text:
Isn't sexy son hypothesis circular?
Sexy son hypothesis.
It states that females are attracted to certain traits in males, because these traits will be attractive in her sons either. But isn't this circular?
Like "I'm attracted to that male because he is the son of an [formerly] attractive male". And you can repeat the process infinitely, going through granddad, great-granddad and so on. Doesn't this hypothesis presuppose some sexy traits that are sexy with no cause?

It's never only one single factor that influences reproduction. "Sexiness" can play a big role in some species, but other factors have a role as well. Also, it is perfectly possible that a factor that has a big role in the present, could have had a very minor role in the past.

@alec_djinn I believe in good genes hypothesis and that attractive traits signalize an individual who has greater chances of reproduction taken his attraction per se out. But it's not what sexy son hypothesis is about.

@rus9384 I think this is clear from the other answers, but "attractive traits signalize an individual who has greater chances of reproduction" could mean traits that mostly improve survival or fecundity (the 'good genes' hypothesis) but it could also mean traits that mostly improve reproduction success (i.e., chance, especially for a male, to successfully mate: 'sexy son'). It's important to remember that fitness is not just about survival, it's about reproduction.

@BryanKrause But sexy son hypothesis is then an addendum to the good genes one?

@rus9384 I think you could view it as that, or look at it the other way around and consider good genes to be an addendum to sexy sons. It's likely that specific case examples will be better described by the particulars of one or the other but I don't see any way that they are incompatible.

@BryanKrause But the point is that, certain features are seen as attractive because they signified greater fitness. And that fitness was not solely to being attractive, because then it again reduces to "these features are attractive because they were attractive". But we know some features could not always be attractive since they were non-existent some time before.

The process is self-reinforcing but the argument is not circular (no tautology implied).
As soon as some male traits are considered more sexy than others, then there is selection for females to like those traits even more, which causes those traits to raise in frequency, which increases the selection for liking these traits. In other words, in this model, the state where there are no sexy traits in males is an unstable equilibrium.

"As soon as some male traits are considered more sexy than others" And they are in the first place because they signalize (maybe formerly) good genes? But I agree mostly there is a double selection for traits in species with sexual reproduction. Sexual selection is just a layer above non-sexual selection.

@rus9384 they don't have to signal good genes they jut need to draw the females attention, A problem bird researches have is it turns out many female birds prefer males with sexy colorful plastic bands around their legs. Something that just happens to draw a females attention is beneficial in and of itself.

@John Well, female birds prefer those male birds who are more noticeable, because even before that preference has developed in them more noticeable male birds had more offsprings. Why? Whom does the female bird notice first? That one male she chooses. Of course then those females who had a preference towards such males actually had an advantage: their male offsprings could have more offsprings. I already though about that about a year ago.

@rus9384 Could you please to a reference for the claim that female birds like "more noticeable" male birds? I have already heard something along these lines but I would love to see a reference.

@Remi.b I'd wish to provide a reference but this one idea is the one I came up by myself. Sure, I'm not the first.

Taken by itself I can agree that it might seem circular. However, in practice, all traits act and occur in a pre-existing background, i.e. in organisms with their genetic background and their living environment. All that is needed is a preexisting difference in fitness (for instance connected to the related good-genes hypothesis), that a new gene for female preference of sexy traits can act on. Then the process can become self-reinforcing. The major difference between the sexy sons hypothesis and the good genes hypothesis lies in whether the traits signal increased chance of mating for future sons or if they signal higher quality/viability of offspring (see e.g. Huk & Winkel 2008). My point is that traits that first signaled the latter (quality) can later signal the former (sexiness/mating chance).

Well, good genes hypothesis is an intuitive one. With one amendment though: those traits which displayed greater fitness in the past (a few tens or hundred generations ago) appear attractive now. But sexy son hypothesis does not add anything to it. Also "higher quality/viability of offspring" contains "increased chance of mating".

@rus9384 Yes, that is my point, that past viability effects of offspring is probably often the original trait that might later get caught up in runaway sexual selection due to sexy son. I agree that higher viability of offspring usually leads to increased chance for mating (unless there is a negative tradeoff between viability and "attractiveness"/display traits), but the opposite doesn't have to hold. You can have "increased chance of mating" without "higher quality/viability of offspring".

Consider the difference between "vanilla" natural selection and sexual selection.
On paper sexual selection sounds strange; while straightforward selection says that a trait spreads because it makes an individual better at life meaning they'll have more descendants, sexual selection says that a trait spreads because it makes an individual attractive to potential mates, resulting in more descendants sure but it suggests that "being better at life" isn't required. And indeed sexual selection is often used to explain traits that make an individual worse at life, like the peacock's tail.
What's going on is that there is a first-order and a second-order process of causality, that are related but distinct. Say for instance you have a trait that makes your offspring 10% fitter. Awesome, they'll be 10% fitter. Except that this means the offspring of your mate will also be 10% fitter... which means other individuals have an incentive to be your mate, meaning you can get a better mate who will also give fitter offspring, so actually you might end up with offspring that are 50% fitter. The latter process is sexual selection, and while it's dependent on the first process to happen in the scenario I described, the causality, mechanics and results are different. You can have one without the other; for example if a trait makes you 10% fitter but this is completely undetectable to anybody else, they won't be able to select you as a mate on the basis of it so you won't have sexual selection. On the other hand sexual selection can indeed in theory function with something that doesn't improve fitness on the first order.
You can see the sexy son hypothesis as a third-order distinct process. It's not just that you have an incentive to mate with a person because your offspring will be fitter; there is an additional incentive involved in the fact your offspring will also be more attractive. This isn't a tautology because it isn't a foreordained conclusion; for example if you have a "love red hair" gene but nobody else does then you'll pick a redheaded mate on the basis of their sexiness, but your sons won't be sexier for it. On the other hand if everyone except you has the "love red hair" gene, you have an incentive to get a redheaded mate even though you yourself don't find them sexy (or not for the same reason everyone else does at least).
This process certainly allows for sexiness to have no fitness-based cause but it doesn't presuppose it; indeed one would expect for there to have been a fitness-based cause at the beginning of the chain if not at the end.


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What are the different types of SNPs?
When I search for this online I get answers such as substitutions, deletions, insertions etc. But I mean in the sense that I have been reading different terms infront of the word SNP such as: lead SNP, tag SNP, sentinel SNP, indirect SNP, direct SNP, secondary SNP, imputed SNP etc.
From my understanding lead/tag/sentinel are all the same (SNP with lowest P value in a locus, representing the variance in that section). An indirect SNP is also a lead/tag/sentinel SNP and indirect because these have not been genotyped but are in LD with the genotyped SNP + having that they have the lowest P value. Also a secondary SNP is a indepedently correlating SNP, and is specifically independent from the tag SNP? Is there a resource defining these sort of categories? Apologies if this is misinformed, I have been trying to learn about GWAS from different studies, and would appreciate any help to clarify this.

see https://biology.stackexchange.com/questions/73617/gwas-terminology-tag-vs-lead-vs-index-snp

Thank you for this, the paper in the answer was great for the lead SNP definition, although I am still a bit stuck especially with understanding secondary SNPs.

source: Stack Exchange

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

sort: votes


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How can different ion channels of the same type have different cell responses?
The NMDA receptor is an ion channel and contributes to synaptic plasticity and memory. It is said that calcium ion flux through the receptor is critical for this mechanism. However, there are other ion channels that let calcium ions into the cell, how come they don't contribute to synaptic plasticity (to my knowledge)?

Can you please add references?

It is not just an ion channel. The name itself suggests that it is a receptor i.e. it responds to a ligand. Perhaps you can read a tiny bit more about NMDA receptor and the answer would become obvious.

cross posted to https://psychology.stackexchange.com/questions/21753/how-can-different-ion-channels-of-the-same-type-have-different-cell-responses although it might get a more detailed answer here

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


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How do fatty acid and polyketide synthases handle the varying size of their substrates?
Polyketide synthesis involves six modules, each containing certain common constituent enzyme activities (KS, AT, KR) that are involved in extending the chain (see e.g. Dutta et al.(2014) ). The growing polyketide, attached to acyl carrier protein, is passed on from one module to the next.
An analagous situation is seen in the single Fatty Acid Synthase complex. How can the same enzymes in later modules recognize what is a structurally different intermediate? Surely this contradicts the idea of substrate specificity of enzymes.

I've looked at the paper very quickly (I've other things to do this evening.). Am I correct in thinking that your question is as follows — restricting it, for the moment, to the polyketide synthase in the paper? "There are six modules in PK synthesis, each containing some common enzyme constituents (KS, AT, KR) that are involved in extending the chain. The growing PK, attached to acyl carrier protein, is passed on from one module to the next. How can the same enzyme in later modules recognize a different intermediate?" If that is correct I will rewrite the question for you (and answer it).

I had time to answer what I think is your question, so went ahead and modified it and answered it. Let me know if I have misinterpreted anything.

@David Yeah, this is the most correct interpretation of what I mean. Simply to say, I was asking how enzymes on later modules bind to large polyketides even the enzymes are as same as the previous ones and the enzymes on later modules should violate substrate specifity of enzymes.

Although the substrate is different at each stage of chain extension,
  the part involved in the reactions — and recognized by the enzyme — is
  the same. This is a common feature of polymerization reactions,
  whether the catalysis is by a single module (ribosomes, DNA
  polymerase) or multiple modules (polyketide and fatty acid synthesis).

This is illustrated by the modification made below to a part of Figure 1 of the paper cited in the question. An overlay in yellow has been made to indicate the common structural features of the polyketides of different length.

Of course, the rest of the chain may well interact with the enzymes, but as this is not at their active sites it can be in a less specific manner, perhaps in a ‘groove’ containing appropriate interating chemical groups.
The question of substrate specificity is not the point of interest in the paper on polyketide synthase where the focus is on the way the elongating substrate is passed from enzyme to enzyme and module to module (the resolution is also too low). It has, in any case, been addressed in previous work on mammalian fatty acyid synthase, where exactly the same single (dimeric) multidomain complex acts on each intermediate until the chain length is 16-18 C atoms. However the question of chain length is taken for granted and the discussion is about discrimination between chemically different intermediates. Thus in a 2008 paper by Maier et al. a substrate tunnel in the ketoacyl synthase (KS) module of the fatty acid synthase (mFAS) is compared with that in polyketide synthase (PKS):

“Despite the pronounced structural similarity between the KS domains of mFAS and PKS, the selectivity of FAS for saturated acyl chains can be explained by a considerable constriction at the base of the active site phosphopantetheine binding pocket leading into the large acyl chain substrate binding tunnel, which connects both active sites of the KS dimer (Fig. 4, A and B). A number of residues lining this narrow tunnel are highly conserved in mFAS but are substituted with smaller residues in all DEBS (6-deoxyerythronolide B synthase) PKS modules (Fig. 4B), resulting in a wider, more permissive tunnel in the KS of DEBS.”

It is important to think of substrate specificity in molecular terms — e.g. what part of the substrate binds to the enzyme and how specific has the binding to be. In this case the substrate is attached to the long phosphopantetheine chain of acyl carrier protein, so that recognition of that and the part of the fatty acid or polyketide attached to the sulphur may be enough to discriminate against ‘free’ extraneous molecules. And a tunnel is permissive as a binding site: if the chemistry and radius are right, there is no need for the whole of the tunnel to be occupied.
Tunnels of various types are found in other enzymes or organelles involved in elongating molecular ‘chains’, e.g. polypeptides and nucleic acids. The tunnel on the ribosome and that through which RNA or DNA passes has to accomodate chemical disparate molecules (four different bases, 20 different amino acids).

I get it. So the rest of the chain is made to be not on their active sites by its enzyme mechanism and the enzymes recognize the yellow parts, thus the enzymes can do their reactions regioselectively. Perhaps, can you locate me which paragraph on the reference that tells about these active sites?

I have modified my answer to deal with the point you raise, as I think that more generally useful than a conversation in the comments. I'm not sure what level you are at, but if you can get hold of the Science paper I reference and have the time and background to work through it, it will give you a better idea of active sites and substrate binding sites.


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Calculation of Respiration Fluxes in Terrestrial Ecosystems Based on Total Respiration (RT)
Overview
Researchers have been studying a temperate grassland ecosystem with the view to understand it's current status with regard to carbon inputs and outputs and to identify whether the grassland is currently a sink or source of carbon.
Investigation:
The aim of this investigation is to calculate different respiration components within an ecosystem with the energy fluxes within a terrestrial ecosystem consisting of:
Energy Fluxes

GPP = Gross primary productivity
NPP = Net primary productivity
NEP = Net ecosystem production
NEE = Net ecosystem exchange
RT = Total respiration
RA = animal respiration
RS = soil respiration
RM = microbial respiration

Query
I have answered the questions below to the best of my ability but with much confusion (see calculations below).
Am I on the right track? Am I calculating these respiration components correctly?
If anyone is able to help here, your advice and input would be deeply appreciated.
Many thanks!
Table 1: Flux values for temperature grassland

Respiration Components to be Calculated: My answers to the questions
1. Researchers measured the total ecosystem respiration (table 1;
    figure 1) as RT = 1300 g/Cm-2/yr-1. What is included in this total
    respiration?
Rs and Ra are not to be included in this calculation because they are part of the heterotrophic respiration system and they cannot be added to plant respiration.
The respiration components incorporated into RT =1300 g/Cm-2/yr-1 is Rp = 800 g/Cm-2/yr-1 (plant respiration), leaving 500 g/Cm-2/yr-1 to
be designated to roots, shoots, and microbial respiration.
2. The researchers measured soil respiration as  Rs = 900 g/Cm-2/yr-1 and estimat3e animal respiration above ground as RA = 50 g/Cm-2/yr-1. Calculate the respiration values for plant shoots (R,p-s), plant roots (R,p-r), and microbial activity (R,m).
Calculations for respiration components (Table 1; Figure 1)

Fig 1: Visual reprsentation of respiration fluxes

Can you give your reasoning for why you did the calculations as you did?

Hi Oosaka, After doing some really dumb calculations, I went back to the drawing board and tried again. I think these calculations are much improved and all respiration fluxes add to 1300. Is this answer correct? Many thanks if you can offer any helpful advice. Thank you again, you have been wonderful!


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Is the chemical composition of urine detrimental or beneficial for a tree?
Seeing as a lot of people around the world urinate against trees it came to mind that I never thought about how the tree responds to this.
Is it detrimental for a tree if people urinate against them?
When looking on the internet, I found this explanation about urine:

Human urine consists primarily of water (91% to 96%), with organic
  solutes including urea, creatinine, uric acid, and trace amounts of
  enzymes, carbohydrates, hormones, fatty acids, pigments, and mucins,
  and inorganic ions such as sodium (Na+), potassium (K+), chloride
  (Cl-), magnesium (Mg2+), calcium (Ca2+), ammonium (NH4+), sulfates
  (SO42-), and phosphates (e.g., PO43-). What Is the Chemical Composition of Urine?

Of course, it is possible that the small amounts present in urine are negligible in contrast to the amounts a tree absorbs on a daily basis.
What I am wondering: is the chemical composition of urine detrimental or beneficial for a tree?

Tom, this is a wonderful improvement from your previous [now deleted] post, and I'm glad you took the time to do some of your own research and include it here. Really great to see the newly added effort! Thanks! +1

related. Also, my +1 to this question and @theforestecologist comment was not enough to express how much the improvement in this question is appreciated. I wish I could upvote again...

In most instances, plants benefit from animal litter, which is why it is sprayed in fields, and used to get bigger crops. Everything in moderation obviously, there is an optimum influx of animal litter which increases plant growth, which in the case of humans weeing, is much lower proportion than cows. other human activities are a lot more detrimental to trees, i wouldn't worry about weeing on them. a big tree can probably benefit from about 1 cubic meter of wee before it got detrimental. ideally you have to keep the pH at about 6.4

a large tree can probably benefit from about 1 cubic meter of wee for a year before it gets detrimental, but not in the same place at the same time.

@com.prehensible the old saying, everything in moderation seems applicable?

Indeed. for cow urine here is a study: http://www.scielo.br/img/revistas/hb/v27n4/06t01.gif

Here is a book about dry-matter production of urine treated plants. If we consider that trees are large plants, it's fair to apply the study to trees too:
The findings of the study suggested that urine and urine products are equally as effective as mineral fertilizer especially in sandy soil and that splitting the application is a useful strategy to manage urine and urine products for optimum dry matter production.
Some plants do live in harsh environments with chalky pH and other specifics, and they may weakened by it. It's safe to say most trees are unaffected or improved by some urine, although the biggest trees are because of rain and steady underground streams (groundwater).

but just like anything in biology amounts matter, if enough people urinate against a tree it can cause salinity issues. But you need a ridiculous number of people to cause that. Note dog urine is far more concentrated so it can reach the problem levels much faster, trees visited by dozens of dogs in a day suffer for it.

@com.prehensible I am sorry, I completely forgot this question (multiple SE's sometimes clutter my mind). If I understand correctly (correct me if I am wrong), it depends on the kind, size and (in the case of dogs) the concentration of the urine and its amount are all important factors.

And the rainfall too. Sorry am in car can't answer.

Speaking specifically about blueberry bushes as a perhaps extreme example, they thrive in acidic soil and nitrogen-laden soil. However, dog urine is bad for blueberries, as the high nitrogen content overwhelms the plant and damages fruit production. Dog urine is only slightly acidic (pH 6-6.5) and can often be alkaline, which also changes the soil acidity in the direction that is not good for blueberries. The acidity and nitrogen content of dog urine can depend on diet.
If there's a plentiful supply of rainwater and the soil has the right nutrient balance and acidity for the plants and trees living in it, then urine will disturb that balance, strictly speaking, however marginally. More urine could damage plants if it changes the soil constitution outside the comfort zone of what is growing in that soil.


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How are mitochondrial diseases like MERRF inherited?
I am doing a project on the disorder MERRF in Mitochondrial DNA. I have to make a pedigree and explain how it is transferred on from generation to generation. I know that it is inherited maternally, but I am confused about how it is inherited. Would it be inherited inherited like autosomal DNA in a Mendelian fashion? If so, would this gene be dominant or recessive? Or would the children just automatically inherit whatever gene their mothers have? Also, how would the genotypes for Mitochondrial DNA be displayed? Any other useful information on Mitochondrial DNA or MERRF would also greatly appreciated. Thanks.

You will find useful information in Wikipedia's Mitochondrial DNA article.

Thanks for the article. Does this mean that the children will have whatever gene that the mother has?

Mitochondria are primarily thought to be inherited from the mother but there is evidence now that the father can also contribute mitochondria (Schwartz and Vissing, 2002; Luo et al., 2018).
Even if the mitochondria were purely maternally inherited, a cell (including oocyte) typically contains many mitochondria and not all of the mitochondria may have the (deleterious) mutation. This phenomenon is called heteroplasmy.
MERRF is associated with a loss of function mutation in mitochondrial tRNAs (See NIH, Genetics Home Reference). The extent to which a cell will be affected would depend on number of mutated mitochondria it contains. Therefore different cells would be affected differently.
The trait inheritance would therefore not be in the typical Mendelian fashion.


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Why not self pollination for finding the genotype instead of test cross?
Test cross can tell us what's the genotype of a plant is. But we can know that even by self pollinating the plant. For example,
If a garden pea plant has the genotype TT, then self pollinating them will give all tall plants.
If the plant has the genotype Tt, then self pollinating them will give both tall and dwarf plants in 3:1 ratio.
So we can simply say that by self pollination if all the plants are of same type then the parent plant is homozygous. If the plants are in ratio them the parent plant is heterozygous.

Because for test cross you need to phenotype far less progeny to be reasonably sure about parent genotype. Lets say you decide to phenotype N progeny. If the tested parent is heterozygote the random chance of you getting all N plants tall is (1/2)N for test cross and (3/4)N for self pollination.
So for example if you decide to phenotype N=8 progeny plants in case of self pollination (3/4)8=10% of your heterozygous parents will be wrongly assigned as homozygous which is error too high for almost anything serious. In case of test cross (1/2)8=0.4% of your heterozygous parents will be wrongly assigned as homozygous. To achieve the similar level of accuracy with self pollination you would have to phenotype N=19 or N=20 progeny plants.
The difference does not seem like much when testing one parrent but if you need to test many the costs will add up.


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Will being very muscular (to the point that one is characterised as obese by BMI) increase blood pressure?
It is widely accepted that obesity/overweight (which I believe refers to people with a high amount of fat cells instead of bodybuilders who weigh a lot due to lots of muscle cells) have higher blood pressure due to various reasons e.g."larger body mass increase resistance to flow", "increase insulin resistance that increases cholesterol and risk of blocked arteries", "more blood (i.e. plasma) is required to supply the larger body mass thus puts pressure on vascular system", "increased weight takes more pressure to move blood around the body" and etc.
Therefore, based on the arguments above, is it fair to also say that muscular bodybuilders who are obese by BMI metric, have higher blood pressure?

May I ask why is this question downvoted? Is there something wrong with this question?

Perhaps it was downvoted because it's better suited to health or physical fitness sites.  Or because it can be answered with a simple Google search.  (The consensus from skimming a few articles suggests that while it's not a good idea to do serious weight training if you already have serious HBP, it doesn't cause it.)

Thanks for taking ur time. I've done some research on this topic but the answers come in the form of how "exercise or people with lots of fat cells thus are obese affect BP" rather as how "muscular people who are obese by bmi standard affect BP". Even then, the theories given as to why people with lots of fat cell have higher BP are somewhat skeptical, and the theories (e.g. more body mass thus require more blood plasma to deliver more O2) should translate to very muscular people who are obese by bmi metric.

Interesting question! I’ve been studying the effects of BMI on blood pressure over the last four weeks. In my study, those with higher BMI’s did in fact have raised blood pressure in comparison to those in a healthy weight range. However, this was a controlled study where participants were selected and so this solely focused on individuals who were classed as overweight or obese due to excessive fat. Often, BMI isn’t an accurate way to measure body weight, for reasons such as muscular persons being classified as overweight or obese. HOWEVER! This is where it gets interesting, being fat puts strain on your heart, your heart must work harder to support your body. BUT, animal fats play a large part in raised blood pressure. The lipids from animal fats form deposits within your arteries causing a blockage. So would it be safe to say that those of a muscular build consume more animal fats to promote muscle growth? Maybe! Hope this helps :)

Hello Emma. Can you please add some references to support your answer? Good references include peer-reviewed articles, books and websites of scientific organizations.


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Is there animal other than human that can recognize distal causes?
We know animals can recognize proximate causes. For example, if animal A hits animal B and injures it then usually animal B is able to associate animal A with his injury. From our everyday experience with pets and other animals we know that. What about distal causes? Proximate causes are not always the most appropriate causes, sometimes distal causes are more appropriate to identify the responsible agents. Let's modify the previous hypothetical example by bringing another animal, animal C: Animal C pushes animal B so that animal A hits animal B and injures it. If animal B is capable of recognizing distal causes, it'll associate animal C with his  injury (not animal B which is the proximate cause of the injury).

I don't know about your example, but would you consider a bird using a piece of bread to lure fish a distal cause? So if the fish looks for more bread it knows its to eat fish.

@Cell but it doesn't show that the bird is consciously doing that. the behavior you mentioned can be hard-wired in the bird brain so  the bird can carry out that behavior without having the general cognitive capability of recognizing distal causes.

How can using bread (a human invention) as lure be hard-wired? Or putting off eating the bread for immediate nourishment for bigger gains?

@Cell Actual baiting behavior can be specific hard-wired adaptation and the fish may develop the flexibility to use x,y,z as baits . I am not entirely dismissing it as a possible answer to my question. If the fish does it out of its general intelligence then of course it qualifies as "recognition of distal causes". Is there any evidence that it's not hardwired behavior?

What about when my dog brings me his leash to push me to take him out? Dogs do recognize distal causes.


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What does Ercc1-/- / DAT-Cre+ mean?
I really need to know what Ercc1-/- / DAT-Cre+  mean. I think the 1st part means that the mice don't have the Ercc1 gene (knockout). But what about DAT-Cre+?
This question arised from reading the following paper: "Inefficient DNA Repair Is an Aging-Related Modifier of Parkinson’s Disease" (Sara Sepe et al).
Ercc1-/- / DAT-Cre+ mice are mentioned several times, For e.g.:

Ercc1−/−DAT-Cre+ mice are viable and normal at birth. At 26 weeks of
  age, specific deletion of Ercc1 in DA neurons mice elicits reduction
  in tyrosine hydroxylase (TH) immunoreactivity in the SNpc and in the
  striatum (Figures 1A and 1B). Aging profoundly exacerbates SNpc DA
  neurons reduction, as evidenced in 52-week-old Ercc1−/−DAT-Cre+ mice
  (Figure 1C). Damage is limited in DA neurons and other populations
  remain unaffected, as indicated by unchanged NeuN immunoreactivity
  (Figures 1A and 1B). Overall, these findings demonstrate that Ercc1
  function and NER are essential to preserve integrity of the DA
  circuits in time.

Sorry to bother you again but you should add the link to the paper. Moreover, copy pasting the text is better than pasting an image, for better searchability and rendering. I have done the both for you this time.

I have answered your question but the answer was pretty obvious. They mention it in the paragraph just before your excerpt. You should have read the paper more carefully. Questions like this ("homeworks") without adequate effort from the asker are generally not appreciated and put on hold.  "Homework" is interpreted to mean any academic or other assignment, test preparation, or task given in relation to a class, educational setting, or self-learning.

Ercc1-/-DAT-Cre means the mice with Cre recombinase mediated conditional knockout of Ercc1 in the DA neurons. DAT-Cre is the mouse strain that expresses Cre recombinase from the promoter of Dopamine transporter.

Cre-recombinase:loxP (Cre-loxP) system was used to generate mutants
  with targeted deletion in dopamine transporter (DAT)-expressing
  neurons. Specificity of Cre recombinase activity was validated using a
  lacZ reporter that confirmed expression in DA neurons of the SNpc and
  not in other cell types, such as serotonergic neurons of the Raphe
  nucleus (Figure S1).

From supplementary information:

Conditional mutants were generated using the Cre-recombinase:loxP
  (Cre-loxP) system and crossing a strain carrying an Ercc1 allele
  flanked by loxP sites (Ercc1fl/fl), with a strain expressing the Cre
  recombinase under the control of the specific Dopamine Transporter
  (DAT) promoter (Zhuang et al., 2005). We validated the specificity of
  Cre recombinase activity by generating DAT-Cre+ROSA26-lacZ reporter
  (Soriano, 1999), which confirmed expression in DA neurons of the SNpc
  and not in other cell types, such as serotonergic neurons of the Raphe
  nucleus (Supp. fig. 1)


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10 inch spider near Mexico City
Four years ago I found a spider so big that I'll never forget. Unfortunately I don't have a picture but I guess there isn't a lot of big spiders in Mexico. So here are some things I remember:

It wasn't a brown spider, I think it had red legs with some parts black and others white.
Its legs were skinny and very long
The main body was tiny compered with the spam of its legs.
I found it at noon, after I moved to my new house. Unfortunately it wasn't moving when I found it
The spider didn't have any visibly hair.

That's all I can remember. I know that this may be impossible but I don't know what else to do.

It almost definitely wasn't 10 inches, but there are some pretty big spiders in Mexico. There is a species of spitting spider with a 9 inch legspan but it lives in South America not Mexico.
Scytodes globula

The cellar spider has a legspan of up to 3.6 inches and a comparatively small body with long skinny legs and no visible hair, but I can't see how that would be confused for 10 inches.
Pholcus phalangioides

The giant crab spider fits that description to some degree. It has a legspan of up to 4 inches.
Heteropoda venatoria

The golden silk spider is very large with long skinny orange and red legs.
Trichonephila clavipes

Sounds like a Mexican Red Knee Tarantula. they are kept as pets. not dangerous except for irritant hairs which they can project and which can get into eyes.
https://www.google.com/search?q=mexican+red+knee&source=lnms&tbm=isch&sa=X&ved=0ahUKEwiJlvWuyvLgAhULlhQKHbfrD3IQ_AUIDigB&biw=1431&bih=734&dpr=1.65

It isn't the spider that I saw, but you made me remember something else.


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Question on compatibility of blood groups
How come a person with blood group O can donate to a person with blood group AB? Since there are A and B antibodies in the O blood group blood surely this would cause agglutination in the blood of the recipient?
My first hypothesis was that the antibodies and red blood cells were separated through use of a centrifuge or something but blood transfusion has been used for hundreds of years before this machine was even invented? What is going on here? Or was it just that before blood types were discovered only people with identical blood groups could donate/recieve from one another?

Yes, the recipient's red blood cells would be attacked by the donor's blood. However, there are not that many antibodies in the donor blood that would pose a major threat - and the donation is diluted by the many liters of recipient blood! Here is a complete answer, the part at the bottom is relevant to your question.

Good question! It just so happens we already have an answer for it! (See the above links, and thanks to @SPr for identifying it.


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How do DNA viruses keep themselves in the nucleus without inserting themselves into genome?
If I'm not mistaken only RNA viruses insert themselves into the host genome. As an example of DNA viruses, herpes viruses for example do not insert themselves in the host genome.
Then how do DNA viruses keep themselves inside the nucleus? Do they just float around without their capsid? And if the cell duplicates, would the DNA of a DNA virus also be duplicated even though it isn't inserted in the host's genome?

If my question makes some weird assumption, I'm sorry. I'm here to learn and the fact that I'm asking a question is precisely because I don't know all the facts.. Thanks for your answer already!

Hi Yuri. We require that all question posts ask a single question on this site. You need to choose whether you want your 1st (How do DNA viruses keep themselves in the nucleus without inserting themselves into genome?) or second (Can CRISPR remove them too?) question answered. Choose to keep one and delete reference to the other. You may ask your second question in a second post. Failure to do so will result in question closure, but I think you'll not find it too troublesome to split up your post. In both, please indicate explicitly that you've researched each question and how. Thanks

@theforestecologist done!

Great, thanks! Now, if you explicitly add where you've already researched your question on your own and what you've figured out, you'll receive much more positive reaction from our community. (for example, try YouTube, wikipedia, pubMed, Google search results, Google Scholar, a school textbook, etc etc.). Our goal, Yuri, is not to simply be an answer site, but rather a site that promotes self-learning with some expert help along the way :).

Herpesviruses maintain themselves during the latent state as "episomes", circular DNA elements, with no capsid, that are in the nucleus but that are not integrated into the host genome. Host enzymes replicate these episomes, and different viruses have evolved different strategies for ensuring that the episomes are passed on to newly-divided cells.

After they first infect cells, many herpesviruses establish a latent lifecycle with the viral genome existing as circular genetic elements called episomes inside the host cell’s nucleus that are closely associated with, but not integrated into, the host DNA. During latent infection, episomes are replicated during S phase, but new viral particles are not produced and the infected cell survives. The maintenance of herpesvirus genomes as episomes contrasts significantly with retroviruses, which insert their genome within the host cell genome to ensure their replication and inheritance by daughter cells and establish long-term infection. ... EBV uses a mechanism to tether the EBV genome to host DNA, facilitating the equal distribution of episomes in daughter cells with a larger number of cells having at least one EBV genome. In contrast, KSHV uses a clustering strategy that promotes a higher number of episomes per cell, but at the expense of not passing on the episome to some daughter cells

--How herpesviruses pass on their genomes
Another mechanism many herpesviruses use is to establish their latent infection in non-dividing cells, especially neurons, so that there's no concern about daughter cells.

"The maintenance of herpesvirus genomes as episomes contrasts significantly with retroviruses,..." - and contrasts with some non-retroviruses the DNA of which gets integrated into host DNA by host enzymes (by chance).  Does herpesvirus care about maintaining its integrity, in other words: does herpesvirus, by any means,  make sure it's not being absorbed by host DNA? (another question: "without 'being' inserted"?)


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Can CRISPR also remove DNA viruses?
If I'm not mistaken only RNA viruses insert themselves into the host genome. As an example of DNA viruses, herpes viruses for example do not insert themselves in the host genome.
Can CRISPR cut DNA that isn't in a chromossome, like a DNA virus?

If my question makes some weird assumption, I'm sorry. I'm here to learn and the fact that I'm asking a question is precisely because I don't know all the facts.. Thanks for your answer already!

It can cut the DNA anywhere. Why do you think it should be a part of the genome? Read a bit about CRISPR; it was originally discovered as anti-viral defense system in bacteria.

By some definition of "remove". The answer below highlights papers that edited the (DNA) virus to make it less infective.

In eukaryotes only RNA viruses, in some prokaryotes DNA viruses can do it as well, they don't have the same barriers eukaryotes have. .

Yes, this should in principle work, and a number of groups have shows that it works in cultured cells:

We found that CRISPR/Cas9 introduced InDel mutations into exon 2 of the ICP0 gene profoundly reduced HSV-1 infectivity in permissive human cell culture models and protected permissive cells against HSV-1 infection.... Combined treatment of cells with CRISPR targeting ICP0 plus the immediate early viral proteins, ICP4 or ICP27, completely abrogated HSV-1 infection. We conclude that RNA-guided CRISPR/Cas9 can be used to develop a novel, specific and efficacious therapeutic and prophylactic platform for targeted viral genomic ablation to treat HSV-1 diseases.

--Inhibition of HSV-1 Replication by Gene Editing Strategy
There's also been at least one trial in an animal model:

Using a hydrodynamics-HBV persistence mouse model, we further demonstrated that this system could cleave the intrahepatic HBV genome-containing plasmid and facilitate its clearance in vivo, resulting in reduction of serum surface antigen levels. These data suggest that the CRISPR/Cas9 system could disrupt the HBV-expressing templates both in vitro and in vivo, indicating its potential in eradicating persistent HBV infection.

--The CRISPR/Cas9 System Facilitates Clearance of the Intrahepatic HBV Templates In Vivo


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synthesis of zn nanoparticle
Sir the protocol I followed where it has been written... 1st using lactobacillus in Mrs media (50 ml in 250 ml conical)..we allowed to incubate for 24 hrs then added 0.1M znSO4 (50ml) and 0.4 M NaOH(50ml)...followed by a vigorous mixture heating it for 15 mints at 40°C ...white portion observed at the bottom of conical..(.which I also showed)...followed by centrifugation washing it with deionised water again again ...finally pelleted portion collected which allowed to dry to make it powdery form..then it observed under UV spectroscopy by mixture the powdery with  deionise water...
But sir I don't get any pick in UV spectroscopy.. Is  there any method synthesis Zn Nanoparticles using lactobacillus culture?

Can you provide a link to the protocol you followed? Is it from a published paper?

Also, please format your question properly. Use bullet points to explain the protocol step-wise. Moreover, add some more details on how you analysed it and what you expect is the problem. Did you try repeating the experiment at least once more?


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What neurons' projections comprise the olfactory nerve (Cranial Nerve 1)?
Recently, I have been learning about olfaction. To my surprise, I am having a heck of a time finding explicit information regarding which neurons' axons are comprising the olfactory nerve. I am aware that there are several cells types that are relevant in the olfactory bulb: mitral cells, olfactory sensory neurons, tufted cells, and many more. However, I have not been able to find any source that definitively states from which neuron type the projections that comprise the olfactory nerve arise from.
I keep seeing articles that seem to imply olfactory sensory neurons comprise the olfactory nerve, but this doesn't seem right to me. My understanding is that the projections that emanate from the olfactory bulb and terminate in the brain constitute the olfactory nerve. The only thing I can think of is that the "olfactory bulb" is actually being considered "part of the brain"...in which case, the olfactory sensory neurons are technically peripheral neurons.
If that is the case, what exactly are the olfactory bulbs? Are they part of the telencephalon? Are they an outgrowth similar to how the optic nerves are outgrowths of the telencephalon and therefore not "true nerves"?

Olfactory receptor neurons (ORNs) in the olfactory epithelium in the nasal cavity project to the olfactory bulb; this projection is Cranial Nerve 1 and it's more of a collection of fibers rather than a highly organized nerve.
Your surprise or confusion is probably based on this:

My understanding is that the projections that emanate from the olfactory bulb and terminate in the brain constitute the olfactory nerve

...which is false: the olfactory nerve is the step prior to the olfactory bulb. The olfactory bulb is part of the brain.
I'll add that I have seen poor diagrams of the brain that point to the olfactory bulb and label is as cranial nerve 1, which is false or at least misleading.

what exactly is the olfactory bulb, then? It's certainly not a cortical structure. Is it classified as a subcortical, telencephalic-derived structure?

It's part of the forebrain, specifically the telencephalon. It's of course not neocortical, but much of the telencephalon is not, for example it includes the basal ganglia.


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What do the text annotations in an electron micrograph mean?
I saw a photograph taken from an electron microscope, with some text.

I want to know what is the meaning of these numbers and letters?
Thank you! Regards.

The 1.40kX is the zoom (1400x), WD is the working distance (distance between the final lens and the object), 20kV is the voltage used to accelerate the electrons, 20μm is the scale.
I'm not aware of the other two.

Thank you! if the voltage increase, what will be the effect on the picture?

@French_FitGirl The voltage is used to accelerate electrons. High velocity electron beam would have a higher resolving power. However low voltage is often preferable for SEM. You can read more about electron microscopy.


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Small mammal identification
Small skull found in Alberta, Canada. Do not know the region. Skull is about 17 mm in length. Trying to identify the species, narrowed it down to most like a species of vole but can't figure out which one. Below are pictures of the teeth under a dissecting microscope that we were using to ID, upper jaw and then lower jaw respectively.


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Is evolution theory falsifiable by whether mutations result in a loss or gain of genetic information?
If I understand the theory correctly, evolution revolves around the process of adaptation of a being to its environment which results in the increment of survival and reproduction chances for that being.
But I constantly hear debates around whether the mutations that trigger these evolutionary changes result in the loss of genetic information or acquisition of new genetic information. The existence of these discussions gives the impression that if genetic mutations only resulted in the loss of information, evolution, as understood today, wouldn't work.
Is this a valid way to falsify evolution theory?

Can you point to one of these debates that you hear? I most often see this sort of arguments put up as some misguided critique of evolution, to make wrong arguments like "evolution can't result in gain of information."

Your representation of the theory of evolution (that we call the modern evolutionary synthesis) is very biased and very lacking. You might want to have a look at a very short intro to evolutionary biology such as evo101 for example.

@BryanKrause Well I watch (and read) a lot of internet debates between creationists and scientists, but the recent one I'd like to refer to is this one between AronRa and Grady McMurtry. Almost right out of the gate the discussion revolves around the question I'm posting here. This is the video: https://www.youtube.com/watch?v=cvnW6N3oy5k

@Remi.b Usually people ask these questions when they actually don't know and want to see if more knowledgeable people can provide valuable insight. If my position seems to be biased in some way, it's probably because I'm not a scientist and therefore I came here looking for help by asking the question. But thank you very much for the link. I will for sure go through it. Thanks!

It would be so amazing if downvoters were required to express why they are downvoting a question. People come genuinely looking for an answer to a site that's populated with a lot of learned individuals. It's rather disappointing that genuine questions just get stepped on instead of answered.

The issue with the question is that the concept of information of a sequence is very much undefined (see Calculating Shannon Entropy for DNA sequence?). If you'd wish to offer a good working definition for the amount of information of a genetic sequence, we could talk about whether new mutations tend to increase of decrease it.

On a sidenote: I have no downvoted but I can picture why it has been downvoted from the comments you have received. I agree that forcing commenting when down voting would be a somewhat pleasant policy.

@Remi.b I have rephrased my question just to clarify that I'm not trying to push a bias. I've sincerely googled for quite some time and I haven't found an answer. I would think that evolution theory works whether the mutations are only losses of information or not. But I don't know for sure. Any ideas? Thanks you!

@sergeidave Don't worry, I meant that your representation of the theory of evolution is quite wrong but never did I mean that you had bad intentions.

I'm voting to close this question as off-topic because the concept of information content is very much undefined (see for example Calculating Shannon Entropy for DNA sequence?). If the OP can offer a working definition (a metric) for quantifying information from a genetic sequence, then the question would be on-topic.

As @Remi.b says, you have to first clarify what you mean by information otherwise your question would be considered unclear.

Does "information", presumably as encoded in DNA, even make that much sense in evolutionary terms?  Say you have the complete genome of a creature, for instance a mammoth: can you use that alone to create a new mammoth?  Or do you need a female mammoth?  And if you did somehow create a baby mammoth, would it be able to survive without being taught by other mammoths?

You also need to define what you mean by Evolution theory.   Evolution is just a change in the genetic composition of a population during successive generations, its is an observation a factual statement not a theory. There are mechanistic theories explaining how it works (such as the theory of evolution Via natural selection) but no "Evolution theory"

This question may already answer your question, https://biology.stackexchange.com/questions/16106/how-does-the-creative-process-of-biological-evolution-work

This is parroting the claims in Behe's latest book. They have been refuted many times. Rich Lenski has recently put up a series of blog posts starting here, with extensive references, further refuting Behe's claims, and clearly showing how dishonest Behe is in continuing toput forward these claims that he must know are lies.

This might not have a purely objective answer. For example:

Most people lose the ability to digest milk by their teens. A few thousand years ago, however, after the domestication of cattle, several groups of people in Europe and Africa independently acquired mutations that allow them to continue digesting milk into adulthood. Genetic studies show there has been very strong selection for these mutations, so they were clearly very beneficial.
Most biologists would see this as a gain in information: a change in environment (the availability of cow’s milk as food) is reflected by a genetic mutation that lets people exploit that change (gaining the ability to digest milk as an adult). Creationists, however, dismiss this as a malfunction, as the loss of the ability to switch off the production of the milk-digesting enzyme after childhood.

And if you go read a review paper on beneficial mutations (as opposed to a popsci article), it never gets to the topic of information loss/gain. The latter seems to be most a concern for creationists (and those debunking their silly claims).
The closest thing that is of concern to biologists is whether a mutation causes a loss or gain of function of the affected protein. There exist ways to score a mutation as gain-, loss-, or switch of function.

I also note that you've substantially edited your question (toward an emphasis on  whether that issues invalidates the theory of evolution) after I answered it. As a brief and obvious addendum: no, the argument doesn't  invalidate the theory of evolution.
After some searching I found that the argument in question has been put forth by Lee Spetner. Dembski has a somewhat similar argument but not exactly this one. Anyway there seems to be countless variations to it:

An especially good example of silliness is the ID assertion that natural processes cannot create new genetic information. ID advocates have recently been pushing this line heavily as of late (Meyer 2009), even in the science standards of some states (see Matzke and Gross 2006, for discussion and refutation of the information argument), and in the ID movement’s new textbook, Explore Evolution (Meyer et al. 2007). Interestingly, this talking point, at least in the form of a seemingly technical chemical/mathematical conclusion (there are older, more informal versions throughout the creationist literature), was invented in the 1984 proto-ID book The Mystery of Life’s Origins (Thaxton et al. 1984), as a modified version of the creation scientists’ Second Law argument (Matzke 2009). It has since grown into one of the top two or three arguments made by ID advocates.

Thank you for your answer. You are correct, I modified the question because from the comments I received, it seemed it wasn't clear enough. Hopefully I left the essence of the question still intact. Thank you very much for your answer.


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What does the number after Vitamin B signify?
Does the number after Vitamin B signify anything? For example what is the significance of 12 in Vitamin B12?

It appears to be fairly arbitrary, but they were originally numbered chronologically by discovery. However...
From Gizmodo:

These Bs are not necessarily designated in chronological order, as B12 (Cobalamins) was discovered in 1926, B5 (Pantothenic acid) and B7 (Biotin) in 1931, B6 (Pyridoxine) in 1934, B3 (Niacin) in 1936 and B9 (Folic acid) in 1941. The missing Bs are substances originally thought to be vitamins, but later reclassified.

Wikipedia explains that certain numbered B vitamins were originally classified as other vitamin letters when discovered and only later reassigned as a B vitamin.
In conclusion, B vitamins were numbered in order as they were assigned as a B vitamin.

missing numbers are due to specific vitamins being reclassified as either different letters or as non-vitamins.


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Can I train my non-dominant hand and make it dominant?
Are our dominant limbs decided on birth or is there some way in which I can train my non-dominant hand and make it as coordinated as my dominant?

You can find science studies and less thorough reading material on that from google, including for becoming ambidextrous. i.e. scientific american suggests that: It is possible to train your nondominant hand to become more proficient. A concert pianist demonstrates superb skill with both hands, but this mastery is complementary rather than competitive. My maths teacher was obliged to write right handed since he was in school, even though he was left handed. We agreed he was the least legible of our teachers.

Of course you can train yourself and make your non-dominant hand to be equal or even greater than your actual dominant handedness. Handedness is directly wired to the right/left hemisphere of your brain, so by training, you will actually re-wire your brain and acquire new pathways. It's a hard process in terms of breaking habits, otherwise, it's non-invasive and non-painfull, where most humans tend to give up before acquiring this skill justifying it as an unnecessary/low priority goal.
Handedness is not decided upon birth. It's gained in the earlier process (while a child is still in mother's womb) based on personal/individual preference (expressed by sucking a finger btw) toward right-handedness (90%) or left-handedness (9%), cross-dominance/ambidexterity (1%).

https://youtu.be/DU3OdTLuHf0
https://en.wikipedia.org/wiki/Handedness
https://ghr.nlm.nih.gov/primer/traits/handedness


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How to supply oxygen to a culture vessel?
I'm reading this paper:
https://www.jstage.jst.go.jp/article/jpsa/51/3/51_0130043/_pdf
From day 17 of the culture period until hatching, pure oxygen was supplied at a flow rate of approximately 500 ml/h through the previously installed plastic tube.
What kind of hardware is used to achieve this ? I would like to test this method, but I don't have access to laboratory equipment ( meaning .. I'm not going to buy expensive equipment for this hobby project..)
I'm used to incubate eggs inside an incubator, and day 17 is approximately the day when they start chirping, and sometimes hatching, so it's my understanding that at this point the chick starts to use its lungs, and breaks the shell in search of oxygen.
Also I don't understand the airflow in this setup: when I supply 500 ml/h of oxygen, where does the displaced gas go ?

Gases are supplied to culture vessels by design. Flasks, for example, may have filtered caps that allow gas in, or microplates with lids that have enough room under the lid to allow a gas exchange interface with the culture medium. Of course with these traditional culture vessels you need to make careful consideration about fill volume, since the gases won't penetrate 100% through the culture medium.
In the case of your paper they cut a large hole in the side of the cup and plugged it with cotton, then fed a small plastic tube through into the cup. They attach a gas line and feed oxygen through the tube. The cotton plug is where the gas will escape back out without letting contaminants in, as the cotton plug acts as a filter. The system seems to have no other outlet, so it makes sense.
In order to control a gas flow rate, you need a regulator of some sort to act as an output control.


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How many proteins on PDB have unknown function?
I was wondering how many of the files in the Protein Data Bank (PDB) have unknown function. The only paper I can find from an internet search is this one from 2012, which I assume might be outdated. I’d welcome suggestions of how to find this information for myself.

The article cited in the question indicates that the authors searched the PDB with the term “unknown function”. There is nothing special about this — you just type in the standard search field and hit ‘Go’. I conducted a search of this type myself:
http://www.rcsb.org/pdb/results/results.do?tabtoshow=Current&qrid=91CA3A5F

Which returned 4384 structures out of approx. 149,600 in the data bank.
Of course, it is evident from the first page of the results that the number of unique proteins is smaller than this because a single study may examine different forms of the same protein.
I admit that I was surprised to find that people had spent time and money determining the structure of so many proteins of unknown function, but it appears that there is at least one blanket initiative to determine the structures of bacterial proteins of unknown functions because of their roles as potential pathogens. The idea would seem to be that they even if their mechanism of pathogenicity is unknown they could still be targeted on the basis of their structure.

There are a number of structural genomics projects.


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DNA replication - how many times and when does it occur?
I’m currently learning about DNA replication in both prokaryotic and eukaryotic cells. And my lecturer has mentioned that replication is a once in a lifetime activity. And I’m not sure what this is implying because I’ve searched up that DNA replication occurs during cell division (cell cycles), which occur repetitively as organisms develop.

Perhaps your teacher was talking about unicellular organisms.

This sounds like a difference in perspective of when exactly cells "die". If you consider that, in a cell division, a mother cell "gives birth" to two daughter cells, you could argue that the mother cell has "died". It makes sense to think about cell division in this way because it puts both daughter cells in the same level, without one being "special" due to it being the mother cell itself while the other is considered the "new cell".
If you face cell division like this, any cell (eukaryote or procaryote) will only really duplicate their DNA once: they duplicate their DNA -> they split into daughter cells, in which they "die" -> (eventually) each daughter cell duplicate their DNA -> and so on.
Like I said this is just a particular POV we can adpot when we try to understand and describe cell cycle and cell division (although it is a common one for researchers in the field).


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What species is this fly?
I am looking for an ID of this fly at genus or preferably species level.
Location: The Netherlands.
Size: approx. 7-8mm
Habitat: indoors, attic.
Timing: usually appears late winter, early spring

Apparently, this is a Pollenia sp
https://forum.waarneming.nl/smf/index.php?topic=447650.0.
One of the common species from this genus, Pollenia rudis, is often found overwintering in groups in attics and is therefore known as the cluster fly or attic fly.


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What does it mean for Caenorhabditis species to be "pseudoparasitic"?
In this Wormbook chapter, Kiontke says that some Caenorhabditis species live "pseudoparasitically" on warm-blooded animals. What does it mean? What is a pseudoparasite? I understand a parasite to be in association with a host where the relationship is beneficial for the parasite and harmful for the host. How is pseudoparasitism defined?
I have found several definition:

Something in the blood that is mistaken for a parasite: not applicable to Ceanorhabditis as no Caenorhabditis has ever been found alive in blood
A false parasite; may be either a commensal or a temporary parasite (the latter is an organism accidentally ingested and surviving briefly in the intestine): could be this
an object or organism that resembles or is mistaken for a parasite: could be this
interpreted to be parasitic but not actually parasitic: could be this
This definition actually sounds like the definition of a parasite and only applies to invertebrates, so not applicable to Ceanorhabditis

In conclusion, I would say that some Caenorhabditis are pseudoparasitic of warm-blooded animals, which means they are commensal and cause no harm. However, I don't see the point of saying they are pseudoparasitic. I would rather just say commensal.

It might just be my opinion, but I think part of the issue approximates something like: The more you know about a subject, the pickier you become about how you would describe something. I remember this being true in undergrad calculus, when the professor would lay out a concept, but also hint that it's not the full picture because of more advanced concepts that they knew, and we couldn't know unless we pursued a PhD in Mathematics.

Why don’t you Email the authors themselves?  When I contacted Walter Sudhaus many years ago he was very helpful.


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Do all gene mutations in pathogens lead to more harmful consequences for humans?
It seems that the concern we always hear is that bacteria and viruses mutate to dodge our treatments either through random mutations or survival of the fittest. Do harmful living things ever mutate to become not harmful?

Mutations are random; the (pathogenic) bacteria (or any living being) will randomly acquire mutations that may be beneficial, deleterious or neutral to its fitness. Only beneficial and neutral mutations will survive the selection. Random mutations and survival of the fittest are not two independent mechanisms. The random mutations can alter the fitness as I mentioned and natural selection ensures the survival of the fittest.
Many pathogens have reduced genome (number of genes) compared to their free living relatives (Weinert and Welch, 2017). This is because they lack most of the genes required for synthesis of different metabolites required for survival. They rather obtain these metabolites from the host and hence they have the parasitic lifestyle. It is not possible for the pathogens to acquire that many genes to stop being pathogenic and become a free-living organism. It may be possible via lateral gene transfer wherein a bacteria may obtain an entire gene (or a set of genes) from another bacteria but the likelihood of that happening to convert a pathogenic bacteria to a non-pathogenic bacteria is negligible.
It is certainly possible that pathogens might lose the activity of some of the pathogenic genes (for example those required for toxin production) due to mutations. However, they may no longer be efficient pathogens and would be outgrown by the others who still retain those genes.

Its also worth mentioning pathogens often evolve to be LESS harmful, not killing your host is a good thing, most of the really deadly pathogens are are ones that jumped from a different host species, and have not had a chance to evolve to be less harmful.

@John that would perhaps not be that straightforward. It depends on several parameters so making a general statement on that would be risky. AFAIK, there is a post here that exactly addresses that topic.

@John it's often even more simple than jumping from different host species. A commensal microbe that finds itself in the wrong niche on the same host can all of a sudden become a big problem. A happy bug in your colon is an unhappy bug in your urethra, for example. Much of infectious disease comes from inconclusive negotiations for symbiosis.


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How fast can muscle fibers relax
I can find a great deal of information about how muscles contract, and how we divide them up into fast twitch and slow twitch and so forth.  However, I can't seem to find anything on how fast a muscle fiber can relax.
How fast can a contracted muscle fiber stop providing force when the motor neuron stops innervating it?

To clarify, are you sure you mean to ask what happens when a "motor neuron stops innervating" a muscle? Or do you mean to ask about the normal physiologic process of muscle relaxation.

I thought they were phrasings for the same thing, but perhaps I used the wrong term.  A physical example of what I mean:  I am doing a bicep curl.  At a point near the top of the curl, I relax my muscle as much as possible and let the weight (and my arm) fall.  I'm interested in how quickly my muscle can stop resisting that falling movement.


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Winter is getting shorter and warmer. Does this mean deciduous trees can photosynthesise for longer and thus absorb more carbon dioxide?
As springtime is starting earlier this year, I wondered if that would mean deciduous trees had more time to photosynthesise and, therefore, they could absorb more CO2 or have longer periods to grow, etc.
Also, is there any evidence that colder climate deciduous trees would fare better or worse as conditions change for them?

yes, you can see from the growth rings that they vary year upon year based on warmth and water. Deciduous trees fair differently to climate change depending on species, the ones on the far ends of their ranges can get outcompeted by other trees. http://www.euforgen.org/species/ check the ranges. don't know what references to add.

A warmer climate in this regard is beneficial to photosynthesis and plant growth. The thickness of the tree rings are constrained by the length of the growing season according to University Corporation for Atmospheric Research:

In some areas the limiting factor for growth is water availability, in other areas (especially at high latitudes) it is the length of the growing season.

Thanks for the downvote but I do not understand why. If you want me to react you have to write something. Is the question about if buds burst earlier and leaves fall later? Is the cited source not fitting?


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How do astronauts eat in space?
If there is no gravity in space how does the food enter the stomach?
My guess is that it is due to the movement of the esophagus.Am I correct?

swallowing does not require gravity. you can test it by yourself if you stand on your head and eat something

Have you ever eaten lying down? What did you notice (or not notice?) This is very easily answered with a simple google search. They even have videos of astronauts eating in space.

swallowing of food or water from mouth to stomach is done with the help of peristalsis action of esophagus
Then rhythmic, unidirectional waves of contractions will work to rapidly force the food into the stomach. This process works in one direction only and its sole purpose is to move food from the mouth into the stomach.
In earth it also happens but it is assisted with gravity but in space Peristalsis action is the only process by which food or water is taken to stomach .

Welcome. In this community we require answers to be accompanied by suitable sources, preferably journal papers.


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What is Growth and how can we define it to be a defining property of life?
I was reading a book and it said that internal/intrinsic growth is defining property of life and not extrinsic growth as saying accumulation of dust on a book makes it a bit bigger, even if it is by a few mm but since it's just a deposition of material and it can be removed, so it's not living. Now, if we see intrinsic growth then I had a doubt. Say we took a piece of log and dipped it into the water. Then the log will also grow in size and this growth is from inside, but the log of wood isn't living. So, I was in doubt that how can I define growth for a living.

There has been a lot of debate on this topic actually and there is no universally agreed upon definition of life. Almost any point that you raise can be refuted with a non-living counter example. Therefore, I think that this question will most likely accumulate answers that are primarily based on opinions rather than facts.
However, if you just refer to growth in living systems it almost always means replication (of cells/genetic material).

All rudimentary definitions of life I've ever come across include growth as only one of many properties. I doubt a log of wood also conducts reproduction, homeostasis, or metabolism (to list a few other features). Similarly, a computer virus reproduces, thermostats self-regulate, and abiotic chemicals may 'metabolise', but somehow these don't confound us. I think the questioner can't proverbially see the wood for the trees :-)

Actually this question came in my mind when I encountered a question that said whether plasma membrane is living or not.My mind instantly drifted towards coacervates prepared by some scientists in order to explain that how 1st form of life would have originated. Then I thought that if I prepare a phospholipid bilayer and add all sorts of protein and stuff in it,can I call it living? Will it show growth? If not then what is life and what is living. How do we define growth in a way that it can best explain life.

If you are just asking what does growth mean in the context of living systems then it almost always means replication of a unit: cell or genetic material (cell division, DNA replication etc).
Note that increase in cell volume or the inter-cellular space (accretionary growth) also happen in living systems and they are also considered growth. However, at a gross level these processes are indistinguishable from what is happening to wood that is dipped in water.
So growing is not an exclusive feature of living systems but still one of the defining features.


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What sort of fish is this?
Just saw a meme online with this fish on it. Is this a real fish? Can some aquatic expert identify this for us?

That is a blue parrotfish (Scarus coeruleus):

(photo: Marc Tarlock via Wikimedia Commons)

Mgk - C'mon. Parrotfish are AMAZING! Some of them can change sexes as adults! They are responsible for most of the sand on earth! They are good eating! You can actually hear them crunching coral when snorkeling! Surely you can say more than "this is a parrot fish." (Can you tell I like parrot fish?)


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How do viral vaccines work?
I have read that a vaccine against a pathogen typically works by using a dead or weakened version of that pathogen and then inciting an immune response against the pathogen so that the immune system then recognizes that pathogen in the future and attacks it immediately.
However, suppose that a person gets vaccinated against a virus. Why couldn't the virus infect a few cells before it runs into immune system cells and starts replicating as normal? Does the immune system somehow recognize virus-infected cells?
Also, how would a vaccine against a virus that attacks immune system cells work (like HIV, for instance)? In this scenario, wouldn't any immune cell that tries to destroy the virus get infected itself?

Look at the normal reaction of your body during infection by a new virus, how (the steps are : detection of the infection, inflammation, processing and presentation of antigens, replication, mutation and selection of the B-cell-antibody pool) it needs 2 weeks to create potent B-cells-antibodies, how it is much faster when enough of the viral proteins contain "antigens" already seen for which your body previously made long-term memory B-cells.

Vaccines containing these weakened or killed viruses or bacteria are introduced into your body, usually by injection. Your immune system reacts to the vaccine in a similar way that it would if it were being invaded by the pathogen — by making antibodies. The antibodies react to the vaccine (virus/bacteria) just as they would the live pathogen — like a training exercise against an antigen. Then they stay as amemory in your body, giving you immunity. If you are ever exposed to the real disease, the memory is activated and antibodies are there to protect you.
Moreover if a cell gets infected virally, infected cells produce and release small proteins called interferons, which play a role in immune protection against viruses. Interferons prevent replication of viruses, by directly interfering with their ability to replicate within an infected cell.

It is better to use the term "pathogens" instead of "germs" especially when the OP is very well aware of the former. Also, it would be great if you could provide some references

Edited your answer for terminology. If not acceptable, please feel free to roll back.

It depends on the particular vaccine.  Generally we can divide vaccines into two groups: live and "dead".
Live vaccine contains weakened (attenuated) pathogen, which (in case of a virus) theoretically can infect our cells.  However, as it is attenuated, it is not doing it very efficiently, thus even naive immune system has no problem with defeating it.
"Dead" vaccines contain either inactivated ("killed") pathogen or only some of its parts (antigens).  As it is not active virus, it can not infect your cells.  It is just presented to your white blood cells as a "dummy" for "target practice".  And by "target practice" I mean things like activation and proliferation of competent lymphocytes, followed by formation of immunological memory - exactly as if the organisms was infected by a virus.
Our body is "blindly" creating a variety of lymphocytes, and each of them is able to fight with pathogens with certain antigens.  As the lymphocytes has been created "blindly", most of them seems to be useless.  However, if there happens to be a lymphocyte able to recognize a virus antigen, the lymphocyte is indeed useful.  It proliferates, "learns" to recognize the antigen even better, fights the virus (or its antigens) and is preserved as memory cells, just in case of reinfection.
Of course I am oversimplifying here, but I hope I managed to grasp the big picture. ;)


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Why do high cholesterol levels result in a buildup of fat in blood vessels?
As is well known, high levels of cholesterol can lead to a buildup of fat in blood vessels, which can lead to them being constricted which makes it more difficult for blood to pass through. In fact, this can end up with the formation of fatty deposits that, if they suddenly break, could result in a clot that causes a heart attack/stroke. Therefore, the resulting buildup of fat because of these high cholesterol levels is highly important.
My question is why do higher levels of cholesterol result in a buildup of fat at all? Why do fatty acids care that there's more cholesterol around? I know cholesterol and fats are both lipids, but beyond that, I don't see the connection.

I assume this isn't a homework question, but you still should have made an attempt to answer this before and shown it here. If the inside of a blood vessel were perfectly smooth, this probably wouldn't occur. But blood slushing along in those blood vessels all day every day do cause some "wear and tear" which is when lipoproteins get involved.

@anongoodnurse I did do some research. Apparently there are cholesterol deposits, where cholesterol is the raw material for the deposits, however, there are other types of deposits and I was unable to find information there.

The point of my comment is to show your research. Anyone can say they did the research and found nothing helpful. Showing the attempt is what counts.

The phrase "high cholesterol", and the measurement itself is a marker for high levels of a particular lipoprotein, Low density lipoprotein (LDL). Because cholesterol and triglycerides are not soluble in plasma, they are packaged by the liver into soluble particles called lipoproteins. Packaged in lipoproteins, these lipids are transported throughout the body, for use by different organs and tissues. As these lipids are dropped off, the lipoprotein is converted from one form to another, with characteristic biophysical and physiologic properties. The LDL is a late stage of a lipoprotein before reuptake at the liver (and other organs, but mainly the liver) via the LDL receptor. We happen to know that people who have high levels of circulating LDL are at risk for, e.g., cardiovascular disease because of The Framingham Study, and that if you can reduce circulating LDL levels you can decrease the risk for these diseases. The molecular basis of this risk was demonstrated to be, in large part, failure of clearance of LDL particles because of ineffective receptor mediated endocytosis, as described in this wonderful 1986 paper in Science.
From this presentation:

Some LDL cholesterol circulating through the bloodstream tends to deposit in the walls of arteries. This process starts as early as childhood or adolescence.
White blood cells swallow and try to digest the LDL, possibly in to digest the LDL, possibly in an attempt to protect the blood vessels.
In the process, the white blood cells convert the LDL to a toxic (oxidized) form.
More white blood cells and other cells migrate to the area, creating steady low steady low-grade inflammation in the artery wall.
Over time, more LDL cholesterol and cells collect in the area. The ongoing process creates a bump in the artery wall called a plaque. The plaque is made of cholesterol, cells, and debris.
The process tends to continue, growing the plaque and slowly blocking the artery.

There is a good overview of the general physiology here in Robbins The Pathologic Basis of Disease. Chapter 5, Genetic Disorders, reviews the physiology, and the relevance to disease, in the section on Familial Hypercholesterolemia. The review is relevant to hypercholesterolemia in general.

So with more cholesterol, it gets packaged into LDL at a higher rate. So does LDL cause a buildup of fat? How does it do this? Is it the actual raw material of the buildup?

@Korvexius it turns out to be quite complicated. Inadequate LDL uptake by the liver causes a number of problems. There are some direct effects of high levels of LDL (because they aren't being taken up), and also some indirect effects. Atherosclerosis is in many ways a disease of inflammation as much as it is a disease of lipid accumulation. LDL probably plays a bigger role through initiating an inflammatory process in vessel walls than it does by depositing lipids directly.

@DeNovo - I think an explanation of the genesis of atherosclerosis was what the OP was really asking for.

@anongoodnurse It sounded to me like they were trying to figure out how cholesterol molecules could cause fatty acid deposits. I figured learning what a lipoprotein was (and what exactly "high cholesterol" means) would have been more helpful than reading about foam cells.

@DeNovo - I agree there needed to be a discussion of cholesterol and lipoproteins, but the question was about atherosclerosis - the entire first paragraph, in fact. Also, see the follow-up question.

@anongoodnurse I'd welcome an answer from you with an overview of atherogenesis! I'd have to look through a review myself to make sure i wasn't misremembering anything.

@DeNovo I would also like to see information on the direct cause of fatty acid deposits in your answer if you could. The question is less about atherosclerosis and more about the deposits.

@Korvexius - Atherosclerosis is about the fatty deposits. Research.

@DeNovo - Apparently you're correct. The OP doesn't want to know about the genesis of atherosclerosis; they want to know how fatty deposition in blood vessels starts. Clearly any answer I wrote would not be helpful.

@anongoodnurse DeNovo is right - I'm well aware atherosclerosis is about fatty deposits and have no idea why you assumed otherwise. But my question directly relates to how those fatty deposits build up, rather than the obvious conclusion that atherosclerosis is an after effect of this buildup.


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What exacly happens at chromossome level during fecudation and in the first zygotic division?
I was reading about the viability of animal hybrids and found the following sentence here:

Previously, this idea was not widely accepted, because, in general, different species have different numbers of chromosomes, the structures within cells that contain genes. This difference can prevent the normal development of the embryo, as each chromosome that came from the male parent must be aligned with an equivalent chromosome from the female parent when the fertilized cell divides for the first time. Without this proper alignment, the cell usually cannot divide and, thus, dies.

However, I couldn't find more information about the first zygotic division and this alignment of homologous chromosomes. This bugged me a little since, during mitosis, there's no alignment of that chromosomes.
So, anyone could clarify what exacly happens at chromosome level during fecudation and in the first zygotic division? How can this block the development of an "embryo" formed by two very distant species' gametes?


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when you are to non-culturally detect the presence of E. coli in the soil from a cow pasture?

You are to non-culturally detect the presence of E. coli in the soil from a cow pasture. You do this by extracting the total DNA from a sample of the soil and PCR amplifying with E. coli-specific primers that bind to a gene only found in E. coli that amplify a region of the DNA 167 bp long. Propose a postive sample that could be tested alongside your experimental sample.
A. Known Shigella DNA
B. Water
C. Number of Injections
D. Muscle DNA
E. Known E. coli DNA

I think the answer is (E) Known E. coli DNA. That would be the positive control in this context. For a positive control, you need something that you would know the response for. E. coli specific primers would amplify the known E. coli DNA. Water is obviously wrong. I could be wrong. Am I missing something?

To the homework close voter: this user has made an attempt to answer, so has fulfilled the requirements of the homework policy.

Yes, you're correct. The question is asking for a positive sample that would be amplified by E. coli specific primers. Known E. coli DNA would do the trick.

@user50592 you're welcome. If you'd like to mark this as the answer, click the gray checkmark next to it. I would also recommend you take the [tour] and visit [help] to learn about this stack exchange site.


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Can MHC class I be used for presenting peptides of extracellular origin by non-professional APCs?
Wikipedia says that: "The antigens presented by MHC class II are derived from extracellular proteins (not cytosolic as in MHC class I)."
So does this mean that MHC class I cannot be used for peptides derived from phagocytosis by non-professional APCs? (i.e. peptides that of extracellular origin?).
For example, when non-professional APCs that can undergo phagocytosis (Eosinophil, neutrophil, dendritic cell) engulf bacteria, will they present their antigens using MHC I although the peptides are of extracellular origin? or will they not present any MHC at all? thanks!

when non-professional APCs that can undergo phagocytosis (Eosinophil, neutrophil, dendritic cell) engulf bacteria

Dendritic cells and probably neutrophils are professional APC, so this part of the question is a little confusing.
You're asking about cross-presentation, which is the process by which extracellular antigen can be presented to CD8 T cells on MHC class I.  Cross-presentation is mainly performed by certain sub-classes of dendritic cell. A number of other cell types have been shown to be capable of it, but it's not clear how important they are in vivo.
A decent review of cross-presentation is Understanding the Biology of Antigen Cross-Presentation for the Design of Vaccines Against Cancer.  A review of a related but somewhat different concept (MHC recycling) is Endocytic Recycling of MHC Class I Molecules in Non-professional Antigen Presenting and Dendritic Cells.


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what is the difference between homozygous and heterozygous duplication?
In a genetic test result it's written
homozygous duplication

or
heterozygous duplication

Does it mean four copies of the same gene for homozygous duplication and three copies for heterozygous duplication?


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Pain perception in animals with nerve nets
Are animals with nerve nets, like sea urchins and jelly fish, theoretically able to feel pain? They have output and input organs which would make them "vulnerable" to feel pain but on the other hand, they don't have brains. I was wondering if they show any signs of "pain" when they are attacked or eaten?
And if they don't show any signs of pain is there the possibility to measure something that could be interpreted as pain?
Edit:
The word pain is here meant in a way, that it responds to an outer force with behavior which one could interpret as an inner-process that shows discomfort. The important parts are here the words "interpret" and "show signs of".
Pain is here thus meant as a behavioural response that could lead to an interpretation of an inner-process


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Why can we hear above 8 kHz
Why have humans developed ears capable of hearing sounds that are (never?) heard in nature.
Is it known why humans developed the ability to hear up to 20 kHz when all the relevant noises are below 8 kHz? (at least in my experience) Or why was it beneficial to hear in that range?

Your question seems to be based on a false premise, because indeed there are sounds in nature >8kHz, including sounds at higher frequency than human hearing (for example, mice vocalize up to 60 kHz or so).

@BryanKrause Yes of course there are some sounds but why would it be beneficial for us to hear them?

@user1136 How does that help with sounds that aren't in high frequency ranges? Doesn't this only work with very high frequencies? How is it helpful for a human to localize mice and other small animals?

Sounds in nature aren't usually pure tones.  They have overtones at higher frequencies, and these are very important in distinguishing between sounds.  Think of several musical instruments all playing the same note: you can readily tell the difference between a piano, a violin, and a trumpet, can't you?

@jamesqf But why don't you hear the tone that's over 8 kHz only the part of the tone that is deeper? Or do you?

You do hear those tones - that is, the ear reacts to them.  But the brain interprets them as a single sound instead of separating them into pure tones.  Similarly, the eye has just 3 color receptors (for most people): the brain combines signals from them to produce the 10 million or so different colors that a human can distinguish, but you don't see the separate RGB signals.


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How to compare models of evolution to make assumptions about selection?
I'm having trouble understanding the concept of comparing models of evolution with LRT. I have following models: M0 (neutrality), M1A (negative selection) and M2a (positive selection) with following results from Maximum Likelihood:
M0: w=0.81; lnL=-5702.55
M1a: wo=0.50, po=0.65; w1=1.0, p1=0.35; lnL=-5650.21
M2a: wo=0.46, po=0.64; w1=1.0, p1=0.25; w2=2.38, p2=0.11; lnL=-5632.10.
I want to do the Likelihood Ratio Test to compare the models and make assumptions about the selective pressures on the analyzed sequences. So, first I compare M0 and M1a and calculate LRT=2(lnL1-lnL0)=104.68.
Now I want to take a look at a Chi table, but what am I using there? Am I supposed to used the po value for the M1a model? And if that value exceeds the value of the p-value in the table then the simpler model is chosen?

The answer to this question depends strongly on how you are formulating the different models. Are you for example computing this from dN/dS from a sequence alignment? Or based on explicit phylogenetic models? Those can have quite different formulations. The model names you are using out sound like they might come from PAML, but it's not clear. There are some exercises for this specific case elsewhere.
I am assuming that what you are really asking is how many degrees of freedom to use when e.g. computing a p value.
For this question, you have to think about the LRT a little. What it is really asking is "do I explain the data better by adding parameters to a model (while accounting for the fact that likelihood will by definition increase with more parameters)?"
So what you need to first establish is what the parameters of your models are. Assuming that the models are "nested", you can just use the difference in the number of parameters as the degrees of freedom. "nested" in this context means that the base model (e.g. H0, probably M0 for you) doesn't have parameters that are missing for the alternative model (which is assumed to have more parameters).
More flexible than the LRT are things like the AIC, which gets rid of Chi square and just computes a value from likelihood and model parameter number. This works well in practice and is nice because it's more flexible and a little less convoluted model comparison technique than the LRT. You can additionally use the AIC to compare non-nested models, which doesn't really work for the LRT.
I hope that this helps.


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Can muscles work as brakes?
When I walk downhill I lose potential energy.  If I descend 100m in, say, 10 minutes I lose potential energy at a rate of about 114J/s (114W).  Where does the energy go?  Not into kinetic energy provided I don't run or fall, not into heat, for there is little friction to create such heat.  My leg muscles appear to be acting as very efficient brakes, absorbing the potential energy but turning it into what? Chemical energy?

Yes, muscles do work as brakes; it's a process called eccentric contraction.
The energy balance of an eccentric contraction is a pretty difficult question. Some fairly recent research (Linari et al., 2003) found that a low velocities more energy is consumed (i.e. released as heat) even during eccentric contraction, while at high velocities, the muscle does store some energy from the eccentric motion. In frog muscles, at least.

So muscles do work a regenerative brake... in some conditions.
It's an active research topic where exactly this (non-heat) energy gets stored. Current models (in the previously cited paper) cannot account for all of what's measured experimentally; only 34% of it could be explained.


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How much oxygen does a human need to breathe?
So, I know that the title isn't very precise, but so is my current knowledge of the subject. It begs the question of what unit are we talking or maybe percentage? Let me explain the situation.
Earth's atmosphere consists mostly of 21% oxygen and 78% nitrogen. O2 is the compound we use to breathe, but nitrogen on the other hand is just a non-toxic gas and is not necessery. Well, it is as it increases pressure which is essential for human existance, BUT it can be substituted by other non-toxic gas like Argon.
On Earth's highest mountains oxygen percentage is on a similar level, but the pressure is lower. Hikers have to use oxygen tanks. If I deduce well, with lower pressure, human needs more percentage points of oxygen than in higher pressure.
Now I am writing a simulation of space ship, in which there is a security system, which controls oxygen in the cabin when pressure drops and it should always keep oxygen amount correct for any pressure given.
How can I calculate the perfect oxygen amount in air and what would be the actual unit of it? Any idea of a unit I have come with would be $\frac{kg}{m^3}$.

Probably the term you are looking for is the partial pressure of oxygen.


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Why do wild animals not eat in captivity?
I have rescued possums before but this is the first full grown opossum I took in. She was skinny unlike the one I have now for 3 years and healthy. I would not normally take in a grown animal like this, but she looks like she hasn't eaten for a while.
I have put all the recommended foods in a cage for her, but she won't eat. I understand that they eat everything so why the hunger strike? Will she starve or eventually eat for self preservation?
Where I live if you can hunt them you can breed them for livestock or what ever. Some places have no regulation unless the species is endangered which this one is not.
https://www.youtube.com/watch?v=YEVL0xuJuPQ Possum Snuggle.

Please do not try to keep a wild animal as a pet as someone untrained.

"But while possums thrive in the wild, examples of these creatures surviving in captivity are rare. Another point is that it is illegal to keep possums without a wildlife rehabilitation permit. [...] Vets don’t have the experience to deal with their health issues." https://www.animalwised.com/possums-as-pets-general-guidelines-and-tips-1401.html

@BryanKrause revised.

note there is no state in the US that does not have some regulations concerning keeping opossums as pets.

I'm voting to close this question as off-topic because the frame for this question makes it seem like it is about how to care for a wild opossum or predict a specific animal's behavior. If you can edit this to make it clear it the title is the actual question (why do wild animals not eat in captivity), and include your research, I will retract my close vote.

Could possibly be closed as personal (veterinary) medical question as well (as it is currently framed)

@Muze The legality in your jurisdiction doesn't have much influence on my suggestion not to keep a wild animal as a pet or livestock if you are not trained to do so. I'm far from an "animal rights activist," but I believe in a basic respect for especially vertebrate animals, which every farmer I have ever met has, along with sufficient training to care for them.

@BryanKrause I let the possum out of her cage. Now she is eating and wandering the house. I do have experience raising them. I would not have taken her in, but she looked emaciated.

Many wild animals will not eat in captivity because they are under stress, few mammals react well to captivity. weird smells and sounds, restricted movement, inability to hide, there are dozens of stressful aspects to captivity that trigger the flight or fight response for small mammals. Lack of appetite is a common stress response in mammals and even when very hungry they are often more focused on escape than feeding. This is one reason keeping wild mammals as pets is regulated in every US state, and is highly discouraged, you are basically killing the animals slowly.
In opossums and many mammals lack of appetite is also one of the early signs of rabies infection, so yet another reason laypersons are discouraged from trying to keep wild opossums as pets.
Source 1
Source 2

If it doesn't answer your question then I have no idea what you are trying to ask, If you are asking for a specific diagnosis for one individual that is very off topic.


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What regulates cyclic AMP?
After reading a textbook chapter on GPCRs I am still confused by what regulates cAMP.
I took in my notes that cAMP is made by adenylyl cyclase and destroyed by cAMP phosphodiesterases (also another question within a question, are phosphodiesterases the same as phosphatases?)
So is cAMP regulated by GPCRs or is it regulated by cyclic AMP dependent Kinase A (PKA)?
I did find this article, but I'm not sure if I am understanding this correctly to answer my own question, but it seems like they are saying GPCRs regulate cAMP?
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2720142/
Thanks

Phosphodiesterases are not necessarily the same as the phosphatases. A phosphodiester has 2 ester linkages, like in DNA. So a phosphatase could specifically cut off phosphates with a single ester linkage while ignoring the phosphodiesters.

Have you consulted a basic biochemistry text such as Berg et al (available on NCBI Bookshelf)? Start there.

Not helpful as you do not provide a direct answer to my question or even provide the link to the text you are referencing. Here is a google search of Berg et al:
https://www.google.com/search?ei=v46SXPWTNqqMggeL4ZUo&q=berg+et+al&oq=berg+et+al&gs_l=psy-ab.3..35i39j0l9.3621.4609..5211...0.0..0.92.752.10......0....1..gws-wiz.......0i71j0i67j0i131j0i20i263j0i10i67j0i10.4283tGmD09U