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How to relate human metabolic model reactions and cancer drug targets / reactome items?
Trying to find a way to take a cancer drug (from CancerDR, for instance) and infer the metabolic reactions that are affected by it in the Human Metabolic Model.
Essentially, I would like to know which HMM reactions are affected by a certain cancer therapy drug, especially the ones found in the Cancer Cell Line Encyclopedia.
Example:
Searching for the reactions that are associated with the HSP90 protein, which is targeted (to some extent) by the 17-AAG agent.  That way, I can trace back the relevant section of the HMM and mark it as 'affected' by that agent.
This could be a very broad or naïve question, but I am afraid I don't know enough to be able to determine that.
If someone can only provide some tip or guidance, that will be greatly appreciated as well.
Thanks very much!

What exactly do you mean with reactions in the CCLE? Can you provide a link to the relevant resource in the CCLE?

Sure.  I believe you have to create an account, but it's free: Cancer Cell Line Encyclopedia data; go to the last section, "Pharmacological profiling".

Short answer:
For drugs with targets having a direct effect on reactions in the model:
Find the gene name for the target protein -> Find the Entrez Gene ID (or other gene identifier, depending on the model) -> Search the model file or database for reactions having a gene association with the gene identifier.
AND/OR:
Find the EC number for the target protein. -> Search the model file or database for reactions associated with the EC number (likely to miss many reactions or be imprecise).
EC numbers can be found in the UniProt database, while the HGNC database at http://www.genenames.org/ can be used to look up genes by name and find their Entrez Gene ID and other resources, including links to UniProt. Many other databases can also be used.
For drugs with targets having an indirect effect on reactions in the model:
Model/estimate in-direct metabolic effect yourself by using data on known regulatory effects to create new gene-reaction associations or modify the bounds on reactions affected by the drug.
Long answer:
To knock out or constrain a reaction based on data about a drug, you have to go from an entry in a drug database to an EC number or gene identifier consistent with the annotation in the model you are using. However, There is currently no standard annotation nomenclature for gene-protein-reaction (GPR) associations in metabolic models, and in general only direct GPR associations are encoded in model files.
Assuming that you have a metabolic model in SBML format (for example the RECON 2 model), reactions may have a gene association and/or be associated with an Enzyme Comission (EC) Number.1 However, several model reactions catalyzed by distinct isozymes (different enzymes catalyzing the same reaction) may be associated with the same EC number, and many reactions may not be annotated with an EC association. Therefore you might want to use the gene associations directly. Both gene associations and EC numbers are recorded in the "notes" tag for each reaction in the SBML file, and is not part of the SBML specification. (A proposal has been published for improving support for gene associations in the SBML format.2)
Using EC numbers:
Using EC numbers is the simplest, but not the most precise or possibly even usable solution. It is simpler than using gene associations, because genes may described using any of a number of identifiers depending on the database while any reaction is associated with at most one EC number. Once you know the target protein, you can look it up in the UniProt database, and find its EC number (if any) in the field "protein names". A simple example: The DrugBank entry for the cancer drug Fluorouracil (http://www.drugbank.ca/drugs/DB00544), links to the UniProt entry for one of its targets, Thymidylate synthase (http://www.uniprot.org/uniprot/P04818), where the EC number is given as 2.1.1.45. Searching the RECON 2 SBML file (or searching in BiGG at http://bigg.ucsd.edu/bigg/main.pl) for occurences of this number will show that it is associated with the "TMDS" reaction.
The IUPHAR database (http://www.iuphar-db.org/index.jsp) may also be useful.
Using Gene associations:
Genes are conceptually at least one step removed from the reactions their products catalyze, so one might argue that using EC numbers which actually correspond to reactions would be better. However, it is thinkable that a drug might affect only one of several enzymes which catalyze the same reaction and thus share an EC number. Furthermore,  annotation of reactions with EC numbers in metabolic models may be poor. Thus you may want to use gene associations to determine which reaction are affected by a drug.
Unfortunately, due to the large number of databases, a single gene may be described using many identifiers or symbols in different databases. You thus have to identify the gene coding for the product which is the target of the drug, and obtain the correct identifier for that gene which corresponds to the nomenclature used in the model.
Assuming again that you are using the RECON 2 model, it is an update of RECON1 which was made using the BiGG database3. Gene protein reaction (GPR) associations are therefore recorded using the gene names in BiGG. When ignoring the decimal and any following numbers, BiGG gene names appear to correspond to Gene IDs in the NCBI Gene database.5 A question on how to identify BiGG reactions  was also discussed at BioStar.6 However, you have the opposite problem: Finding a BiGG gene name from another gene identifier.
Using Fluorouracil as an example again, the DrugBank entry lists "Cytochrome P450 2C9" as a targeted enzyme, with the effect being inhibition. Following the link to the UniProt entry P11712 (http://www.uniprot.org/uniprot/P11712), we find that it has an EC number 1.14.13.- However, this EC number corresponds to a class of reactions (or rather, enzymes). There are also listed several additional EC number at the single reaction level, but as these may not cover or be associated with all relevant reactions, we'll use the gene association. Going back to the DrugBank entry (or just reading on the UniProt page), we find that the gene name is CYP2C9. Looking up this name at a suitable database, for example the HGNC database of human gene names at http://www.genenames.org/, we find the entry for CYP2C9 (http://www.genenames.org/cgi-bin/gene_symbol_report?hgnc_id=2623) and that its Entrez Gene ID is 1559. Searching for this gene identifier in the BiGG database, we find that four reactions are associated with this identifier (The actual association is to "1559.1"): P4502C9,P4502C92,P4502C93 and P4502C94. Note that none of these reactions have an associated EC number.
Defining your own GPR associations
Keep in mind that even in genome-scale metabolic models, a large number of reactions and processes are missing. While the term metabolism in its widest sense may be used to refer to all reactions occuring in a cell, metabolic models have so far been mostly limited to covering transport and inter-conversions of small metabolites. Processes involving signalling molecules and regulation of enzymes have been mostly or completely left out, along with critical processes such as DNA replication, DNA repair and apoptosis.  Because of the limited scope of the models, gene-protein-reaction (GPR) relations do not generally take regulatory effects into account, being limited to describing direct relations between one or more genes encoding (part of) a protein which directly catalyzes a reaction.
One could also model a very large number of indirect regulatory effects, but as current metabolic models generally do not specify these, you may have to construct them yourself. To find reactions in a metabolic model which are affected by a certain drug, you may have to "travel" several steps of interactions from the original target of the drug. You may consider using protein-protein-interaction network (PIN) data to help in this. You will have to consider the strength/importance of the interactions, something which may require a high degree of manual curation.
For example, if your drug affects HSP90, which is needed for correct folding of certain enzymes, you may consider creating a GPR stating that the gene for HSP90 (or rather, HSP90 itself) is needed for any reactions catalyzed by a specific enzyme to be active. This would be an indirect GPR, as HSP90 does not itself produce any part of the enzyme that catalyzes the reaction. As an alternative to on/off regulation through a GPR, you may consider searching for data on the ratio of correctly folded and misfolded enzymes in the presence and absence of HSP90, and apply bounds on reactions catalyzed by the affected enzyme to reflect this.

Again, I am amazed at your answers :).  Thanks so much for your help!


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Binding of Multivalent Antibody to mutiple epitopes?

A multivalent antibody molecule such as Immunoglobulin M Immunoglobulin A etc bind to more than one antigens or epitopes but I am confused about that wheather these multivalent antibodies bind to identical epitopes or can bind to different epitopes? means if one molecule of Immunoglobulin M being pentameric can bind to 10 epitopes at a time the 10 epitopes that it binds Will be identical or can be different..? Confused about that..       2. And also another Question I want to ask that as Immunoglobulin G,Immunoglobulin D and Immunoglobulin E are monomers but all of them have 2 antigen binding sites so we consider them as Mutivalent antibodies or not and if we cnsider them as multivalent antibodies then what are the Examples of monovalent antibody that Specifically only bind to One antigen molecule or epitope? Because as far as i Have studied Antibody or Immunoglobulin molecule hae specific "Y" structure that contains 2 binding sites. Similarly in this case also want answer that these momomeric ImmunoglobulinsG,D,E each binds to 2 identical antigens or epitopes or can bind to two different epitopes. Means that if Immunoglobulin G is binding to two epitopes these epitopes will be identical or can be different...??? :/

Please separate this into two questions.

Any one Plasma Cell that is producing antibody is making one kind of Heavy Chain and one Light Chain. In an IgG, there are two heavy chains each associated with a light chain. Together, a heavy and light chain have one epitope binding region - so in toto, an IgG is multivalent because each heavy chain : light pair can bind a single epitope for a total of two.
If a Plasma Cell is making IgM, it still is making only one kind of heavy chain and one light chain. Because they are pentameric, that does add up to 10 binding locations, but as Matt says above, sterically, all of these sites are unlikely to bind at the same time.
This multivalency is important in crosslinking antigens. Crosslinking is required for the original B Cell Recpetors to activate the B Cell, and it is also useful in clumping antigen in a way that it can be eaten by macrophages or otherwise interfering with the function of the antigen.

Non-engineered IgM (such as is produced in vivo) has the same binding domain on all "arms" of the pentamer. They don't bind to more than one antigen, instead they can bind to multiple copies of the same epitope. Due to steric hindrance, a single IgM molecule generally will not bind at all 10 binding sites.

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Mushroom Identification: White mushroom growing on tree (South America)
Near the place I live in I noticed a little white mushroom growing on a tree trunk (a dead palm tree). I was curious to identify it, but from the little I learned so far white mushrooms are the worst to identify. I’m on Brasil, near the tropics in an Atlantic Forest predominant area, and I haven’t yet found a field guide for my region (if anyone knows any, or a field guide from a region that grows similar mushrooms I’d love to hear suggestions).
Also, I'm very novice when it comes to mushroom identification (still learning the basics), so if I missed some important characteristic, or misinterpreted something that can be spotted in the pictures I'd love to hear it. The whole point of identifying this mushroom is learning.
Below are some characteristics I noticed and some pictures from the mushroom:

Region: Brazil southeast coast, state of São Paulo, predominantly Atlantic forest
Grows in very small colonies, but every fruiting body comes from an individual point (No Cespitose)
Presence of Volva
No presence of partial veil (No Annulus)
Pileus Color: White with some brown spots
Stipe Color: White
Wasn’t able to get a spore print, but when it grew old (at least I think that's what happened) and shrunk it looked like the spores where brown as can be seen in the pictures
Narrows gills? (The fruiting body is small, so maybe relatively speaking it isn't narrow)
Fruiting body leaves white stain in wood
Margins of the Pileus are cracked

There's a new colony growing, so I might be able to collect a sample once it grows big enough and gather more information, as a proper spore print, since my guess of the spores being brown might be a mistake (maybe those brown things in the dead mushroom are not spores).

Pictures:
Older colony

Recent colony

Shrunk fruitbody

Does it have a hollow stem? stem and cap size? The gills are like a Marasmiellus, and it's larger. A image of the gills in daytime and perhaps a lengthwise cross section would be cool. What's the region? There are s many more species of tropical mushrooms.

@com.prehensible Not sure about the hollow stem (would have to wait the new colony to grow so I can get a sample). Cap was about 1.5-2cm in diameter on the bigger ones, stem also about 1.5-2cm long. I'll update the question with a more specific location: it's Brazil southeast coast, state of São Paulo, on an area that is predominantly atlantic forest. Can you indicate a good field guide for this region? By the way, I looked at some pictures of different Marasmiellus species and some do look very similar to the ones growing here!

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Why does muscle blood flow decrease during exercise?
My questions semi-relates to these two items: Where does extra blood come from to fill your muscles during exercise? , and Blood pressure during exercise .
While reading Exercise Physiology by Dr. Brooks, I've come to the following quote, which is a bit puzzling to me:

Muscle blood flow increases exponentially with metabolism. At maximum exercise, some vasoconstriction occurs in active muscle in order to maintain blood pressure. Maximum muscle blood flow is largely determined by the amount of active muscle. The larger the portion of active muscle mass, the less total muscle blood flow.

Questions:

Why is it that the larger the active muscle mass, the lower the total muscle blood flow? I'd expect it to be greater.
Say that I am doing the bench press, does that qualify as an exercise with large active muscle mass?

I think that vasoconstriction from the quoted part refers only to maximum exercise. Because, in general, blood flow in the active muscles during exercise increases.

Re #2, think about the difference between doing it with heavy weight & few reps, vs light weight & many reps, or in the extreme, a highly aerobic exercise like rowing where endurance rather than strength is needed.

@jamesqf not sure I am following the comment james. Are you saying that Q#2, only applies to endurance / aerobic exercise? i.e anaerobic exercises like bench press would not necessarily qualify?

@angryip: No, I'm saying that apparently (I have never seen detailed studies) blood flow increases during aerobic/endurance exercise, but doing things like a bench press with heavy weights gets the muscles "pumped", which seems to decrease the blood flow.  (This is just my casual observation, of course, and could easily be wrong.)

@jamesqf interesting. I'll try to dig it up in this book and observe

I think there might be some missing context here leading to confusion of which muscles are being referred to in that passage.
During exercise, blood flow increases in active muscle due to local vasodilation. Cardiac output also increases, which ensures that total blood flow in the body is sufficient to meet the increased demand.
At higher levels of exercise, there is also systemic vasoconstriction. Systemic vasoconstriction acts to maintain blood pressure. You simply have too much total muscle for maximum cardiac output to supply all the muscle with full vasodilation plus the rest of the body without a loss of pressure. For an athlete with greater maximum cardiac output, it would be possible to fully perfuse more muscles at high effort than for someone untrained.

At maximum exercise, some vasoconstriction occurs in active muscle in order to maintain blood pressure

Because vasoconstriction is systemic, it has an influence on all the muscles, including the active ones. You should think of this vasoconstriction as relative to already dilated vessels, not necessarily compared to rest.

Maximum muscle blood flow is largely determined by the amount of active muscle.

This sentence could be rewritten as:

Maximum blood flow through a given muscle is largely determined by how much muscle is active in the rest of the body.

That is, the maximum blood flow through an arm muscle would be greatest if your legs are resting.

The larger the portion of active muscle mass, the less total muscle blood flow.

This is I think the most confusing sentence...I believe what they are referring to is the total muscle blood flow for a given muscle (total meaning over time rather than over space), which will be maximum when fewer other muscles are active at the same time.
Joyner and Casey 2015 explain all this in more detail; their Figure 8 is most directly related to the question but the rest of the background is also useful.

Joyner, M. J., & Casey, D. P. (2015). Regulation of increased blood flow (hyperemia) to muscles during exercise: a hierarchy of competing physiological needs. Physiological reviews, 95(2), 549-601.

that makes a lot more sense! thank you! the wording in ch 16&17 of the book is a bit challenging to understand.

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Determine planar phyllotaxis characteristics
Is there any method to fast and precise count the number of spiral and the divergence angle on a planar phyllotaxis pattern?

The example of spiral phyllotactic arrangement of emerging flowers on Gerbera hybrida. (doi: 10.1093/jxb/erw489)
I'm looking for a method for characterizing any phyllotaxis pattern.

I've found a following protocol for counting spirals on sunflower heads: http://www.turingsunflowers.com/media/Resources/count/Measure_and_count.pdf


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What is silicalemma and what is plasmalemma in diatom algae and how do they differ?
I try to understant the morphology (cytology?) of diatom algae. Does someone can describe what is silicalemma and what is plasmalemma in diatoms and how do they differ? Or they are the same?


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Are there cases when genus name is equal to the name of a higher taxon?
Are there any cases when the name of a genus equal to the name of a higher taxon: family, order, class, etc. in botany and zoology?

I doubt so.... Familiy names typically end in -cae or -dae while genus names typically end in -us/ -um/-a and others but not in -dae/-cae.

I answer for botany: no.
The International Code of Nomenclature for algae, fungi, and plants has strict requirements on names:
Article 16.1 has:

The name of a taxon above the rank of family is treated as a noun in the plural and is written with an initial capital letter. (...)

Article 18.1 has:

The name of a family is a plural adjective used as a noun; it is formed from the genitive singular of a name of an included genus by replacing the genitive singular inflection (Latin -ae, -i, -us, -is; transcribed Greek -ou, -os, -es, -as, or -ous, and its equivalent -eos) with the termination -aceae (but see Art. 18.5)

And article 20.1 has instead:

The name of a genus is a noun in the nominative singular, or a word treated as such, and is written with an initial capital letter.

On later article it is explained how to latinize names, with simpler rules (compared to Latin).  So genus are singular and higher rank are plural.
Additionally, for botanical nomenclature, an name for ranks between family and phylum rank is made usually by concatenating a genus name with some suffixes (which are rank specific, see article 16.3, 18.1). So reading a name, one could derive also the rank.  Just few families still have a old name, but still ending with 'ae' (e.g. Compositae, Cruciferae, etc., Art 18.5).  Now (just since 2011-2012 version) there are more exceptions in code, but for historical reasons and for names outside plants in stricter term.
Note: Some old names are automatically corrected with new rules (see e.g. 18.4), so we should have not equal names.

And what about zoological nomenclature?

Previously there were an other answer, mainly for zoological nomenclature.  I think it is potentially possible: zoology is also more complex: much more diverse and sectoral. I expect that on botany, if not you, one of your colleagues, will remember some high taxa name.

If you take all the taxons into consideration, yes, it can sort of happen - particularly on the genus/species level. The confusion is generally avoided since species are usually referred to by genus and species, using the name twice, whereas the genus is simply referred to by the genus name.
For example, the genus Vulpes includes all true foxes. (Wikapedia)
The genus Vulpes includes multiple species, such as the arctic fox (Vulpes lagopus), the swift fox (Vulpes velox), etc.   One of the most widely distributed species of fox, however, is called the Vulpes vulpes, also known as the red fox.
As Remi.b said in his comment, this is very unlikely to happen in higher taxons, since there are general rules that are followed in their naming, and it changes from level to level.

Hmm, why the downvote, I wonder.  I won't bite if you drop a comment... :)

But do you know any exception when a genus name equal to the name of a higher taxon?

Ah, I see what you mean.  Sorry, I was misreading the question, my bad. I'm not aware of any, but I'll dig around a bit.

Your answer is confusing the term species with the specific epithet. As the species name is a binomen, i.e. composed of two words, it cannot possibly be confused with a genus name.

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Autophagy in eukaryotic cells
What is autophagy? How and under which circumstances is it used by the cell? I believe The reason for autophagy is some kind of recycling, am I right? But why does it occur in infections?

Autophagy is a cellular process that is occurring all the time, but it can be elevated during times of need (see below).
In autophagy, cargo (can be anything - mostly macromolecules but also bacteria/viruses etc) is taken up by a lipid membrane which folds on itself to form an autophagosome, which is like a vesicle but have markers on it that makes it specialized in carrying out autophagy. These autophagosomes are then transported to, and merge with, lysosomes, releasing the cargo into the lysosome to be degraded. The broken down materials are then released back into the cytosol, where other processes can make use of them. That is the "some kind of recycling" you are referring to.
There are two types of autophagy - selective and general. In selective autophagy, receptors on the membrane of the autophagosome specifically selects for ligands (e.g. p62, ndp52 selects for ubiquinylated substrates, which usually marks molecules for degradation). In general autophagy, the uptake into the autophagosome is random.
So, you can think of general autophagy as maintaining a basic level of turnover - to ensure everything in the cell is not worn out; and selective autophagy as a response to specific ligands that needs to be degraded.
By this logic, autophagy activity increases during infection because those infectious agents, once gaining entry into the cell (either through phagocytosis or by forced entry), will need the autophagy machinery to transport it to the lysosome to be degraded. Interestingly, some bacteria actualy hi-jacks this process to ensure its survival in the cell. Here's a good review to get you started if you are interested.
Note that the proteasome also recycles macromolecules, although the things it can recycle is limited by size.

I like your answer. But in most sources I read there is a distinction between normal phagosomes which have one membrane layer and autophagosomes which have 2 to 3 membrane layers. Which is the only distinction I found so far.  Are there any other reasons to differentiate between these two processes?

Like I said, autophagosomes can take up any cargo - this includes other vesicles and phagosomes.
The autophagosome is double-membraned, so when it fuses with the lysosome, the inner membrane is 'released' into the lumen of the lysosome, whereas the outer membrane fuses with that of the lysosome. Thus, the outer membrane of the autophagosome would resemble more of the lysosomal membrane (and they do share similar markers and it's often hard to distinguish the two in microscopy). This is different from the the membrane of phagosomes, which originate from the plasma membrane.

Having said this, no one is sure as to the origins of the autophagosome membrane - where the lipids are sourced from.

To answer your question - you can distinguish the two processes as their place of origins, phagocytosis originates at the cell membrane and autophagy originates inside the cell. The phagocytotic process may feed into the autophagosomal process, although it may not be an requirement.
If you read the review I suggested, you'll appreciate that some bacteria that is taken in using phagosomes, break out of their phagosomes and replicate in the cell. This is when autophagy can come in and restrict their replication.
So I, a very crude distinction would be - phagocytosis outside, autophagy inside

Any papers by Daniel Klionsky and Beth Levine should definitely be used for reference, they are the two biggest names in the field today.


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Why do mammals in the wild retain the "trait" of menstruating with blood?
This question intrigued me a lot since if animals in the wild did have menstruation with blood flow, wouldn't all that blood be attracting every other predator in the vicinity?

Yes they do, most if not all mammals menstruate. Any dog owner can confirm this for example. Please research and try to answer your question before posting here. A 5 minute search for "mammal menstruation" for example would have answered it for you. If you want to know why that does not call in predators, [edit] your question accordingly.

Edited the question. I wasn't able to find why they would retain this trait.

I've always wondered the same thing about crying babies - would attract predators.

I would guess that the answer is something like this: ever since the development of the placenta enabled females to carry their offspring longer and to develop more fully.  Upon birth they were stronger and/or their brains were more fully developed (in the case of humans).  The increased gestation time, made possible by the structures of the womb and placenta is probably an adaptation whose advantages are much greater than the increased risk from menstruation once a month.
Some anthropological studies indicate that in preindustrial societies that women do not menstruate very much as adults though.  If you subtract out the time that they are carrying infants and nursing, which both prevent menstrual cycles, females will miss years of menstruation with only a few months in between. I would assume this is a factor in the risk of menstruation for many animals.

Yeah! I guess in the wild most mammals will miss quite a lot of menstrual cycles.


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delta coronavirus: Why isn't similar viral load in vaccinated people causing as severe adverse effects as in unvaccinated people?
In latest news, it is reported that:

if vaccinated people get infected anyway, they have as much virus in their bodies as unvaccinated people. That means they're as likely to infect someone else as unvaccinated people who get infected.

But vaccinated people are safer, the document indicates. "Vaccines prevent more than 90% of severe disease"

I've understood in general viral load is related to severity of the sickness. Do we know why would it not be in this case?

I believe the news report you cited is not accurate in its reporting.  Of course, it's not actual science, and we will wait for the release of the actual science, but here's my understanding (which may end up being wrong):

if vaccinated people get infected anyway, they have as much virus in
their bodies as unvaccinated people.

This seems to be incorrect. My understanding is that the CDC info looks at vaccinated people who were infected AND developed COVID symptoms, not all vaccinated and infected people. Also, the tests did not look at the virus levels in the whole body, just in the nose and throat. Obviously, the nose and throat release virus into breath which is exhaled, so that directly impacts how contagious a person might be.  However, what should be important for the person's own level of illness is the amount of virus in the lungs and other internal systems, not the nose and throat.
This mis-reporting would seem to account for the apparent discrepancy you noted.

I'd say this is consistent with my understanding, too: there's a sampling bias here. I think the reporter misunderstood and should have written "if vaccinated people get infected anyway and are symptomatic, they can have as much virus in their bodies as some infected unvaccinated people". Those nuances don't always make it to the news articles.

I now found these links from CDC: 1 and 2, which claim "Real-time RT-PCR Ct values in specimens from 127 fully vaccinated patients (median = 22.77) were similar to those among 84 patients who were unvaccinated, not fully vaccinated, or whose vaccination status was unknown (median = 21.54)." - so not sure if discrepancy is fault of the news report.

@eis The data in your MMWR link seems consistent with my and Bryan's description. In particular, the MMWR did not discuss "if vaccinated people get infected anyway", but rather (mostly) symptomatic people who were then discovered to have been vaccinated. That is, the group studied was selected from among those who were already known to be sick, not a random sample from among vaccinated individuals in general.

@Armand however, I think "some" are not consistent - it would seem from the data that pretty much all examined people did have roughly as much virus (in their throats and noses). Of course, the amount of people involved in this study is small and there is selection bias, but at least in this study the levels seemed to be similar in all samples they had, if I'm reading this correctly.

@eis You may have misinterpreted the whisker plots in Fig. 2 from CDC. The larger an RT-PCR Ct value, the less target was present. Normally, Ct values as small as 38-40 are considered very weak/negative results. The plot shows that some of the vaccinated infected had Ct values this small, while none of the unvaccinated group did.

First of all there is one error in the article: Vaccinated people do not get infected anyways. Vaccination prevents somewhere between 80-90% of infections (see reference 1). There is no perfect protection against infection, but in the symptomatic cases the viral load goes down much faster in the vaccinated people than in the unvaccinated (reference 2):

The figure show the Ct-values of the PCR from infected patients (figure 1 from reference 2). The lower the Ct value, the higher the viral load. However, this is only a test for the presence of viral RNA, it does not state how infectious these patients are. There are good indications (see reference 3) that vaccinated patients are not as infectious as unvaccinated patients.
And this might be the reason why vaccinated people have less severe disease when they get infected. Lower viral loads (or a faster reduction), less infectious virus which both means less cells in the body can be infected and affected. To sum up: Yes, vaccinations are highly recommendable as well are boosters.
References

Impact and effectiveness of mRNA BNT162b2 vaccine against SARS-CoV-2
infections and COVID-19 cases, hospitalisations, and deaths
following a nationwide vaccination campaign in Israel: an
observational study using national surveillance data
Virological and serological kinetics of SARS-CoV-2 Delta variant
vaccine-breakthrough infections: a multi-center cohort study
Longitudinal analysis of SARS-CoV-2 vaccine breakthrough infections
reveal limited infectious virus shedding and restricted tissue
distribution


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Why are some scorpion species fluorescent under UV light?
It's known for some scorpion species such as Pandinus imperator, Heterometrus Petersii etc. to be shining under UV light. That makes them easier to capture and collect by humans.
Is there any evolutionary advantage for this property?
Usually, in articles you stumble upon the phrase "It is not known" for this matter (example). Maybe someone knows of recent discoveries.

As far as I can see from different articles, this seems to be a study in progress. Dr Kloock from the California state University states that scorpions might be more active when not exposed to UV light. If not fluorescing, they know that they are hidden and have a lesser chance of being preyed on. He argues that scorpions are less active on full moon nights rather than other days. (reference) Dr Kloock has also stated that the pigment could get used up on repeated exposure to UV light. He made an observation that scorpions whose pigments got used up were more active than those still fluorescing when exposed to UV light mimicking the moon and the stars. (reference) Dr Gaffin from the University of Oklahoma, in his studies have reported that scorpions might be converting UV light to turn it into the colour blue-green which is what they see best effectively turning their body into one big eye. His studies are consistent with Dr Kloock in that scorpions try to hide and avoid UV light (reference). Some scientists have also hypothesized that scorpions might glow to warn predators or that the pigments that make it glow are the accidental by products of certain chemical reactions in its body (reference). There is no definite proof on this subject though.


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Why do I breathe out of BOTH nostrils?
After reading the question why do I only breathe out of one nostril I realized that breathing out of both isn't common. I have always breathed out of both, and when I get a stuffy nose, or a runny nose, it's on both sides. If only one side is stuffed, I'll just lay on my side a bit to even it out until I can breathe out of both again. I've always though that was totally normal! What does it mean that my autonomous nervous system is not alternating my breathing?

If you're concerned, talk to a doctor - we can't give you medical advice here. Speaking biologically though, as you can read on the page you linked, we don't really know whether the nasal cycle serves any purpose. The only explanation I've heard is to reduce desensitisation of the olfactory sensors from overstimulation (basically giving each side of the nose alternating breaks). Assuming that, the only effect of a genetic variant that doesn't have a nasal cycle would be a weaker sense of smell.

@Armatus The nasal cycle may also be an artifact of the way our autonomic nervous systems works in bilaterally symmetric animals. Another hypothesis is nasal defense. I included some links in my answer to the one-nostril question, if you're interested. :)

The odds are that you're noticing the equality of patent nostrils in the middle of a changeover, when both are equally patent. Also, the shape of your nose may be permitting the congested side to still be fairly patent. Your nose is doing what it's supposed to be doing (and everybody suffers bilateral congestion during colds, allergies, etc.) If it were not, you would be plagued by dry, painful and bleeding nares (um... are you?)


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How far does the diaphragm stretch when it contracts?
How far, exactly, does the diaphragm stretch during tidal breathing, and what is the maximum length it can stretch? I have been wondering about this for the entire day today, and I can't seem to find an answer.


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Is the diaphragm made of two muscles?
Is there a 'crural' and 'costal' parts of the diaphragm as suggested in this paper or is it just a single muscle?

@aliential so it's incorrect to consider there to be a 'crural' part of the diaphragm?

@aliential please do not answer in the comments; comments are reserved for comments, answers for answers. Comments are used to ask for clarifications or to suggest edits. Answers are there to answer the question. Placing answers in comments repels other users to generate a proper answer.

The delineation of muscles is often arbitrary. E.g., quadriceps femoris can be thought of as one muscle or four, depending on how you look at it. A debate over semantics is generally not useful in these situations. Understanding the crux of the matter is more important. In this particular paper, the crux is that the costal and crural parts of the diaphragms work somewhat independently in certain activities.


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Why do sieve elements need to be alive
I am studying high school biology and I got these two pieces of information in khan academy and wikipedia:

Sieve elements in phloem are living cells because the translocation includes active transport which uses energy that is only produced in living cells. (Starting from 10:36 https://www.khanacademy.org/science/in-in-class-10-biology/in-in-life-processes/in-in-transportation-in-plants/v/phloem-translocation-life-processes-biology-khan-academy)
All of the cellular functions of a sieve-tube element are carried out by the (much smaller) companion cell. (https://en.wikipedia.org/wiki/Phloem)

So this is my question: if the sieve elements do not actually produce the energy, why do they need to be alive? The argument that the required energy is only produced in the living cells is no longer relevant since the energy does not come from sieve elements themselves, but instead companion cells.
If being alive does not serve a specific function, then being dead cells like those that make xylem should cost less energy. However, this reasoning does not match with the fact that sieve elements do have organelles.
I am not sure about statement 1 since it is not from a formal wiki and I may be just getting an oversimplification of the functions of sieve elements.


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Which cells in our body perform lactic acid fermentation?
Does lactic acid fermentation in humans happen only in the muscle? I have read in this Wikipedia page that human muscle cells sometimes respire anaerobically to produce ATP and lactic acid. Does it happen anywhere else in our body?
My research:
Cells which lack mitochondria or do not have enough supply of oxygen perform lactic acid fermentation for the energy.
Aerobic and anaerobic respiration:
The NADH gets converted to NAD+ during the process of fermentation. Aerobic respiration and anaerobic respiration follow through glycolysis, the Krebs cycle and finally the Electron Transport Chain (ETC). The difference between aerobic and anaerobic respiration is that, in anaerobic respiration another molecule , other than oxygen, is used as the electron acceptor in the ETC.
Fermentation:
But during fermentation, there is no ETC ( or Krebs cycle). Because of the lack of oxygen, the cells performing fermentation have glycolysis followed by some extra reaction ( to get back NAD+)  for their energy requirement in the absence of oxygen. During glycolysis NAD+ gets reduced into NADH. Then the NADH oxidises in the ETC to form NAD+. This can again be used in glycolysis. But there is no ETC in fermentation. So, the pyruvate (or a derivative of it) after glycolysis acts as the electron acceptor and oxidises the NADH back to NAD+ in fermentation. Based on the electron acceptor during fermentation, it can be classified as lactic acid fermentation or alcoholic fermentation.
The two main type of cells that perform fermentation are the erythrocytes (RBCs) and SKELETAL muscle cells. As mature RBCs lack mitochondria, which is essential for aerobic respiration, they only performs lactic acid fermentation. Skeletal muscle cells on the other hand perform lactic acid fermentation when the energy requirement is higher than the rate at which the muscles cells can get oxygen. This is usually during strenuous exercises.
I would like to know if any other cell in the human body might be doing this. So the answer might be a cell which lacks mitochondria or that experiences hypoxia and needs energy.

Welcome to SE Biology. There are two situations in which lactic acid fermentation /anaerobic glycolysis occurs — that in which the tissue has insufficient oxygen, and that in which there are no mitochondria to oxidize NADH. A little reflection might suggest to you an example of a cell in which the latter situation exists.

Thank you for that, I have researched some more and would like to know cells in our body that may not have a mitochondria.

What may be the reason for the negative votes on this question? Was it because of no research?

Hello Patrick, yes that's probably the case. It might also be the use of "fermentation". Whilst perhaps not technically incorrect by some definitions, it isn't the usual usage of the word as it would normally apply to microbial activity, not what happens in (healthy) human cells.

@JiminyCricket. — No, I put that in because anaerobic respiration is wrong (it covers bacteria that use metals rather than oxygen as an electron acceptor). I don’t like it really either. Perhaps anaerobic glycolysis would be better.

@JiminyCricket. — Just realized why I changed to that title: that was the subject of the Wikipedia article the poster linked to.

Would it be wrong to call anaerobic glycolysis , as you mentioned , as lactic acid fermentation in animal cells? Lactic acid is the product formed and glycolysis is the only energy extraction pathway followed by some reaction to get the NAD+ back. That would be a choice of word usage then?

I'd use anaerobic glycolysis, but other's mileage may differ.

Certain human tissues can be considered completely aerobic (e.g. liver) or anaerobic (e.g. erythrocytes) in their energy (ATP) production. However it is wrong to think, as some other recent questions or comments have seemed to imply, that the only other tissue that displays anaerobic metabolism — glycolysis followed by conversion of pyruvate to lactate — is skeletal muscle. Certainly the mitochondrial content and blood supply of white muscle during excercise leads to it being the major producer of lactate, but most tissues also have the capability for anaerobic glycolysis, and there exists a spectrum in the relative contribution of aerobic and anaerobic metabolism to energy production.
The primary literature on this is quite old and tends to be of the observation and measurement variety. I will list some lactate-producing tissues with linked ‘medium old’ references, as modern ones tend to have a narrow focus.
Most well established are:

retina

Sertoli cells of the testis

renal medulla

brain astrocytes

Somewhat less so, perhaps, are:

adipose tissue

skin

In addition, it should be noted that many tissues produce lactate in abnormal medical conditions, reviewed here and, from a more surgical viewpoint, here.

This is answered on the basis that no other pathway other than anaerobic glycolysis produces lactic acid right?

The historical papers generally measured the production of lactate by tissues. This was assumed to be from pyruvate in a reaction catalysed by lactate dehydrogenase, and subsequent work confirms LDH as the sole enzyme producing lactate. The origin of the pyruvate may or may not be shown to be glycolysis, depending on the study (there are 60 years' worth of papers for you to follow up). However in many/most experiments glucose is the only source of carbohydrate precursor for pyruvate, so this is quite reasonable. In any case there are not a lot of alternative precursors for pyruvate.

This article tells about lactate being the neuronal energy source. I am posting this to ask why you placed brain on the "somewhat less" category. Thus, it is hypothesized that the astrocytes produce lactate which is then taken up by the adjacent neurons and oxidized for fuel.

@Patrick — Yes it looks pretty solid. The source I quote also talks about the "astrocyte–neuron lactate shuttle". This is not my area (as I always say), I just have  a vague memory of things I have encountered and know how to search. I'll change it. The answer would be better with a paragraph after each entry, but there's only so much time one can devote to these things.

Well, first, fermentation and anaerobic respiration are separate things. At the elementary level, fermentation only involves glycolosis whereas anaerobic respiration involves all stages of respiration. Anaerobic respiration, which is what occurs in muscles cells once their store of ATP have dried, is incredibly inefficient, with 2 ATP produced per glucose (with Aerobic respiration producing up to 38), and so one would heavily doubt anaerobic respiration occurs in anywhere but muscle tissue, where it is occasionally necessary.

In muscle cells aerobic respiration occurs most of the time. I agree with your difference of fermentation and anaerobic respiration. How would you explain the lactic acid formation using anaerobic respiration. Skeletal muscle cells perform lactic acid fermentation.


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What evidence is there on the medical effects of circumcision?
If this is the wrong place to post this question, then I will delete it and post it were it belongs.
I have heard many conflicting things about circumcision.  I have heard that it reduces the rate of STDs, including AIDS, and cancer in the man and his wife.  On the other hand, I have also heard that circumcising babies can cause psychological harm and increases the rate of urinary tract infections.  Are there any reliable studies on this issue and what do the conclude?
Thank you for any and all answers.

This question has already been answered over at the Skeptics site in great detail.
See Does circumcision reduce HIV risk? and Does circumcision lead to a net increase in quality of life?. The answers are well-sourced and there are answers addressing both sides of the issue.

This is community wiki since it doesn't really add any new information outside of links to another stackexchange site. Feel free to add more links and resources if you wish.

Thank you for the information.  I will go to the skeptics site and read those links.

authors: خالد العيساوي


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Calculating Rate of Growth without a Population
Lets say that by studying individuals of a rare species, you have determined that species gestation period, age of sexual maturity, average time between pregnancies, maximum lifespan, and average number of individuals born per pregnancy. However, you have never had enough specimens at the same time to establish a breeding population.
How can you calculate the maximum rate of growth of a population from just the information already gathered? If not, what other information would be needed?

is this a homework question?  Given this information, you can write down a life table and calculate a growth rate: http://web.mit.edu/7.01x/7.014/documents/populations.pdf

The breeding lifespan of an individual is (maximum life span $L$ - age of sexual maturity $M$).
Call the time between pregnancies $\tau$ and the gestation period $g$. Then the average number of pregnancies per (female) individual is then $(L-M)/(\tau+g)$.
If the average number of individuals per pregnancy is $N$, then each reproducing individual produces $N(L-M)/(\tau+g)$ offspring in their lifetime.

If this species has males and females (gonochoric/dioecious), and a 50/50 sex ratio, then the number of females per female is $N(L-M)/(2(\tau+g))$.
This is a growth rate per generation: the generation time is approximately (mean time between birth of mother and birth of offspring) = $(M+(L-M)/2)$ (it's a little more complicated than this); the growth rate per unit time would be approximately equal to the ratio (growth rate per generation)/(generation time).
Other things you might need to take into account: survival of juveniles up to $M$; menopause (unusual).


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How to determine whether a newly discovered dinosaur is not a young one and not an entirely different species?
Every once in a while, there is an official announce that a new species has been discovered. For example, paleontologists have recently discovered a dinosaur they named Nanuqsaurus hoglundi, which really resembles Tyrannosaurus Rex, but in a smaller version. It also lived during the same era. Is there something that indicates it's a cousin of the T-Rex, and not Mr. Rex's son?
Other small dinosaurs include the Compsognathus, the Microraptor and others. Why were they classified as new species when they were discovered?
Considering evolution over a few million years, my guess is that some earlier species may have been smaller and evolved into more complex animals, bigger bodies, horns, frills, etc.

Diagnosing extinct species is even more difficult than extant taxa (see this question). Because systematists describing fossil species (usually) only have skeletons, they compare to other fossils. You are correct that diagnosing a species from only a skeleton can be tricky. What defines what you call a genus, a species, etc.? How morphologically dissimilar can two skeletons be before you call them different species? The running joke is that if you found fossils of a chihuahua skeleton and a great dane skeleton, you would certainly call them different species. But by modern biological species concepts, they are the same species. Then there are extant species that are essentially indistinguishable in terms of their skeletons, but do not interbreed, and so are probably different species.
Sometimes there is consensus, and sometimes there is not. This disagreement can lead to a description of a new species by one person being reclassified ("revised" is the term used) as another species. There are lots of examples of this among dinosaurs. Most famously, Brontosaurus was revised as actually being Apatosaurus. More recently, and relevant to your question, Nanotyrannus is thought by some to be a juvenile Tyrannosaurus rex.
So then how did Fiorillo and Tykowski, who described Nanuqsaurus hoglundi, decide that it was (1) not just a juvenile T. rex and (2) that it was a new species? Their rationale is laid out really well in their paper, primarily in the sections "Diagnosis" and "Description". You rightly picked out the two questions that paleontologists reading this paper would want to know.
Nanuqsaurus is not a juvenile:

The dorsomedial edge of the maxilla is marked by deep pockets separated by pronounced transverse ridges. These together formed a strong peg-in-socket articulation between the dorsal margin of the maxilla and the ventrolateral edge of the nasal. The same kind of deeply interlocking naso-maxillary contact is a well-documented character that is also present only in developmentally mature individuals of the derived tyrannosaurines Daspletosaurus torosus, Tarbosaurus bataar, and Tyrannosaurus rex 2, [6], [20], [21], [22]. The nasal-maxilla contact is either smoothly grooved or bears only weak scalloping in immature individuals and more basal tyrannosauroids 2, [6]. The presence of this feature in DMNH 21461 is evidence that the material also represents a developmentally mature individual.

What they are saying here is that maxilla (part of the front of the upper jaw) in Nanuqsaurus has a very characteristic relationship to the nasal bone in which they form a peg-and-socket joint. This relationship is found in tyrannosaurine dinosaurs like Tyrannosaurus, Daspletosaurus, and Tarbosaurus. But more importantly, it is only found in adult tyrannosaurines. So they conclude that Nanuqsaurus is an adult.
Nanuqsaurus is a distinct species from Tyrannosaurus and other tyrannosaurines

In all three hypotheses of phylogeny, Nanuqsaurus hoglundi was found to be a derived tyrannosaurine, the sister taxon to the Tarbosaurus + Tyrannosaurus clade (Figure 6). This node was supported by a single unambiguous character, the presence of a dorsoventrally tall, paired sagittal crest on the frontal. The age of Nanuqsaurus hoglundi (70-69Ma) is consistent with its place in the recovered hypothesis of tyrannosauroid phylogeny, positioned in time between the more basal Daspletosaurus torosus (Middle to Late Campanian) and the more derived Tyrannosaurus rex (latest Maastrichtian) among other North American tyrannosaurines.

The authors ran a phylogenetic analysis of characters coded for Nanuqsaurus and about 20 other taxa. Nanuqsaurus has enough shared characteristics to put to solidly among tyrannosaurine (near Tyrannosaurus, Daspletosaurus, and Tarbosaurus). But, importantly, it has a characteristic that none of these others have: "the presence of a dorsoventrally tall, paired sagittal crest on the frontal."
Based on its being an adult and having a character that is not found anywhere else among tyrannosaurines, Fiorillo and Tykowski name a new species. I'm simplifying what they did, but that's the general idea. To their credit, they acknowledge that there is not a lot distinguishing the new species and discuss in much more detail their rationale and the implications of their results.

Thanks a lot for your answer! Just a small detail... You seem to have linked the same article 2 times. Nanotyrannus should like to what website?

I fixed the Nanotyrannus link.

authors: Бауржан Сарбаев


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What are the exact differences between stereocilia and microvilli?
This is a question in an old exam of Histology. I tried to answer the question, and I've made many searching attempts, but without resulting in any fixed/exact information. In some articles on the web, I've read the stereocilia and microvilli have both actin core, and this website states that stereocilia doesn't have actin filaments! I'm just feeling lost at this point. And now, I'm just searching for an exact answer for that question.
Note : It may be a super easy question for you. So please note that I'm a novice self-learner at Histology.

Both are actin based.

Is this information come from a trusted resource ?

Haha well I don't know… do you trust me?

http://www.uniprot.org/locations/SL-0293 and http://www.uniprot.org/locations/SL-0302

Thanks. But I still need to know the differences between them.

Stereocilia are basically modified microvilli. They are much longer than microvilli, and lack the villin protein.
According to Ross histology textbook, they both contain actin filaments.


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How can we determine the polarity of fat molecules?
I'm trying to solve a question in a biochemistry quiz, which is asking for classifying a set of lipidic derivatives, by increasing polarity. Unfortunately, we didn't cover the classification of different liposoluble molecules by polarity in Biochemistry class. I find myself buried in details every time I use google seeking a good explanation. So:
How can we determine either if one molecule is more/less polar than other ?

For example, classifying Cholesterol, Triglyceride, Phosphatidylcholine, Phosphatidylserine, by increasing polarity.

PS : I'm not searching for the answer of that example too. I just need the exact method for determining how strong a polar fat molecule is. I'm sorry for my bad english.

Please read our homework policy, then [edit] your question to include what you've learned so far, what your thinking is regarding the polarity of the different molecules, and where exactly you're stuck. We're not here to do your homework for you, but we are here to help you learn.

This is not homework. I'm just practising some random exercises from the internet in order to develop my knowledge and skills in Biochemistry. I asked for the method, not the answer to the exercice. And this example I provided is not the set provided in the exercise. :)

You determine polarity, generally, by looking at the composition and the functional groups on the molecule, and the geometry of the molecule. Do you expect a separation of charge, or something uniform? Water is polar because the draw on the net electrons for the molecule is to the oxygen atom, resulting in a more negative charge in that region. Carbon dioxide is nonpolar because of it's linear geometry, even though there are two oxygen atoms.

Not that. For example, a fatty acid have a hydrophilic region and a hydrophobic region right? and a phospholipid also do. But, they differ in composition of the polar head (Hydrophilic part). So, I want to classify these two molecules, by their hydrophilic part polarity. Which one is more polar and can interact with water more than other. Got it ?

http://chemistry.stackexchange.com/questions/18589/how-do-i-figure-out-the-relative-polarity-of-organic-compounds
I managed to find a good answer in the chem stack exchange. Otherwise you'd use column liquid chromatography and a gradient elution technique to determine experimentally which one is more polar.

As mentioned in the chemistry-SE post, dipole moment can be empirically calculated based on electronegativities of different atoms. I guess there are other ways to calculate the net dipole moment (perhaps by spectroscopic techniques or subjecting the molecule to electric fields). I cannot comment further on this question would be suitable for physics or chemistry SE. I suggest that you edit your question such that it is about experimental techniques to calculate dipole moment. You can also narrow down your question by describing the kind of "fat" molecules you are interested in.


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What has to duplicate before cell enters M phase?
What has to duplicate before cell enters M phase?

DNA
histones
centrosome
mitochondria (any other organelles?)
condensins (not sure?)

have I forgotten anything?
Thank you in advance!


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What makes synaptic vesicle release probabilistic?
The fusion of synaptic vesicles (SVs) with the plasma membrane of the active zone (AZ) upon arrival of an action potential (AP) at the presynaptic compartment is a tightly regulated probabilistic process crucial for information transfer (https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4773589). In a typical forebrain synapse, only ~15% of APs arriving at the presynaptic terminal cause fusion of a synaptic vesicle.
My question is, what factors make this process probabilistic? What happens at the molecular/cellular level that an action potential can lead to the fusion of synaptic vesicles one time and not another time? Is it due to some differences between different synaptic vesicles, how the vesicles are positioned inside the synapse, variations in the synapse's environment, differences between action potentials, etc?

From the source you provided, the answers seem to be outlined well from the authors' sentence that states:

The Pr [release probability] of SVs [synaptic vesicles] at the AZ [active zone] is set by a complex interplay of different presynaptic properties including the availability of release-ready SVs, the location of the SVs relative to the voltage-gated calcium channels (VGCCs) at the AZ, the magnitude of calcium influx upon arrival of the AP, the buffering of calcium ions as well as the identity and sensitivity of the calcium sensor. These properties are not only interconnected, but can also be regulated dynamically to match the requirements of activity patterns mediated by the synapse.

Below, I use an analogy to provide a framework for understanding how these factors come together to mediate Pr as a whole, but you can read a scientific review on that here:  https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3059705/.  However, the actual molecular/proteinaceous machinery that underlie these phenomena are pretty well explained in your source (particularly in the sections "SV Proteins Regulating Pr" and "Recruitment of Calcium Channels to the AZ").
To use an analogy, think about the presynatpic terminal as the 100 meter dash at the Olympics.  The track only has so much space, so not everyone can run the race at the same time.  That's why there are multiple heats of the race.  The first point from the authors is availability of release-ready SVs, which your source discusses as part of the readily releasable pool (RRP) of vesicles.  Think of those SVs as the runners in a heat, lined up in the start position waiting for the gun to go off.  Their equipment is ready (starting blocks set, shoes tied, proper uniform and tag on, etc.). They're all in position, awaiting the signal, and they will take off as soon as they get that signal.  Therefore, the more SVs you have in that position with equipment/molecular machinery prepared to "go" in response to a signal, the more likely you are to have SV release.  The second point is location of the SVs relative to VGCCs.  In our example, this would be equivalent to having a lane closer to the person shooting the start pistol.  The closer a runner is to that, the more likely they are to hear the pistol go off and start the race.  Conversely if the person with the start pistol is at the finish line, it's possible less runners will hear it go off and miss their cue to start running. Since SVs require calcium to undergo membrane fusion and release their contents into the extracellular space, the closer these vesicles are to calcium channels the more likely they are to get that necessary substance for fusion/release. Third, the magnitude of calcium influx upon arrival of the AP, which we can think of as the volume of the start pistol.  If the start pistol is loud (a high volume of calcium comes into the cell), it's more likely the runners will hear the shot go off and start running (SVs will fuse to the membrane).  However, a very quiet start pistol (low influx of calcium) is less likely to be heard by the runners (less likely to bind SV proteins important for fusion). Lastly, they list buffering of calcium ions as well as the identity of the calcium sensor.  What's important to remember about the process of SV fusion is that it requires free calcium that can bind to the necessary vesicle proteins, so any other proteins (calmodulin, calbindin, the list goes on forever) that bind free calcium and make it unavailable to the vesicle will decrease the likelihood of successful vesicle fusion and neurotransmitter release.  This would be like someone giving the runners ear plugs before the race, which dampens the sound of the start pistol and decreases the likelihood of runners hearing their cue to start.  Again, there are nuances not covered in this analogy, but I'd recommend going through your source again with this framework in mind to pick up where those nuances come in.


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Immune response to IgA positive bacteria
If certain bacteria can be coated with IgA in vitro, does that mean they are likely to elicit an IgA immune response?
Edit
I'm working on a project that involves IgA-Seq analysis. Bacteria are coated with IgA and then sorted for how much IgA they actually ended up having on them. I'm a biostatistician, so I don't know the biochemical details. But I'm assuming that the IgA binds to receptors on the surface of some bacterial more than others. I was wondering if that was related to immune response. I tried googling, but couldn't find much.

Can you clarify what you mean by "coated with IgA"? Do you mean the bacteria bind to the constant region of the IgA heavy chain, or the variable region (which would presumably be shared with other isotopes during class switching)?

Hi @iayork. I added some information to the question.

Depending on the precise details of the experiment, I don't see a particular reason to suppose that being coated with IgA should mean that they'll elicit an IgA response.
I'm assuming that the "coating with IgA" means that the IgA is binding like an antibody, through the variable region binding site on the antibody to some epitope(s) on the bacteria. The way antibody class switching works is that the epitope binding region of the antibody remains the same while the constant regions switch from IgM to IgG or IgA, etc. That means that the ability to bind to the bacteria appeared in a non-IgA antibody, so the ability to bind, per se, is more or less separate from the isotype of the antibody.
The factors that drive a response toward IgA are heavily influenced by location - a response on a mucosal surface is much more likely to drive IgA than one that's systemic (simplistically, because the cytokines and cell types involved are different in the different locations).
An alternate possibility is that the IgA is binding the bacteria through its constant (Fc) region, analogous to Protein A.  If the bacteria have evolved an IgA-binding capability in this way, one might guess that they did so because they need it as a defense, and if it's specific to IgA one might guess that it's because they tend to have an IgA-dominant response. But that's an inference, not a strong argument. As a counterargument to that, Protein A does (sometimes) bind to IgA and that's likely more of a side effect than a primary thing.
So I think the answer is "probably not, but you'd need more information to have a good answer."


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why do our eyes not go red in response to body temperature?
I know that blood flow increases/decreases in response to temperature change, which is why (lighter-skinned) people go red when they are hot.
I know that the eye contains lots of blood vessels.
Why do our eyes not turn red when we are hot?

Skin turns red when light skinned people flush because it contains few absorbers, so photons diffuse through it long distances. During this time green and blue light is absorbed as photons encounter blood vessels. Red photons are not and so the skin appears redder.
The whites of the eyes are strongly scattering and have relatively few blood vessels, so changes in blood flow has a small effect on color.  The (wavelength-independent) scattering dominates over absorption.
The pupils open up on the approximately 22 mm gap between the cornea and the retina. You don't see changes in color here because the entire retina strongly absorbs all colors of light. The few red photons scattered by blood are very unlikely to be exactly aimed at the pupil. Instead most scatter back into the retina and are absorbed. This is compounded by the scattering anisotropy of blood, which causes most incoming red light to be scattered in the forward direction - directly into the strongly absorbing retina.


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What is the scientific name of this parrot?
I found this parrot at Nehru Zoological Park which is located in Hyderabad city of India.It's head to tail length is between 30cm-35cm.Can anybody tell me the scientific name of this parrot?

Looks like a male plum-headed parakeet (Psittacula cyanocephala)
wiki: the plum-headed parakeet


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What is the name of this plant which is located in Hyderabad city of Telangana State,India?
I found this plant in Hyderabad city of Telangana State,India.Many people of Hyderabad city have planted this flowering plant.I don't know the name of this plant.If it's flower treated as a circle,the flower has diameter of nearly 6cm length.Can any one tell me what is the name of this plant?

From the twisted overlapping appearance of the petals it is a member of the Apocynaceae family.  So I searched for "Apocyanaceae india" and found images consistent with your picture.  Good chance it is Allamanda blanchetii or Purple Allamanda.  Here is a picture comparable to yours (source/CC0).

Here's a bit about the plant and Wikipedia has a short page.


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Like Mother Cape Buffalo,do remaining mammal mother species also try to protect their babies from being eaten by predative animals?
Some statistics say that on earth there are approximately 5500 mammal species.I have seen a video of Mother Cape Buffalo protecting it's calf from being eaten by predative animals.Like Mother Cape Buffalo,do remaining mammal mother species also try to protect their babies from being eaten by predative animals?

This seems really ill-defined.  Do you mean some/most individuals of every mammalian species, or every individual mother?  For the latter, H. sapiens provides an obvious counterexample.

I edited my question.

Propagating their species to the future is an important & continuous function of plants,birds,mammals & many other living organisms. Parental care is part of the evolution. If
all the mammal mothers start to abandon or cannibalize their own babies then all the mammal species will become extinct. As propagation is an important function,these extinctions are not at all supposed to happen. As mammal species are surviving & propagating to the future, it's clear that almost all mammal mother
species protect their helpless babies from predators.

There is quite a bit of evidence showing that mothers of a number of mammalian species will sometimes kill and eat their own young.  E.g. https://www.nationalgeographic.com/news/2014/3/140328-sloth-bear-zoo-infanticide-chimps-bonobos-animals/

It's a hard question to answer definitively, because it's almost a black-swan problem. By definition, all mammal species secrete some form of milk to nourish their offspring (to my knowledge there are no known exceptions to this) [See "Mammalogy: Adaptation, Diversity, Ecology" by Feldhammer et al.]. It could be argued that the mere proximity of smaller young to their larger mothesr would deter some predators who might otherwise prey on those young. So, from a behavioral perspective, it's difficult to completely separate parental feeding from other protective parenting behaviors.
If you are only interested in more specific exceptions, it's not uncommon for some mammals to reject and abandon their offspring, or even cannibalize their young. But these behaviors are generally based on situational or environmental cues, like whether the mother has enough nutrients available to raise the young.
If you think about the evolutionary implications, it seems fairly straight forward why this is the case. Most mammals give live birth. For all parenting bahavior to completly vanish from a given population, there would have to be a greater fitness advantage for offpring of mothers who completly abandon their young at birth compared to those who provide nourishment and therfore (arguably) protection from predators.

Likewise, from the opposite side of the evolutionary perspective, mothers who would always fight to the death to protect young would be at an evolutionary disadvantage (since they could have no future young) to those who would expend only "reasonable" efforts in protection.


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Can any one explain me the structural difference between Proteins and Peptides?
I have read in books that Proteins and Peptides are fundamental components of cells which carryout important biological functions.Can any one explain me the structural difference between Proteins and Peptides?

Welcome to SE Biology. Have you tried to research this yourself? You should do this before posting — I am sure you will find an answer. If not, [edit] stating what you have found and why you are still unclear on the topic. See our help on asking good questions.

Dear users of Biology Stack Exchange,I have been banned from asking new questions in Biology SE by the system.It's showing that "you have reached your question limit" and "sorry,we are no longer accepting questions from this account".That's why I'm editing my questions.Your up votes may help me in getting out of this ban.So,please upvote my questions if you like them.I didn't know about question ban previously till I had got imposed and no one told me about that ban.I would have improved my questions if I knew that.So,please help me in getting out of this ban with your upvotes to my questions.

Dear David and theforestecologist ◆,I'm unable to ask questions on Biology SE.Whenever i click on "Ask" option it's showing that "sorry,we are no longer accepting questions from this account" and it's telling that I need to edit my questions.I'm editing my questions for the second time after the question ban had imposed on me but the ban remaining as it is. Today i need to post a question and it's telling i should wait 6 months for posting that!! It's 'horrible' and facing this ban is 'too hard for me'.Please,can anyone help me in getting out of this ban? I will be thankful for that.

You need to ask about this on meta, if it will allow you. Then one of the mods will explain the situation to you. @theforestecologist is better placed than me as he is a moderator (the diamond indicates this) but you need the ampersand to alert anyone to a post. He should see the one I have included.

David and @theforestecologist ◆, i have already asked a moderator of Biology SE about this question ban nearly 25 days ago.He told me to improve the questions i have asked previously.I'm doing that and I'm also asking other people to help me in getting out of this question ban.

OK, the "homework questions..." is a close option that is often used when one thinks the question shows insufficient research. If you look at the Help on asking questions, it says "search, and research". This question is really basic in relation to the definition of this site as being for "for biology researchers, academics, and students", so you would be expected to search on the internet on sites like Wikipedia or NCBI bookshelf.

In terms of structure: both are composed of amino acids.
A peptide is when at least two amino acid are linked together.
A protein is composed of multiple amino acids and have a secondary, tertiary and even quaternary structure.
In terms of function: larger molecules have more complex functions.
Peptides can act as a intracellular or extracellular ligands which will activate a signal.
Proteins have a large array of functions (enzymatic, structural, receptors etc)
This article explains in more details the differences in proteins structure and functions:https://en.wikibooks.org/wiki/Structural_Biochemistry/Proteins

pls include pictures :)


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Crossbreeding mouse and chinchilla
The MGI Mouse Genome Informatics website states for the Mus musculus 129 strain, popular in biomedical research, that:

Origin: Dunn 1928 from crosses of coat colour stocks from English fanciers and a chinchilla stock from Castle.

Source
However, according to wikipedia, Chinchillas are in the suborder Hystricomorpha, whereas the house mouse is in the Myomorpha suborder of the Rodentia order. From my limited knowledge about species hybridisation, this seems like quite the evolutionary distance for these species to hybridise. How plausible is it that the 129 mouse strain was actually bred through hybridisation efforts between chinchillas and house mice? I'm also open to the possibility that I might've misinterpreted some relevant information.

"Chinchilla" is both a separate rodent, and also a name for a Mus musculus mouse coat color/pattern. Here it's used in the latter context. You may be more familiar with the word "agouti" which is a different color. See for example:
AFRMA Fancy Mice:

Color is to resemble that of the Chinchilla rabbit, with a pearl-gray background, evenly tipped with black, and a slate blue base to the hairs. The belly and the inside of the legs is to be white, the outside of the legs to match the top color. Eye color is black.

Varieties - Ticked - Chinchilla (chi):

The mouse shall be as near as possible to the colour of a chinchilla with slate-blue undercolour and intermediate shade of pearl-grey. Hairs to be evenly tipped with black. Colour of feet on inside white, with remainder of foot the same colour as body - as in the standard for tans. Belly white. Eyes black.

I would have assumed the name was derived simply from the chinchilla, as in a "chinchilla mouse" has a coat that reminds someone of a chinchilla, but that first quote seems to suggest that the route is a bit more circuitous, and perhaps there was first a breed of rabbits which had a coat that reminded someone of a chinchilla coat, and later used the same word to describe a mouse as looking like the rabbit that looks like the chinchilla. I have no other evidence for this, but find it a bit entertaining.

It makes much more sense if 'chinchilla' is a coat phenotype rather than the separate rodent. Thanks for clearing up this confusion!


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Term for Marsupial with Offspring in Pouch
Is there a term for a marsupial that has a offspring in its pouch? 'Pregnant' doesn't sound right, cause she has already given birth to the offspring. But this is still a distinct life-stage for the offspring, so I feel like there should be a word that refers to it. 'Carrying' would work, but it is also used to refer to pregnant non-marsupials, so it would just cause confusion. Is there a better term available?

They definitely aren't pregnant at that point (well, not unless they have another one in the pipeline), as they have given birth.
Carrying is often used as it is generally clear that you are talking about a particular species or group of animals.
Another term that is fairly commonly used is "Pouch Young" (e.g. use in last line under "Hit by car" at a wildlife rescue org). This is generally not used to refer to the baby animal rather than the mother though as in a sentence like "Do they have pouch young?".
I think the proper term would be "in marsupium", the marsupium being the pouch for which the group Marsupial is named. Of course, some other animals, such as isopods, and even the a family of plants (the liverworts) have marsupia, so depending on the context, this might not be much help.


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Source for Specific Models of Birds' Habitat Suitability
This source gives a very detailed analysis of what habitats are best suited for many different species. However, this is a government funded project and, to the best of my knowledge, not published in a peer-reviewed paper. In addition, this project has officially been depreciated for 18 years.
There are 2 features of this project that are very attractive to my own project. First, each habitat is ranked as a value between 0 and 1. Second, it ranks 31 habitats, each with very precise differences (e.g. a conifer palustrine forest habitat is ranked separately from a deciduous palustrine forest). Compare this to other sources, such as the IUCN Red List which only says 'Yes' or 'No' to whether a species has been observed in a habitat and only tracks 18 habitats that are very broad groups (e.g. all forests are ranked together).
Can anyone direct me to a more modern and/or peer-reviewed source that has one or both of these benefits?

A quick google reveals several databases of bird habitats, which appear to be at least somewhat more recent.
I believe that the one closest to what you describe is here (there may not be a single publication but they do have a lot of associated publications on their site). But this climate change geospatial database (with a newer version here) and this more local database may also be helpful.

Thanks. I think I missed those when searching because I always included terms like "dataset" or "database".


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Can prawns and lobsters live out of water for more than six hours?
I live in Telangana which is a state of India.I like eating Non-vegetarian food.People of our state eat pond fish more comparing to other aquafood.In many places near me,I've seen people cutting alive fishes in to pieces with their big knives.I won't feel good to see this.So,usually I bring the pond fishes home and keep them aside for atleast 40 minutes with no water in contact to them.In these 40 minutes I prepare other ingredients needed for the recipe.After these 40 minutes,generally as there is no response from those fishes I start cutting them into pieces.In the same way I don't know how much time it will take for prawns and lobsters to die without water.Do they live more than six hours without water?
This question is not related to the experiments carried out by the biologists on lab creatures.They are great people.I encourage their experiments whether it involves humane killing or inhumane killing because their experiments on one creature may help millions of remaining creatures.

TL;DR version is they are gill breathers and need to be in a humid and moist environment to have a considerable longer life span outside sea water.
Dr. Cowan's on being asked the same question about lobster said:

“Gills work best in seawater, but if lobsters are kept in containers of seawater with no aeration, they quickly use up the oxygen and suffocate,” she said. “That it why it is imperative to transport lobsters in containers with no standing water.” - New York Times

Many lobsters, shrimps and even crayfish & crabs are transported in boxes with a small amount of water in the bottom and they survive for several days like that. However the long term side effects of this are still to be discovered as most crustaceans transported this way get cooked.


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Long brown needly things fallen from tree?
I was walking next to a row of trees (I think coniferous) and found many of these things on the ground:
A parallel bundle of 2-4 medium-brown needly things, about 15 cm long and 1 mm in diameter, not quite as sharp as a saguaro spine, a bit stiffer than a blade of grass, connected at one end by a darker brown bulb about 3 mm in diameter and 7 mm long. Very easy to pull apart.
What is this thing called?
EDIT: thanks to nextworldplz' answer, here's a picture of what I was describing (turns out to be specifically ponderosa pine needles):

... pine needles?
These are the leaves of coniferous (evergreen) trees. It sounds like they might be from Pinus ponderosa, a species of pine.

Yup, I think that's it. lol. I was originally thinking "aren't pine needles shorter?"

If they are brown, they are dead pine needles.  Unlike deciduous trees, which shed their leaves in the fall and grow new ones in the spring, conifers replace their needles more or less continuously: https://sciencing.com/pine-needles-6455979.html  Needles also vary in length according to the species.


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Problem with Caspr antibody in western blotting
I have been working on optimizing western blotting for Caspr (contactin associated protein), but I am having difficulties and would like suggestions.

I ran my proteins on a 40% acrylamide gel,
I used TBST for washing and BSA as blocking buffer.
I incubated the blot with primary antibody overnight.
The secondary antibody is linked with HRP.

I could  not find any bands in the blot.(Same problem was faced in case of contactin) What might be the reason?
Edit:-

I repeated the experiment a couple of times and found that secondary antibody(Anti-mouse,1:5000)wasn't working anymore.
I made freshly diluted secondary antibody again and found bands.
The old secondary antibody dilution was only few months old.What may have gone wrong with it?

What percentage is your gel? And: Did you do Ponceau staining of the membrane?

The resolving gel was 8%. Yes, Ponceau staining was done.

And there you did see bands I assume. How old is your antibody dilution?

Do you have a positive control (actin or something)?

Usually you visualize the bands on the blot by exposing the blot to X-ray film or otherwise visualizing the HRP reaction, because you can't just see the reaction on the blot. Can you show us a film or other exposure of the blot? The blot itself looks ok but it's hard to say what the problem is without seeing such an exposure.

There were bands in ponceau staining. The antibodies are 2-3 months old.


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What is the current thinking on the typicality (or otherwise) of fossils as representatives of their species?
Since fossil records represent a tiny percentage of species populations, how do paleontologists determine how typical those specimens are?
Is there any research or analysis to determine how the distribution of fossil specimens within a species corresponds to the distribution of specimens of the species population as a whole?

Your title seems a bit iffy, but your question seems to be of palaeontology rather than biology.

Welcome to Biology.SE! The typos/automiscorrections in your title make it very difficult to understand what you are asking! In addition, as i think @David was suggesting, this might be better suited to the earth sciences site. ——— You may also wish to go through the help pages starting with [Ask] questions effectively on this site. Thanks!

Ugh... sorry about the title typo. I've corrected that. Regarding the appropriate site - both this site and the Earth Sciences one have a palaeontology tag (and this site has 50% more questions with that tag, so it's hard to know which is the more appropriate site. However, this question is much more aligned with biological processes than physical one, so (absent any other information), this feels like the right place.

Tags do not justify posts. To learn what is on topic here read the Tour and the Help. The representative nature or otherwise of fossil specimens is not biology in terms of this list.

I disagree with David, I think it is completely on topic for exactly the reasons described: this is about the biological side of paleontology (though David is also correct that tags do not determine topicality).


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Can stomach acid destroy a virus?
I was reading about a viral list of dubious coronavirus tips on The Verge and reached this tip:

“Even if the virus gets into your mouth, drinking water or other
  liquids will wash them down through your throat and into the stomach.
  Once there, your stomach acid will kill all the virus,” one tip reads.
  Loren Rauch, an emergency room doctor in Los Angeles who has a
  master’s degree in epidemiology, told Mother Jones this advice was
  “totally bogus.”

I asked a friend, who has a PhD. in cell biology, about this and she said that it's true that a virus would be killed by the stomach acid (i.e. due to high acidity, or low pH value, of stomach acid which could easily break the structure of the virus); however, she added that it's NOT true to think that drinking water would wash the virus from your respiratory system (i.e. trachea or lungs) into your stomach, so drinking water regularly does not necessarily help if it's in your respiratory system.
I was a bit confused since the doctor referenced in the article considered the whole advice as totally false; on the other hand, my friend thinks at least part of the advice, i.e. the virus being killed by stomach acid, is true.
Now, my question is not limited to coronavirus and I am not seeking medical advice or treatment here. I just want to  know if my friend is scientifically correct, i.e. whether stomach acid is able to destroy the biological structure of a virus (any virus, and not necessarily coronavirus)? And if so, how does this work biologically?

Unless you only eat sterile food , your stomach kills a lot of stuff . I think the question is "what doesn't a stomach kill"?

Study on MERS coronavirus and HCoV-229E: "rapidly lost most of the infectivity in fasted-state simulated gastric fluid (FaSSGF; pH 2.0)" but "survived FeSSGF" (fed state, which is less acidic). See Figure 3. IOW, on empty stomach, the gastric acid rapidly deactivate the MERS coronavirus and the 229E coronavirus, but if there is food in the stomach then the virus survives.
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5687858/

You know why rotovirus and polivirus vaccines are oral, not injected?
Becuase it's the immune system in your stomach that needs to be primed to kill those viruses, they are primarily GI infections (yes, polio is primarily a GI infection, it only sometimes infects nerve cells.)


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How does brain activity change when focusing on something within peripheral vision, as opposed to the fovea?
Normally when looking around, we mentally focus on what we see within our fovea, as that is where we have the greatest visual acuity. However, it is still possible to focus (both physically with the eyes and mentally with our attention) on an object in our peripheral vision.
Can we detect any changes in brain activity when this happens? Do different regions of the visual cortex or prefrontal cortex become more active?

What have you already read on the topic? The best Biology.SE questions are questions where you can support your question with a basis in something you've read. In other words, show the research you've done to come to this question. Every StackExchange site has some version of this requirement.

This may work better on [psychology.se], with the eyes and CNS being so intimately connected and the question being regarding brain activity. You'd need to show your background reading there also.

That makes me think of the test where frowning faces are placed on a monitor in peripheral vision, amidst smiling faces, smilies... The brain cannot consciously see and register them, and the subconscious brain is wired to turn the eyes towards any frowning face is peripheral vision, as a primitive defence system that exists in the cortex, which operates faster than conscious thought.

I know for sure that there has been extensive research on this, particularly on experiments with monkeys --with functional Magnetic Resonance Imaging (fMRI) or Electroencephalography (EEG). Just do a short research on the web and you will see the avalanche. Sensory visual attention is one of the most investigated areas.


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Why is the nitrate concentration in a root hair cell higher than the nitrate concentration in soil?
For the exchange of nitrates and other mineral ions to occur between the root hair cell and the soil, the root hair cell needs a higher concentration of mineral ions and nitrates than the soil so that active transport can happen from the soil to the root hair cell. Please can someone explain how and why the root hair initially has more nitrate ions than the soil and what the point of absorbing these minerals is if the root hair cell already has more?
Sorry if this questions is worded badly or some of the information is wrong.

Comments have been moved to chat; please do not continue the discussion here. Before posting a comment below this one, please review the purposes of comments. Comments that do not request clarification or suggest improvements usually belong as an answer, on [meta], or in [chat]. Comments continuing discussion may be removed.


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Recent developments in the diagnosis of Parkinson's Disease
I was reading a research paper titled - "Discovery of Volatile Biomarkers of Parkinson’s Disease from Sebum" by Drupad K. Trivedi. I am Providing a short summary of it.

Discovery of Volatile Biomarkers of Parkinson’s Disease from Sebum

Parkinson's disease (PD) is a neurodegenerative disease that is difficult to diagnose early. However, a "Super Smeller" individual was discovered who can detect PD by odor alone. Early studies showed that the odor was present in the sebum (skin oil) of PD subjects. In this study, the volatile metabolites of sebum samples from control subjects and PD subjects were analyzed using thermal desorption-gas chromatography-mass spectrometry (TD-GC-MS) and validated by a separate group. The results identified a distinct volatiles-associated signature of PD, including altered levels of perillic aldehyde and eicosane. The odor of these compounds was confirmed by the "Super Smeller" to be highly similar to the scent of PD. Additionally, the study used machine learning approaches to validate the biomarkers. Further analysis showed that the compounds eicosane, perillic aldehyde, hippuric acid, and octadecanal were consistent and differentially expressed between PD and control samples. The presence of these biomarkers was confirmed by the "Super Smeller" through qualitative smell analysis. The study also demonstrated that these biomarkers were not associated with medication use in PD subjects. The findings suggest that analysis of volatile metabolites in sebum could potentially be used as a non-invasive screening method for PD. However, further research with a larger sample size is needed to validate the results and understand the underlying mechanisms of PD-associated odor.
I have read several research papers on this topic, but I am still unclear about the accuracy of these compounds for detecting Parkinson's disease and whether they have been validated in other experiments. I would greatly appreciate guidance from someone with more knowledge on this subject. As part of my college club, I need to write an article on this, and it would be helpful to have more insights.

So - you are at college and you have done the relevant literature search and looked at the paper's references? And what did they say?

Have you searched for relevant papers which cite the Trivedi et al. paper?  A basic such search is easy to do with Google Scholar.  Was the Sinclair 2021 Nature paper of any help?

A small point: the problem with PD isn't so much with the diagnosis as the treatment, although clearly, any approach to treatment may be enhanced by some understanding of the possible implication of these volatile substances in the pathogenesis of PD itself: "the underlying mechanisms etc.''.  So, the matter is certainly worth pursuing from that angle.  Why don't you write to Trivedi himself if only to broaden your perspective?


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Why are smaller mammals more prone to cancer and tumors
especially rats and mice usually develop cancer and tumors very fast, reducing their life expectancy.
From an evolutionary point of view, how come that these mammals are so prone to cancer and tumors even though they reproduce at a very fast pace?
Shouldn't they develop a resistance towards these illnesses through natural selection?
Source: https://www.thesprucepets.com/rat-tumors-1238498

Can you please add a source supporting your claim? Additionally both animals are not getting very old at all (a lot of mice for example only 2-3 years), so what do you mean by "in just a few years"?

Counterpoint: the naked mole rat is a small mammal that rarely gets cancer.

Here's some clues: https://www.researchgate.net/figure/An-illustration-of-Petos-Paradox-Cancer-is-a-disease-of-uncontrolled-cell-growth-and_fig1_318415292 and https://www.google.com/search?q=mammal+body+mass+cancer+frequency&sxsrf=ALeKk03Cg1u3LNP84BVSv3Z71LdGxNvdMA:1583687276279&source=lnms&tbm=isch&sa=X&ved=2ahUKEwiXxKbsrovoAhWo0eAKHehgDg0Q_AUoAXoECGEQAw&biw=1227&bih=646#imgrc=8T1PWiyWvtwtLM and try the web search for the same words.

Do we really have data on anything other than lab rats and mice, which are often bred to develop cancer, or have cancer given to them for experiments?  WRT the natural selection argument, almost everything in nature gets eaten by something else long before cancer or other age-related diseases develop.

The topic is called Peto's paradox, you can find references to studies on the wiki page, here's a summary:
A rat cell is more likely to get cancer than an elephant cell in the same time span. Mice have cancers in 2 years as often as humans have in 60 years.

Studies find that 4 ton elephants have only 4 times more blood cells than a 12 gram shrew. They have big mammal cells that divide at a slower rate. Rats can double their body weight every 10 days when they are teenagers, as if a puppy with a lot of appetite could become an adult dog in 30 days.

It is thought that the genetic safeguards that have evolved to protect large mammals against cancer would slow the growth and reproduction rates of small mammals. For example, an elephant has 14 copies of the cancer suppression gene TP53, humans have three copies, hyraxes and manatees have one copy.
Evidence for the paradox began to emerge in the 1970's. Studies from zoos on many mammal species have confirmed that big animals are protected from higher cancer rates.
https://en.wikipedia.org/wiki/Peto%27s_paradox

You could also look at it as a large slow growing animal had better be resistant to cancer or it is unlikely to live long enough to reproduce, simply due to the high turnover rate the impact of cancer on a small short  lived line of animals is much less.


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What is the name of this bug?

I found this bug in my garden in India this morning.

That is a tortoise beetle (Family Chrysomelidae (Leaf beetle), subfamily Cassidinae). It looks very much like the Indian Green Tortoise Beetle Chiridopsis bipunctata. https://indiabiodiversity.org/observation/show/338651
I am almost sure it is in the genus Chiridopsis.


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How does a pine cone open?
When a pine cone is wet, it remains closed. However, when it's dry it opens again.
From the perspective of physics or biomechanics, what is the mechanism that allows a pine cone to open and close as I've described?

From How Do Pine Cones Open (Nature):

The scales of seed-bearing pine cones move in response to changes in relative humidity. The scales gape open when it is dry, releasing the cone's seeds. When it is damp, the scales close up. The cells in a mature cone are dead, so the mechanism is passive: the structure of the scale and the walls of the cells composing the scale respond to changing relative humidity.

As to the reasons why:

Pine cones usually appear open because this is considered a more favourable condition for the seed dispersal and germination. This usually happens when the weather is warm and when they touch water or in cold conditions, they tend to close to avoid destruction.

As to the physics/biomechanics of the pine cone opening/closing, there is an interesting article titled Hygromorphs: from pine cones to biomimetic bilayers that discusses objects that respond to environmental humidity to change their shape.

Using the pine cone as an example that opens when dried and closes when wet, we quantify the geometry, mechanics and dynamics of closure and opening at the cell, tissue and organ levels, building on our prior structural knowledge.