evidence ethylene (gas) has any detrimental impact on human health? The only thing I was able to find is that the IARC doesn't consider it a carcinogen. But carcinogenesis is not the only way a substance can afflict human health, is it? The ATSDR only has ethylene glycol and ethylene oxide. But maybe it's oxidized after being emitted so the latter is relevant, isn't it?


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why can you avoid onions making you cry either by protecting you eyes or your breath?
i was wandering why onion makes me cry when i'm cutting them, so i tried three different things :

first i tried cutting onions with swimming glasses, and it worked (i didn't cry)

then i tried cutting onions without breathing, and it worked too.

it doesn't makes sens to me ! it seems like the second experiment contradicts the first (and vice versa) : my eyes are not protected and yet i don't cry !

and finally, i tried with my nose obstructed, but breathing from my mouth, and it also worked

but i think that is just a variation on the second experimentation, which add an important precision : blocking breathing is not exactly the action that avoid tears, it's not breathing through the nose
i tried to read and understand this paper, but it's way above my capabilities
in the answers to this question, Why does cutting onions cause tears?, it's specified that the lachrymal gland can also be activated in the nose, but it doesn't explain why blocking one of the two way is enough ?

Holding one's breath while chopping onions won't prevent irritation; maybe not breathing results in less gas movement in general, but cutting the onion will cause air movement and eventually the lachrymatory factor will reach the eyes, so breath holding doesn't confer any protection against onions. As to your last question, what way are you referring to?

Does breathing increase the air flow (and onion fumes)  past the eyes?

@anongoodnurse well, try it, i works perfectly ;) it does prevent irritation. And not only for the first few seconds, but one whole minute each time. And i was speaking of the two ways that lachrymal gland can be activated : through the eyes and through the nose. Protecting eyes, or protecting breath.

about the air flow, my third test already covered this question : when i was blocking only my nose, i was breathing, so the air flow was "normal", but i didn't get any tears

I will try it next time I chop an onion, thanks! I'm old, but I can still learn some new tricks. But will you believe me if I report that it didn't help? Or if I tell you that the scientific literature doesn't support your experience? And it has been studied, both for reasons of curiosity and economics (to develop a "tearless" onion.)

well ;) i would have no reason not to believe you, and i would be glad to know ! but that wouldn't change the fact that it works for me :) and for some of my friends that where curious with me :) Actually one of my friends already observed this phenomenon, and as a biologist herself she has an hypothesis : if the lachrymal gland receives a contradictory message : irritating gaz from the eyes but not from the nose, or the opposite, the reaction doesn't start. It might differ among peoples ? i don't know how to verify this hypothesis anyway :/


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can mammalian expression vector be used in e coli to produce plasmid
I would like to use this plasmid (mammalian expression Flag-HA-USP53 (Plasmid #22606) - Addgene) to produce plasmid in e coli to purify plasmid. Would this work? I am starting out with this vector because it is already available and has the insert I need.

Short answer: Looking at the plasmid map, yes, this should work.
Long answer: It depends on the plasmid. To be able to replicate a plasmid in bacteria, you need a origin of replication (ori). To find out if this is present, have a look at the vector map provided by Addgene:

It shows the ori on the left side of the map. Additionally an antibiotic resistance gene is helpful to be able to select for bacterial cells whic have taken up the plasmid in the transformation, which is also present in form of the ampicillin resistance gene.
Generally speaking most expression plasmids will carry both feature since bacterial transformation, growth in culture and mini (or midi or maxi) prep it is by far the fastest, easiest and cheapest method to produce large amounts of plasmid.

To add to this, note that the linked Addgene page has a section titled "Growth in Bacteria" with specific instructions for growth temperature, strain, and selection

Thank you. Very helpful.


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Why does the body not develop immunity to rabies during the period of incubation?
Rabies typically has an incubation period of 20 to 60 days and most cases develop only after at least a month after the bite from the infected animal.
Nevertheless, rabies is nearly always fatal and the host seems to consistently fail to develop an effective immune response to the virus, even though it has been exposed to the virus for weeks or even months.
It generally is supposed that an immune response takes about 10-14 days to develop. In other words, if the body is presented with a novel viral pathogen, it takes 10-14 for the body to recognize the pathogen and begin making antibodies to defend against it. However, this does not seem to hold true in the case of rabies, which can be present and motive in the body for many weeks before causing fatal infection, yet the body still fails to mount an immune defense. Why is this?

I hate to ask, but what did you find on searching for an answer? There's a very simple reason that it's not like a lot of other viruses in terms of exposure and development of immunity. Incidentally, there are people in areas of high incidence of rabies who have developed antibodies without known exposure. The mechanism for this is unclear.

@anongoodnurse My research was to read the chapter on Rhabdoviruses and specifically the Lyssaviridae in Field's Virology. I didn't find any explanation there of why immune response does not develop.

Gosh, then I think you should read better sources... It's a really interesting virus, one I've spent a considerable amount of time reading about, and have had several personal encounters with. It's fascinating, really. There is suggestion in the literature that the longest incubation time recorded for the virus is 18 years! Can you imagine how well it hides from the body's immune system? I'd try Google if I didn't know.


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Anyone Know What This Is?
So I don't know much about plant structure or biology in general but I found this little guy while on  X10 and x40 lenses on our school microscope while looking at a leaf. I'm not sure if it's part of the leaf or if it's something that attached to it (I did find bits of filamentous algae on the leaf so it could be something aquatic?). I will provide both pictures and if I can, the videos I took of it. It has a spring shaped tail that seems to connect it to the edge of the leaf that's causing it to spring back rapidly after it moves out from the leaf.link to the pics shown as well as the videos taken at the same lens strengths as well as other stuff I found
EDIT: I am from Michigan, and based off of a lab that I'm doing today in the same class the plant is an Elodea, a freshwater aquatic plant. Don't know if that info helps any but hopefully it does!

Welcome lilgyz. Could you give us a bit more to go on such as what country/area you're living in, what type of plant was the leaf from, perhaps a picture of the whole leaf?

I'm from michigan. Unfortuantely I don't know what kind of plant it is nor did I get a picture of the plant but I can if I can figure out what plant it was


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How many of their caches do chickadees retrieve?
Chickadees are scatter-caching birds and I've heard they can hide as many as 10,000 seeds for retrieval over the winter. How many of these cached seeds actually end up getting used in a typical winter? And can the chickadee really remember all of the locations?

I'd guess about the same percentage as squirrels and their acorns, and yes, they remember where every one is hidden, but they have a hell of a time finding their car keys.


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What are these animals, and what happened here?
While walking along the northern shore of Lake Ontario, I noticed the following strange scene:

Here is a closer angle:

What are these animals, and what is the likeliest cause of this?

Oof! :'-(  Looks more like a raccoon to me. Seeing its head might help...

A picture under the fish's head would help as they could be entangled somehow - fishing line?

This question could focus more on species ID rather than CSI to avoid further close votes. Really interesting albeit disturbing scene though and thanks for asking :)

That's likely a raccoon and a dead fish (salmon, perhaps).
For the animal on the left: notice the ringed tail, foot anatomy, and lighter foot color, and variable (light/dark) fur color:

 University of Arizona

 Furbearer Conservation

 University of Nebraska-Lincoln Extension
Note: Since you mentioned opossums, I include the above to show the vast difference in foot anatomy between a raccoon and and opossum. An opossum's foot is also not white like that.
The fish, in my opinion, is too degraded to get an accurate ID. However, based on size, upper jaw size, and coloration (dark dorsal + tail fin with lighter belly), I think it's quite possible this is a salmon, of which 3 species can be found in Lake Ontario.

 Fishing Booker
Possible species include Atlantic, Chinook, and Coho. See here for descriptions and pictures of each along with many other Lake Ontario fish species. I invite you to stare at your photo longer to convince yourself to which specific species it is.

Oh yeah, and there's just no telling what happened. Though, notice the raccoon's foot is buried. This suggests these animals possibly have either been here for a while and/or were carried here and deposited from wave action. The former seems unlikely given the easy meal both would have provided to some other predator. It may very well be the salmon was caught on fishing line (perhaps snapped by an angler), which caught it up near shore where a raccoon got entangled Then they got swept up, drowned, and then their tied-up carcasses deposited on the beach and covered in moving sand. Who knows...

And in a few 100,000 years they'll dig up the fossils and note the epic battle between the 2 species a la fighting dinosaurs, concluding that racoons were partially aquatic and descended into the depths to hunt their prey.

I was wondering why would a decapitated raccoon end up on beach. Your theory makes sense @theforestecologist


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Are there any biometrics that can measure tiredness (sleepiness)?
Are there any biometrics that can estimate how tired someone is? I specifically refer to tiredness in the sense of sleepiness (as opposed to physical tiredness that might happen after a workout, for example).
For context, I'm trying to quantify "tiredness" through methods other than counting hours slept, and I'd like to explore some other way(s) of measuring (approximately or otherwise) how someone is. Also, regarding granularity/accuracy it's okay if a metric can't accurately detect a sudden slump (as may happen after a heavy meal), that would still be of interest (more accurate/granular is better, obviously, but not vital).

I would pretty much guarantee that artificial intelligence and a learning algorithm of eye movement And  Iris dilation would be able to tell when the eyes are alert and when they are lethargic.

Most of the sleep-deprivation studies I've seen measure cognitive impairment as a way of quantifying sleepiness, similar to some of the metrics taken in drug and alcohol intoxication studies.
Here's a recent proof-of-concept study using a phone app designed to measure things like simple attention, arithmetic ability, episodic memory, working memory, and executive functions like cognitive conflict and behavioral adjustment (using something called a Stroop test). They also included a subjective "sleepiness" survey self-reported by participants on a 1-10 scale.
It's a Frontiers journal, so I would take the results with a grain of salt, but the methods seem well defined to me (a non-expert), which is more than I can say for many of the Frontiers articles in my field of Microbiology. Seems to me like it would be prudent to include some control metric that isn't expected to fluctuate with sleep-deprivation, but, not being an expert in the cognitive science, I'm not sure what that would be.
Reference:
Holding BC, Ingre M, Petrovic P, Sundelin T, Axelsson J. Quantifying Cognitive Impairment After Sleep Deprivation at Different Times of Day: A Proof of Concept Using Ultra-Short Smartphone-Based Tests. Front Behav Neurosci. 2021 Apr 13;15:666146. doi: 10.3389/fnbeh.2021.666146. PMID: 33927603; PMCID: PMC8076531.

Lactate production is a direct measurement of fatigue, also described as tiredness. You may want to consider ATP Synthase production and the results as they relate to temperature and oxygen.

lactate can measure muscle fatigue it is basically useless for mental fatigue.

Mental fatigue happens because muscle fatigue happens. That’s how we measure an athletes performance, you need a brain in order to contemplate.

mental fatigue has little to do with muscle fatigue.


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What is this bone from?
This object showed up on my fire escape in New York city. It appears to be some kind of bone. It's a bit smaller than an adult human hand. What animal is it from?

Given the size and thin/elongated ilia as well as the urban location, I think a domestic cat and/or a raccoon are likely candidates. I'm leaning toward cat.
Cat pelvis:

 VCA Hospitals

 Ventral view of domestic cat pelvis; Source: BoneID
Raccoon Pelvis

 Anterior view of raccoon pelvis; Source: BoneID
I'm not an expert in differentiating these two species' bones. I will note that your specimen is more or less in between the sizes of these two species. Your size is probably closer to the raccoon, but a cat is just more likely given the location.
The most noticeable trait that stands out to me is the size/pointedness of the ischial tuberosity, which better matches that of the cat.

I could not for the life of me definitely identify it from the first picture alone. I saw those sockets and thought "hips", and those articulations and thought, vertebrae, but I never saw such a pelvis. This is why you have a gold badge in identification. Fantastic!

@anongoodnurse, teaching 11 years of anatomy + that arduous comparative vert anatomy course I took all those years ago in college help a lot :p.

I'm still in awe. Makes me want to take a comparative vert anatomy course!