text:
Explain asymptomatic viral infection (ie covid) with no symptoms
There are a lot of people that are testing positive for covid that have no symptoms (ie they are asymptomatic).  This raises the question - does the current test have an unacceptably high rate of false positives?  From a physiological point of view, doesn't an active viral infection of any sort generate tissue damage and hence some sort of response (immunological, inflamatory, histochemical, etc) that DOES lead to outward symptomology?  Viral replication necessarily causes tissue damage (is there a human virus of any sort that does not?).  Tissue damage, especially in the upper airway and lungs, would (it seems to me) cause a response (coughing, perhaps fever, etc) yet we are told that covid is capable of causing asymptomatic infection.  Is this really plausible?  We seem to only have these swab tests as the only indicator telling us these asymptomatic people have the covid infection (or the virus is present in their airways).  This is, naturally, a huge public health and social problem if these tests are false-positives.

Typhoid is an example of an infection that even when it causes symptoms - the symptoms are not readily visible by a bystander (ie caughing by someone with covid).  Is there any other example of an upper respiratory or lung infection that does not cause symptoms ?  The covid test was necessarily rushed into production and that leaves a reasonable chance that it may give false positive results.  And even if covid is somehow able to replicate in the lungs and upper respiratory tract without eliciting an inflamatory response, then how can that person be contageous IF THEY ARE NOT COUGHING?

Pine Street Inn homeless shelter in Boston - Of the 397 people tested, 146 people tested positive. Not a single one had any symptoms.  Testing of the entire crew of the aircraft carrier Theodore Roosevelt - at least 655 Roosevelt sailors have now tested positive - the majority have displayed no symptoms.

Widespread testing of asymptomatic people has until now not been a priority or even seen as necessary or needed or useful.  When it is done, however, it is turning up lots of positive results.  This to me is unexplainable.

'how can that person be contageous IF THEY ARE NOT COUGHING?' because they are breathing and speaking.

As far as asymptomatic caries of other respiratory diseases: in one study Asymptomatic rhinovirus infection outnumbers symptomatic infection four to one among university students

@Peggy Do you want an answer or not? Your responses in comments lean towards "not", which makes this a bad question.

@Bryan Krause: what you consider "bad" about the question could be implying that tests should indicate "symptomatic infections" only - at the same time, it's been said that there are asymptomatic infections that are "infectious". So, the question seem unclear about "infectious infections" that are not symptomatic. Am I allowed to set up some "draft answer" based on definitions? To me, Stackexchange has got all the forms and frames needed to discuss - peers should be more tolerant towards "draft" questions. e.g.  answers her  to me "do not answer the question", however, they are (answers).

There are many examples of asymptomatic virus infections.  For instance,  person can be infected with HIV for years before noticable symptoms appear.  Then there's the varicella-zoster virus that gave you chicken pox when you were a kid, only to lie dormant for half a century before reappearing as shingles.

@jamesqf In fact even flu can be (and often is) asymptomatic.

It isn't just Sars-Cov-2. Many diseases and medical conditions are known to be asymptomatic in some people. The most famous asymptomatic carrier of a bacterial disease was Mary Mallon ("Typhoid Mary"), a woman who was permanently infected by the Salmonella typhi bacteria. She had no ill effects from the infection but spread it to many other people until she was forced into quarantine.
The underlying issue is that our immune systems are highly variable from person to person.

Tissue damage, especially in the upper airway and lungs, would (it
  seems to me) cause a response (coughing, perhaps fever, etc)

It isn't that binary. Your respiratory system is constantly being damaged by pathogens and pollutants, but your body is constantly repairing the damage.. As long as the rate of repairs can keep up with the rate of damage, you may not notice anything. When you feel sick from something like Sars-Cov-2, it's an indication that the pathogen is causing damage faster then it can be repaired. The balance between these depends both on how fast your immune system responds, and how efficiently your repair mechanisms work. Both of these can vary widely between individuals, depending on both genetics and the environment.

First, the 60% asymptomatic numbers for the Roosevelt are fairly consistent (adjusting for age) with those from the Diamond Princess: about 50% at the peak of the infection, but in a much older population. (Also you can be pretty sure the Japanese were using a different test kit [in February] than the US.)
Second, asymptomatic when tested, doesn't mean you won't develop symptoms later, as the damage accumulates. (In fact, accumulated lung damage is the main problem with Covid-19; see q on Skeptics on the death of Rooselvelt sailor.) Nonetheless, the presymptomatic people can shed enough virus to infect others:

We report temporal patterns of viral shedding in 94 patients with laboratory-confirmed COVID-19 and modeled COVID-19 infectiousness profiles from a separate sample of 77 infector–infectee transmission pairs. We observed the highest viral load in throat swabs at the time of symptom onset, and inferred that infectiousness peaked on or before symptom onset. We estimated that 44% (95% confidence interval, 25–69%) of secondary cases were infected during the index cases’ presymptomatic stage, in settings with substantial household clustering, active case finding and quarantine outside the home. Disease control measures should be adjusted to account for probable substantial presymptomatic transmission.

And yeah, this asymptomatic presentation is not unique to Covid-19 among respiratory diseases. Influenzas cause this too:

We identified 235 virologically confirmed secondary cases of influenza virus infection in the household setting, including 31 (13%) paucisymptomatic and 25 (11%) asymptomatic cases. The duration of viral RNA shedding was shorter and declined more rapidly in paucisymptomatic and asymptomatic than in symptomatic cases. The mean levels of influenza viral RNA shedding in asymptomatic and paucisymptomatic cases were approximately 1–2 log10 copies lower than in symptomatic cases.

It does seem to be that case that the less "sick"/symptomatic shed less virus, in influenza at least, and probably by analogy in Covid-19 as well.
The degree of asymptomatic presentation can vary between strains (and likewise by age group) even for viruses that are pretty similar, like the "common cold" CoVs:

(If you want to know more about the specificity of Covid-19 tests, ask on med SE. Your question was pretty broad, and I can't touch all the angles here. I've only shown you that asymptomatic cases in other viral respiratory illnesses are not uncommon.)

To answer your question  it is necessary to distinguish the concepts of:

infection
symptom
test set up

The term infection might even denote the swallowing of a "dose from a  nose", without any replication of virus. On the other side of the ladder, "infection" might refer to a symptomatic disease.  However, "to explain infection without symptoms" implies that there does exist some stage  in between -  and "replication of virus within individual cells of the body" might "explain infection without symptoms" in the sense of the question.
Moreover, defining infection by "infection of single cells"  is the basis for  test set ups: "take" a "dose of the nose": a test would not run the risk of false positive results just to include that rare case of an infection that has not reached the stage of viral replication. (And a test should not run the risk of false negative by setting the minimum that high  that viral replication surely leads to symptoms).
Most important, the key concept "viral replication" explains why there may be contagiousness (there is no such term as "infectiousness", but a contagious person "always" is considered "infected", of course) without symptoms: viral replication does not imply symptoms of the disease.
The above should explain why there is infection=disease without symptoms, in principle.
Cp. https://www.verywellhealth.com/how-do-you-define-asymptomatic-2721956 where they talk of "over-diagnosis" which might be the opposite to "symptomless spread", as you might get treated not because of being sick "just a little bit" (without being infectious). For Diseases that do not exhibit symptoms cp. https://en.wikipedia.org/wiki/Asymptomatic. Maybe you speak of "asymptomatic disease" if there are some persons that do not show symptoms compared to persons that do exhibit symptoms, both groups refering to a common denominator, "viral load" for instance.
To answer the question which refers to Covid-19 one must look at the symptoms of covid. How can it be that viral replication in the case of CoV-19 does not INSTANTANEOUSLY lead to symptoms - if AT ALL?
A common concept is  to differentiate symptoms that  result from the activity of immune cells from those symptoms that result from the destruction of the infected individual body cells, which is a common differentiation.
It seems difficult to find reputable sources googling as with Covid it is mostly "explaining asymptomatic spreading" that is the main issue. Your question pertains to that as well, but focuses on "explain asymptomatic disease" - which might be considered a self-contradictory concepts as it denotes some "hidden disease" that should have certain symptoms that are just not being unveiled.
To "explain asymptomatic infectiousness", compare for instance
https://www.nejm.org/doi/full/10.1056/NEJMe2009758
"A key factor in the transmissibility of Covid-19 is the high level of SARS-CoV-2 shedding in the upper respiratory tract,1 even among presymptomatic patients, which distinguishes it from SARS-CoV-1, where replication occurs mainly in the lower respiratory tract."
One more link: https://www.nejm.org/doi/full/10.1056/NEJMe2009758 refering to influenza (the more viral load in the upper tract the more symptoms - which should not explain asymptomatic transmission)
Some reputable source on "asymptomatic disease" (i.e. not on asymptomatic spread):
"Clinical and immunological assessment of asymptomatic SARS-CoV-2 infections" https://www.nature.com/articles/s41591-020-0965-6
There are attempts at explaining "asymptomatic covid-disease" specifically.
However, for instance, https://www.thelancet.com/journals/laninf/article/PIIS1473-3099(20)30460-6/fulltext specifically names "Lactate dehydrogenase" which seems to refer to the immune system in a corona-unspecific way, i.e. seems to  refer to individuals' being different in strength of their immune systems.
Here is my own personal approach based on the type of target cells of Covid, which are epithelial cells called "pneumocytes II" (target antigen of the spike is ACE2)

As target cells are stem cells their loss of function in  replacing dead epithelial cells (whose apoptosis is a regular one and, interestingly, not caused by the virus!)  might be felt only very late or not at all

The second function of Covid's target cells, pneumocytes II, besides their function as stem cells renewing epthelium, ist the production of surfactant. Hereby, I  tentatively  hypthesize that loss of that function of only leads to symptoms of shortage of breath if the  muscle activity of breathing in (which is supported by surfactant) does not overcompensate the loss of surfactant when the breathing activity of the patient in general is low.

I had to rule out my idea that the inflammatory reaction, in asymptomatic cases, might even be less in degree than with common cold caused by corona virus because stem cells as such should be lesser in number compared to differentiated epithelial cells  - this idea is wrong: counterintuitively, stem cells, i.e. pneumocytes II are much higher in number than pneumocytes type I.

For whom it may concern some explanatory remarks on  "infection and symptoms" in abstract terms:
The term symptom according to commmon usage refers to the signs sick person present with when they feel at uneas.  However, in a more intricate way,   "symptomatic" might be  defined as: infection of single body cells causing replication of virus. In that case, there would not exist any "asymptomatic infection" as that would be self-contradictory: if "symptom" does come with "infection" - of one single cell.
To explain asymptomatic infection the underlying concepts of "symptom" and "infection" must clearly be set apart. The replication of the virus (infection) is different from the symptoms as consequences of this event. Viruses only replicate in cells, thus turning a test to a positive result, and only then (not before infection of single cell, "after contact".)
On the other hand, tests are not set up to turn positive before this replication starts, as it is the basis for contagiousness. Your question may seem to  blame tests for being "false positive". However, tests are not set up to show negative results when it's only the symptoms that do not show, but the cells have harboured viruses that have replicated, thus causing contagiousness. Test are truly positive when they indicate virus replication only, and, on the other hand, presumably only turn positive if there ,in fact, has been some minimal infection of single cells, thus indicating some more virus than has been inhaled.
If there is "infection without symptoms" this might quite easily be explained by the symptoms being caused be the reaction of the immune system, not by the loss of function of body cells. There may be a common situation where epithelial cells  are infected already, implying virus replication, thus contagiousness - without the immune system causing the symptoms, and no  defunct epithelial cells either, thus  resulting in a  test being positive showing "symptomless infection".
For a very up-to-date and surprising alternative answer to your question that refers to insertion of viral RNA as DNA into the genome (retroviral like mechanism ) that is detected by positive testing "without symptoms" see the following reference.
https://www.sciencemag.org/news/2020/12/coronavirus-may-sometimes-slip-its-genetic-material-human-chromosomes-what-does-mean
which is like a review of the reference in some other question at stackexchange Does SARS-CoV-2 kill its host cell or not?

This is a (not very good) criticism of the question, but by no stretch of the imagination an answer to it. Answers should be answers. If you have

By adding some "no stretching" to your comment it becomes much more "substantial" (don't know how to say in English) than what I have gotten used to around here - so sad....

@David Please see - I coorected the criticism you criticized as - yes, indeed - it is incoherent to my commenting on "first comment" of question. Let me know if this is being unclear to you.

This still doesn't answer the question. Symptoms are defined, for xample see here. It does not mean the infection of the body with a pathogen.

@user1136 All this flagging makes me look important. So I should get along alone very well as soon as you have skipped me out :-) What you're saying suits me fine! You are right. I haven't said anything to the contrary. Your reproach is that I haven not answered what the question is about, and you have?

@Chris . "I agree" :-) With your link,  I expected some page with precise definition of covid-19. Then, that page was on general principles. Still, you are right! "Explaining" in the sense of the question needs specifity.  I will edit and elaborate on "replication without symptoms in case of Covid-19".You do not want me to clarify a question that might in strict terms of peerness be an "unfocused question"? I took your job?

Haven''t read yet all what's in your link - I think it's a good link, as "Alzheimer" might illustrate what I was talking about. It should be clear what the test is testing for: for the symptoms that define the disease which are "just" certain effects of certain causes or for, I'd say, pre-effects of symptoms - which, interestingly, in the case of anti-bodies, may be post-symptom-effects as well.

user1136 Please see my comment above, refering to the link you gave. What are you flagging me for? Is it for not answering the question as it is put? If yes I would like to retaliate to just the opposite: your comment does not fit the question as formulated. What I've been trying to do was interpreting the question according to its explanatory text, then answer it as it was put.


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How verified experimentally is the Marginal Value Theorem for viruses?
Reading some Stanford notes on R0, they get to MVT and optimal virulence:

Consider a directly-transmitted infection from which there is no recovery (e.g., Herpes Simplex). The population experiences a baseline mortality rate, µ, and a disease-induced mortality δ. [Then the SI model]

ds/dt = −βsi − µs
di/dt = βsi − (µ + δ)i,

Figure 4: Marginal value theorem for optimal virulence. The ESS [evolutionarily stable strategy] virulence occurs where a line
  rooted at the origin is tangent to the curve that relates β to δ. Two curves are depicted. The
  first curve shows a pathogen in which transmissibility increases relatively rapidly with mortality.
  Point A indicates the optimal balance between β(x) and δ(x) under this case, and the optimal
  virulence is indicated x∗
  . For the second curve, relative transmission is less efficient. Therefore,
  the tangent line from the origin to the curve hits further out (B) along the mortality axis and
  the optimal virulence is higher (x∗∗).

Wikipedia has a page on MVT but it doesn't discuss viruses/virulence at all (although it has some criticism of MVT from other angles/domains). So, how verified experimentally is MVT for viruses?

I'm not an expert but it seems purely theoretical. There are some fairly basic criticisms that can be made of this model. First it assumes that viruses tend to optimize propagation, a perfectly reasonable assumption. The clear prediction is that propagation rate should be inversely related to mortality rate. Quickly checking a list of the most common viruses shows you that this relation is not that strong, if there at all. The second issue is that R0 is a very abstract measure. Viruses do not propagate in a straightforward manner. Rabies relies on animals biting each other, HIV sexual contacts, etc. On average each virus will still have an R0, but I'm not sure it is so sensible to assume it will trade-off with mortality as it relies on the animals behavior (although with rabbis for example the animal behavior is actually modulated by the virus itself to increase propagation). Lastly epidemics usually start with a zoonotic disease randomly mutating and jumping species. They often have quite different effect on different species so here again I am not sure it is completely reasonable to assume that the mortality rate of a virus will tradeoff with infection rate.
It's still a useful tool to think about how viruses should behave. As you noted there also are criticisms about the MVT to describe animal foraging. But mathematically, under some assumptions, it is the optimal solution. So any deviation you see from that tells you your assumptions were wrong.

The answer seems to be "not much". I did find one paper that proposed MVT for viruses but instead of transmission efficiency in abstract terms they used/proposed lysis time as the parameter that might get optimized for/by phages. And as dependent variable they proposed not mortality but host density.
The problem indeed seems to be that before one even bothers to consider such a (MVT) model, the assumption[s] that that parameter gets optimized need to pass the "smell test".

A fundamental issue is whether the phenotype at the
  center of an optimality model has sufficient genetic
  variation that is sufficiently unconstrained to evolve in a
  manner consistent with the model. There might be a lack
  of genetic variation in the phenotype per se. Alternatively,
  there might be genetic variation for the phenotype, but
  such variation lies in a ‘higher dimensional space’ than is
  assumed in the optimality model [32,33]. This means that
  selection acting on traits outside of the optimality model
  can drive phenotype evolution in a way that is not captured
  by the model (as proposed for the evolution of some disease
  virulence models [34]).
Lysis timing has a clear genetic basis in all lytic phages,
  suggesting that it is appropriate for optimality. Large genome
  phages have modular lysis timing genes (holins and
  anti-holins). Mutations in holins have few pleiotropic effects,
  as shown by experiments with site-directed mutations in
  holins. Perhaps more crucially, holins translocated to
  different phage genomes retain their function in the new
  genome [24–26]. These studies establish a mechanism for
  genetic variation in the optimality phenotype that is free of
  major pleiotropic effects. In essence, holins provide a genetic
  ‘identity’ for lysis time [35].
Lysis timing also has a clear genetic basis in phages with
  small genomes, because these phages have genes dedicated
  to lysis. Thus, lysis timing can plausibly evolve through
  changes in the expression and activity of the lysis genes.
  Evidence of genetic variation in the phenotype could be
  obtained otherwise (e.g. by measuring heritability in lysis
  timing). However, knowledge of genes that regulate lysis
  timing not only circumvents the need for such evidence, but
  also reveals that lysis timing is and has been a major fitness
  component in phage life histories.

Subsequently the same authors proceeded with an experimental verification in another paper

Here we employ phage mutants to explore issues of phage latent-period evolution as a function of the density of phage-susceptible bacteria. Theory suggests that higher bacterial densities should select for shorter phage latent periods. Consistently, we have found that higher host densities (≥∼107 bacteria/ml) can enrich stocks of phage RB69 for variants that display shorter latent periods than the wild type. One such variant, dubbed sta5, displays a latent period that is ∼70 to 80% of that of the wild type—which is nearly as short as the RB69 eclipse period—and which has a corresponding burst size that is ∼30% of that of the wild type. We show that at higher host densities (≥∼107 bacteria/ml) the sta5 phage can outcompete the RB69 wild type, though only under conditions of direct (same-culture) competition. We interpret this advantage as corresponding to slightly faster sta5 population growth, resulting in multifold increases in mutant frequency during same-culture growth. The sta5 advantage is lost, however, given indirect (different-culture) competition between the wild type and mutant or given same-culture competition but at lower densities of phage-susceptible bacteria (≤∼106 bacteria/ml). From these observations we suggest that phage displaying very short latent periods may be viewed as specialists for propagation when bacteria within cultures are highly prevalent and transmission between cultures is easily accomplished.

In the same vein, there's a later paper titled "Bacteriophage Adsorption Rate and Optimal Lysis Time".
There might be more papers like this, but it doesn't look like the (more) universalist approach (i.e. transmission vs mortality) from the ecology notes has had much traction with virologists.

Cool. I couldn't find papers but I looked only at viruses, not bacteria (although the basic principle should hold). Even for food intake, which is what MVT was meant to be applied to, evidence are fairly scarce and more qualitative than quantitative.

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text:
Understanding Research Paper Differences
I'm doing a high-level research which led me to the following paper - https://www.researchgate.net/publication/280389511_Quality_of_life_of_patients_with_chronic_lymphocytic_leukaemia_in_the_Netherlands_results_of_a_longitudinal_multicentre_study
As it's mentioned there are many groups of testing and comparison in the research, which are: the general population, total patient group and three groups of CLL patients.
I'm a bit confused about the definitions' differences between "the total general population" and "the total patient group".
I appreciate every advice / help.

This study enrolled 144 CLL (chronic lymphocytic leukemia) patients ("total patient group"). They further grouped these patients into 3 groups according to the treatment they were receiving.
When they refer to "general population" they are referring to norm scores:

For each patient, an individual norm score was
  derived from age- and gender-matched scores of the general population on the EQ-5D [28] and EORTC QLQ-C30
  [29]. These two studies, as reported in Refs. [28] and [29],
  used a panel consisting of more than 2000 Dutch households, representative of the Dutch-speaking non-institutionalised population in the Netherlands.

So these scores are not part of the current study, but they are estimates from a survey of the wider population rather than patients who have CLL (you can assume they do not have CLL). "Total population" doesn't mean "all CLL", it means "all Dutch-speaking non-institutionalized people".

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text:
Do any known viruses contain "junk" or parasitic genomic information?
After reading about so-called "mystery proteins" in this excellent summary of the coronavirus genome (and acknowledging that the "mystery" simply reflects our lack of knowledge about a very new virus), I'm curious if any known viruses can contain parasitic genetic information "along for the ride", or if their genomes are selected, generally speaking, to be as informationally efficient as possible, for what is encoded? In other words, does selection pressure allow for these parasites to contain their own parasites, and are there known examples of such, if so?

Here’s something: https://bmcbiol.biomedcentral.com/articles/10.1186/s12915-015-0145-1

That's a great answer, cheers for that.

I'm curious if any known viruses can contain parasitic genetic information "along for the ride"

Analogous to the parasitic transposons mentioned in the paper linked by canadianer, phage-inducible chromosomal islands are mobile elements that "hijack" the molecular machinery of bacteriophage during lytic infection of Gram-negative hosts.  PICI elements, as they're called, encode Rpp proteins that complex with the phage TerS homodimer, changing the conformation of the complex such that the PICI cos mimic is preferentially bound and packaged into the empty capsid.  Fillol-Salom et al. 2019 1 discuss in detail the mechanism of PICI propagation and provide a good graphical abstract of the process:

Similar elements exist in Gram-positive bacteria, specifically Staphylococcus aureus, called Staphylococcus aureus pathogenicity islands (SaPIs).  Instead of encoding a separate protein that complexes with the phage TerS, SaPIs encode a homolog of TerS that specifically recognizes and packages SaPI DNA into phage capsids.2
Note that this answer does not directly address the question of "junk" DNA in viruses, as PICI elements are dormant in the genomes of the bacterial hosts rather than the genomes of the viruses themselves.  Though, I believe this is relevant insomuch that they parasitize bacteriophage, and are therefore "along for the ride" in the viral capsid.

Citations

Hijacking the Hijackers: Escherichia coli Pathogenicity Islands Redirect Helper Phage Packaging for Their Own Benefit
Role of Staphylococcal Phage and SaPI Integrase in Intra- and Interspecies SaPI Transfer


text:
Is this arthropod non-intrusive and recommended to be left alive?
I am in Portugal (Lisbon) at the moment, and when leaving my room late at night (12 pm ~ 04 am) I usually face about 4 of these arthropods in the corridors:

(For reference, the "line" in the image is a standard separation on the floor. This particular example of the animal is a little smaller than a nail.) They seem to have quite variable sizes and walk primarily on ground. Also, as implicit above, they seem to be active primarily during the late night. (I don't see them much often, if at all, during the morning/afternoon.) They can be quite fast, but if left unharmed do not move much. They also appear to take shelter inside the walls.
From what I searched, it seems possible that they are centipedes. I've seen sites saying that they are useful to keep other less pleasant animals at bay. My questions are: What are those animals, and should I leave them be or not?

Related: Is this an insect? Which one?

This appears to be a silverfish, a very common household "pest" in the Lepismatidae family of insects.

 Photo Credit: Dong-Hwan Choe. Source: UC IPM
Silverfish are silver/grey and (like all members of the Zygentoma order) have three distinct, tail-like caudal appendages from their posterior end -- really, two large cerci with a central long filament.
 [Sources: 1, 2, 3].
According to Wikipedia, you can find them all arround the world:

Silverfish are a cosmopolitan species, found in Africa, the Americas, Australia, Eurasia, and other parts of the Pacific.[8] They inhabit moist areas, requiring a relative humidity between 75% and 95%.[9] In urban areas, they can be found in attics, basements, bathtubs, sinks, kitchens, old books, classrooms, and showers.[3]

They are relatively harmless due to their weak jaws [source], and their presence is typically a larger nuisance than the damage or disruption that they cause.
We have a number of posts already identifying silverfish and asking about management advice. Try yping "silverfish" into the Search bar at the top of the page to search for more information.

Thanks for the insightful response. Taking a look at the sources, it is unclear to me if the amount I'm finding is alarming. Would you know if it is?


text:
Are "sympathetic nerves" the same as "cardiopulmonary splanchnic" nerves?
I've gathered from a number of sources (e.g., Patel (2015), Wikipedia, and here) that the sympathetic nerves leaving the sympathetic trunk to innervate the heart and lungs are called "cardiopulmonary splanchnic nerves".
However, I've noticed that both the 14th and 15th edition of Tortora & Derrickson's A&P textbook seem to suggest that these nerves are simply called "sympathetic nerves," even though they make reference to abdominopelvic and adrenal splanchnic nerves more specifically.  See below from Tortora & Derrickson (2013):

...Then, the axons of the postganglionic neurons leave the trunk by forming sympathetic nerves that extend to visceral effectors in the thoracic cavity (Figure 15.4). Sympathetic nerves provide sympathetic innervation to the heart and lungs.

Here are subsets of images from Patel (2015) [LEFT] vs Tortora & Derrickson (2013) [RIGHT] (my emphasis):

My question: Are "Sympathetic nerves" the same as "cardiopulmonary splanchnic" nerves?

Are these names interchangeable? I can't find further evidence supporting Tortora and Derrickson's usage of this phrase in such a specific manner to refer to postganglionic neurons leaving the trunk to innervate the heart and lungs. Are they acting rogue? Are they simplifying? Any insight would be appreciated.

Cited works:
Patel, T. R. 2015. "Chapter 36 - Anatomy of the Sympathetic Nervous System." Pages 495-506 in Tubbs, R.S., Rizk, E., Shoja, M.M., Loukas, M., Barbaro, N. and Spinner, R.J. eds. Nerves and Nerve Injuries: Vol 1: History, Embryology, Anatomy, Imaging, and Diagnostics. Academic Press.
 Tortora, G. J. and B. Derrickson. 2013. Principles of anatomy and physiology, 14th edition. John Wiley & sons, Inc.

You might consider cross-posting to SE Medical sciences who know more about this stuff.
I think that they are simply using a more general term than other authors. In the same way, most people call crabs crabs, but some people might occasionally refer to them as crustaceans.
Based on wikipedia, it seems that cardiopulmonary splanchnic nerves are a subset of sympathetic nerves. The sympathetic nervous system innervates a large number of organ systems of the body (see image), such that the cardiopulmonary splanchnic nerves are simply the sympathetic nerves that innervate the heart and lungs.
Looking further at the wikipedia for splanchnic nerves, it seems that this is a technical term relating to the fashion in which organs are innervated by the sympathetic nervous system; e.g. in my crude understanding they are organ hookups to the sympathetic nervous system.
In other words, all cardiopulmonary splanchnic nerves are sympathetic nerves, but most sympathetic nerves are not cardiopulmonary splanchnic nerves.

thanks for the answer. However, -1 b/c I feel like it doesn't answer my question. I know what the sympathetic nervous system is, and I know that the cardiopulmonary splanchnic nerves are the part of the sympathetic system that go to the heart/lungs. I also know that all nerves carrying sympathetic signals are considered "sympathetic nerves". I indicated all of this in my post. It appears to me, that everything you've mentioned in this answer repeats points made in my question, so I don't think this is actually an answer to my question. Could you clarify your post if this isn't the case?

IMO you did not indicate all of that. It was not clear that you understood that the sympathetic nervous system could be a superset of nerves of which splanchnic nerves was a subset, and that the authors in question could be substituting a more general term. I am happy to delete the answer if you do not feel that it addresses your question. But if you knew all of that in the first place I am not sure why you are even asking the question? It seems you have answered it yourself before even posting it.

Cardiopulmonary splanchic nerves consist of:

sympathetic nerves
the vagus nerve (a part of parasymathetic system)


text:
Does a tubular sodium reabsorption cause a stimulation of β2-adrenergic receptors?
I read the study "The Role of Aldosterone in Obesity-Related Hypertension" and there is one thing I didn't understand. They write: "According to norepinephrine-induced tubular sodium reabsorption, stimulation of β2-adrenergic receptors leads to activation of the Na–Cl cotransporter through suppression of the serine-threonine protein kinase WNK4 in the distal tubule." Is According to meant like due to? So does a tubular sodium Reabsorption cause a Stimulation of β2-adrenergic receptors?
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4886496/

You've got it backwards. "norepinephrine-induced tubular sodium reabsorption" is the whole process. The β2-adrenergic receptors respond to norepinephrine (this is the "norepinephrine-induced" bit). The receptors then suppress WNK4 in the distal tube ("tubular"), which causes the Na-Cl cotransporter to activate, which in turn causes sodium reabsorption.
This was probably a poorly phrased sentence on the part of the writers, but the sentence follows the same logic as "According to the First Law of Thermodynamics, energy cannot be created or destroyed". The description of the process is just complicated by multiple clauses.


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Glycocylation or glycosylation?
I came across a few sources that refer to glycocylation. Is this the same as glycosylation?
See for instance page 237, or the abstract in this paper.
"glycocylation" - 1210 search results on google
"glycosylation" - 5.98m search results on google

Ever heard of typographical errors or mistranslation from languages where the consonant C is pronounced like an English S? At 1 in 6000, that is the conclusion I would have drawn.

Yes, glycocylation is same as glycosylation. You can check out following links which explain glycocylaion same as post translational modification named glycosylation.
https://www.semanticscholar.org/author/Haudhiya/93411308
https://grantome.com/grant/NIH/R01-DA004166-05
https://quizlet.com/137217422/lecture-10-a-biochem-final-flash-cards/
https://books.google.com/books?id=3RbT3cpdCc0C&pg=PA508&lpg=PA508&dq=glycocylation&source=bl&ots=qIwbK6-ZdP&sig=ACfU3U18W_rG0D53R67_fzAywtMXGye5NA&hl=en&sa=X&ved=2ahUKEwjKrvfJp_foAhW3knIEHWLVB8gQ6AEwFnoECGQQQw#v=onepage&q=glycocylation&f=false

None of these references, except maybe obscurely the quizlet, do much of anything to support the equivalence of the two words.  The abstracts of the first two just mention one of the words, and the full papers are in Indonesian or unavailable, respectively.


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Please help me identify this caterpillar species (Sabah, Malaysia)

I kinda having trouble searching the internet to find this caterpillar name. Does anybody know what kind of species they are?

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If you can get a photo of just one of these from the side it may help even more; from what I can see these "caterpillars" are destined to become some sort of sawfly rather than a butterfly or moth (I think I see more than five pairs of prolegs on at least one of these--a butterfly or moth will have no more than five pairs of prolegs).


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Why do vertebrates have an oesophagus?
As far as I know, the oesophagus in vertebrates has no digestive or absorptive function. It is simply a conduit from the mouth to more distal parts of the gastrointestinal tract. Why have it at all, then? What evolutionary advantage does it give? Why not have the stomach start right where the mouth/pharynx ends?
Could it be to make space for the heart?
A Google search did not yield any useful answers.

Some fish do this, but if you want a neck (and if you live on land you do) you need to space things out. narrower fish use it to give space for the gills.

Because of the lungs - they need their own space to expand and contract.

That's a cool question! I think (just a thought, hence not an answer) the stomach needs space since it moves to churn food, and there are already have two vital 'moving' organs in the thoracic cavity. Additionally, it would be easier to have a lower position for the stomach to transfer the chyme down to the intestines, rectum, anus and finally eliminate it from a point far away from the mouth- for hygienic purposes.

@Varsh04802_Lr That's a possibility. But the words 'mouth' and 'hygienic' should not be used in the same sentence. The human oral cavity is home to hundreds of species of bacteria (see https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1287824/). It's so filthy, some even call it the glorified rectum.


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Can you identify this snake?
On a walk through I’ON Swamp/Natural Forest in Mt. Pleasant, SC, we came upon this snake. We did not get too close for fear it may be poisonous.
It had a very dark brown/taupe exterior with almost a diamond shaped head. It had a reddish, orange belly. It was ~3-4’ in length and fairly large girth.

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there is a Yellow Belly Water snake here in TX that the book says is the same as a Red Belly Water snake in the east. Looks like a good possibility.

How do I upload a photo?

When you are making (or editing) a post there is a picture icon (looks like white mountains on a black background) in the tool bar at the top of the editing field that you click on.

Hard to tell without a clearer picture, but the size and color pattern seem to match the description for the Plain-bellied Watersnake.
See for example the following picture from the Virginia Herpetological Society:

I assume from the location being in something called a swamp that the habitat (in and near slow moving bodies of water) also fits.

That’s it! That’s the same snake we saw on the trail. Thank you!

Great, glad I could help!


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Why do scientists perform most of biological experiments done on rats prior to humans?
Why do scientists perform most of biological experiments done on rats prior to humans?

Scientist gave a third ear to this rat

Source
Here is the another source claiming Researchers wants to COVID - 19 vaccine on rats.

World's scientists admit they just don't like mice

Welcome to Biology.SE! We encourage you to do some research on your own and then, informed by what you have learned, ask any questions you still have (ideally with references to reliable sources). Also that is a mouse not a rat! ——— Please also take the [tour] and then go through the help pages starting with [Ask] questions effectively on this site and [edit] your question accordingly. Thanks!

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

@tyresome I added second sources, still how many sources are needed for my question? Any specific number?

Some sign of researching the answer to question on your own first, please read the homework policy.

Originally for practical reasons.  Rats and mice breed prolifically and are easy to keep in captivity.  (Imagine trying to perform lab experiments on say hippotami, or tigers :-))  I would also imagine, given the large number of rat & mouse traps & poisons sold, that the fact that few people would care what was done to rats might have factored into it.
As time went on, those particular animals became the entrenched experimental animals, as techniques and equipment for maintaining them became readily available.  Indeed, you can readily buy commercial rat & mouse food: https://multipurina.ca/en/rodents/products/  Various lab strains were developed having consistent characteristics such as genetics or susceptibility to cancer.  (Not my field, so someone more knowledgeable could perhaps expand on this.)

You can do a google search. However,
The rodent lineage, which gave rise to the rat and mouse, and the primate lineage, which gave rise to humans, diverged about 80 million years ago. Humans have 23 pairs of chromosomes, while rats have 21 and mice have 20. However, the new analysis found chromosomes from all three organisms to be related to each other by about 280 large regions of genomic sequence similarity - called "syntenic blocks" - distributed in varying patterns across the organisms' chromosomes. (More at genome.gov)

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@tyersome well, this is what he needed


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How a pathologist would analyse this H&E image?
I am working on a project which involves writing computer software to analyse histological images. A typical image looks like this:

It is a Hematoxylin and Eosin stained biopsy of breast cancer tissue.
Being a programmer without biology background, I would like to get insight into how a pathologist analyses such images.
More specifically:

Which cells are cancer cells and which are regular cells?
Can an invasive margin (a curve marking the boundary of cancer invasion into the tissue) be seen in this image?
Can a pathologist provide a TNM classification looking at the image? If yes, what would be the T, N, M, G values for this image?

A single image is not enough for a TNM classification. This system requires knowing the size of a tumor (T), the degree of spread to new-by lymph nodes (N), as well as information about metastasis to other organs and tissues besides the lymph nodes (M), none of which are apparent from a single H & E stain image. Also, histological scoring often requires the user to scan around a slide and review many different fields of view. You'll probably want to collaborate closely with a skilled clinical pathologist for the project you've described.

@MikeyC what can be inferred from such image?

@MikeyC i.e. if a single image is not enough for classification, why is it taken?

My histology experience was looking at inflammation and necrosis in animal tissues, which is why I kept my reply to the commets section. I really only know enough about this to know that I would seek expert collaborators if I was doing what you're try to do. Histology often needs to be evaluated in context. A single image might be enough to identify cancerous or pre-cancerous cells, but you'd also need something like X-ray images to determine a T score along with additional biopsies or lab tests to determine N and M scores.

Here are some reviews I came across that might help give you a sense of similar applications being explored.
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2910932/
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5556681/


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Do larger unicellular eukaryotic organisms have larger organelles?
It seems that many of the giant unicellular eukaryotic organisms (size 1mm and above) are multinucleate but there are some with a single nucleus as well (the genus of Acetabularia). My question is: do they have proportially larger organelles (mitochondria etc.)? If so, can they be seen by a person with sharp eyesight when removed from the cell?

The cell has the amount of organelles necessary to perform its function. If a cell requires a lot of protein, it must have multiple nuclei to produce this protein. If the cell performs many activities that require energy, it needs many mitochondria. So the size and quantity of the organelles will be proportional to their function, not their size. In relation to Acetabularia, it is a single-celled organism visible to the naked eye. The nucleus is visible, but other organelles are not.


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Is there any known pharmaceutical or chemical that could cause infertility in humans in a single dose with few or no other effects?
Is there any known pharmaceutical or chemical that could cause infertility in humans in a single dose with few or no other effects?
The context is that a number of claims are circulating about vaccination being a "cover" for a plot to render males and/or females infertile. I claimed that it is unlikely that there is a known way to make a person infertile with a single dose of a chemical without significant side effects. However I couldn't find a source.
I'm asking as I believe it is important to have scientifically accurate responses to rumors and the like, even if they are outlandish.

People believing this sort of thing usually aren't that convinced by facts.

@BryanKrause, True, but not-yet-believers may be dissuaded from adopting the belief if contradicting facts are shown in rebuttal to the assertion.

@mgkrebbs Sure, but, given: https://xkcd.com/808/ this is a pretty insane claim. If there were some easy way to infertility with just a pill with no side effects we wouldn't be bothering with vasectomies, tubal ligation, etc. It's a losing battle to argue against things that don't have a basis: the burden of proof has to be on the claim not on the skeptics.

I would be interested to hear from someone with relevant knowledge who can lay out exactly why such a chemical is - or is not - possible. For example has any research been done into chemical alternatives to vasectomies?

yes, chemical castration, or chemical sterilisation! They generally have many side effects. The pill makes millions of female temporarily "infertile" every day. I am not sure how important this question is to the claim though. The simple counterfactual surely is enough? I have had many vaccine and am not infertile. Billions of vaccinations given a year. And in the developed world coverage of upwards of 90% for most vaccines. Wouldn't 90% of the developed world then be infertile?

It's hard to understand why, if such a chemical existed and was available at a price cheap enough to be used in mass vaccinations, it would not be available commercially as a less expensive alternative to vasectomy or tubal ligation.

@reubenmcg but are any of those chemical methods permanently effective in a single dose? My understanding is that they're not?

@jamesqf exactly.

Absence of evidence... years or reading science publications I haven't heard of any. If there was a single dose infertility drug with few side effects this sure would be big, big news. Getting the influential people onside before vaccination would be good, including vaccinating oneself.

". If there was a single dose infertility drug with few side effects this sure would be big, big news. "  -- can you add an answer listing publications where that information would be expected to appear?


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What are the short/long term effects of chloroquine on fundamental cell processes?
Does chloroquine, which affects the endosomal membrane traffic pathway (by affecting the acid environment used for fundamental endosomal reactions), have short/long-term effects on cell growth/proliferation/signaling?

This paper provides many experiments about changes to the endosomal system and autophagy and should be a good starting point.
Most of the treatments are done in the 5h to 24h range typical for cell culture studies. In theis relatively short time frame Chloroquine is well tolerated by cells. However, long term treatment will very likely be different.

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Do dogs and cats know the names of other people / pets in the house?
I have a dog named Penny and a cat named Milo. I always wonder if Milo knows Penny's name, and vice versa. So if I call Penny, does Milo know that I just called her? Similarly for humans, if someone is over the house that they're familiar with, do they know that person's name? If someone calls me by name, do my pets know that I've been called?
What about other interactions - not just calling someone (scolding, feeding, asking to do a trick, etc).
I'm looking for a more scientific answer if possible - meaning studies and facts. I've had dogs all my life, and cats for the past 10+ years, so I know they're very smart. But I want more than just "I know my dog knows my cat's name, because she's just so smart". I'm wondering if anyone has ever studied this and proven it one way or the other.

reason for downvote?

Not my downvote, but I would assume because simple observation would provide an answer.  For instance, I can tell my dog and a friend's dogs that he frequently associates with to go to a particular person, or do something with a particular other dog.

I specifically said that I'm not looking for simple observation, I'm looking for scientific proof. That's different. Also, what about cats?


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Are there other examples besides wasps' polydnaviruses in which a parasitic species introduces an immunosuppressant virus in the parasite's host?
An interesting form of mutualism:

Parasitoid wasps serve as hosts for the virus, and Lepidoptera serve as hosts for these wasps. The female wasp injects one or more eggs into its host along with a quantity of virus. The virus and wasp are in a mutualistic symbiotic relationship: expression of viral genes prevents the wasp's host's immune system from killing the wasp's injected egg [...]

I'm guessing suppressing the immune system of the host is done by other parasitic species in various ways, but are there any other examples in which a virus is "used" for this purpose?

Not exactly the same, but Toxoplasmosis leading to loss of aversion of mice towards cats is a behavioral suppression: https://www.nature.com/news/parasite-makes-mice-lose-fear-of-cats-permanently-1.13777#/b1

Summarizes more related-but-not-quite-the-same systems: https://academic.oup.com/bioscience/article/49/4/311/228949


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Why some viruses can spread with aerosol droplets, but others some cannot
Why can some viruses spread with droplet like influenza virus, but some can not like HIV?
Is it due to their physical shape or the protein of their wrapper? Is there any formalized logic decide this before test the virus in lab?
Thanks in advance!

Welcome to Biology.SE! Some of which virus? There are 'a lot' of virsuses...

This is a very general question. I popup this idea during read the book <>

I would recommend first looking at some of the wikipedia pages for some viruses and doing some preliminary research to make your question more precise. This is a very broad question and it is hard to answer unless you can narrow it.

Thank you very much for the help. @MaximilianPress I will check the wikipedia later too. Actually I'm a programmer, love to read books. It's hard for me to start without basic virus knowledges. I will try to ask the question more precisely in the next time. :)

The question you are asking, if I have it right, is about what is called the "mode of transmission" of a virus.
I won't get into too much detail but there are many many factors that play a role. The main one here (in the example of HIV vs influenza) is which cells the virus infects. Influenza infects cells of in the mouth, throat and lungs. So when it grows and ruptures these cells the virus will be let out in your throat, mouth and lungs. So the way it spreads to other people is coming out of these areas on saliva and mucus when coughed or sneezed in droplets.
HIV on the other hand infects cells of the immune system, which are mainly found in the bloodstream as well as mucus cells (that line reproductive tracks). Again without going into too much detail (because mucoid layers are also found in the stomach etc) HIV can spread only from the location where the cells are located that it infects. Because it does not generally infect cells in the mouth and throat it will not be able to access these areas. So it spreads from blood or sexual intercourse, as that is where the cells of the immune system that it infects are located.

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Does this means not all the cells of human composed with same chemical surface? If so that is amazing. How could that be? As I superficial knowledge, all the cells of human are mitosis from stem cells. I though all the surface should be the same...

The surfaces of cells have many markers that are different. The DNA will be the same (with exceptions). But the surfaces will be different. For example: Cancer cells that show a different surface will be destroyed by immune cells.

Got it. Thank you!


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Are the alleles that code for the same phenotype all the same exact sequence?
The idea that you can be homozygous for a gene means that there are limited options or alleles , correct ?
My question is, if the mom has the allele b which codes for a blue eye, and the dad has an allele which codes for a blue eye too, are these alleles the exact same ? Do they have the same nucleotide sequence ?
This is probably a basic question but no matter how I phrase it, I can't seem to get an answer off of google.

Most educational texts ignore the nucleotide variations and only look at the gross effect of the gene, and the gene interactions. Like @Cell says, they only care if the gene works or  not. They dont care about the millions of variations that may cause the gene to not work.

No the same phenotypes do not mean the same sequence. For example some phenotypes are associated with alleles that are caused by non-functional gene products (like proteins). But there many ways to alter a gene to produce a non-functional protein.


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Is there any study to find the plant with the absolute minimum light need?
Is there any study to find plants with absolute minimum light need?
Consider a bathroom without windows that you have occasional artificial light (e.g. white LED light).
Another question is there any numeric system assigning a number to each plant representing its minimum and maximum light tolerance?

That's not so difficult, if you look on the north side of densely forested mountains. ferns come to mind.

Some deep sea plants get very little light.

Not all plants even do photosynthesis.  Consider saprophytes, which live on dead plant or animal tissue.  Or an even stranger example, the mycotrophic plants like the snow plant (Sarcodes sanguinea) that is a parasite on a fungus (which in turn seems to be a parasite of conifers): https://botany.org/Parasitic_Plants https://www.fs.fed.us/wildflowers/beauty/mycotrophic/whatarethey.shtml/Sarcodes_sanguinea.php

@jamesqf thanks for your note. can any of them be kept as an in-door plant?

@PHPst: I don't know, though I doubt it, since they need the fungus that parasitizes/commensalizes with conifers.  In the case of the snow plant (the one I'm most familiar with, since it's fairly common hereabouts), the flowering stalks only appear for a couple of months in the spring, right after the snow melts.  The rest of the year there's nothing obvious above the surface.

@com.prehensible I doubt any mountain can be as dark as a room without any windows.

there are parasitic plants that need zero light, so you may need to clarify.

ZZ plants are the most dark tolerant that you can get, if you get 2 you can always swap them out every 6 months if you want. Other than that, a grow light of some kind is advised.

Gardening forum knows more about low light plants, the question exists there as a duplicate. check this bathroom: https://youtu.be/hC3wNrDYzzE?t=385

@John I reckon the host of parasitic plants needs light, so they indirectly need light

@PHPst well yes but by a definition that loose nearly all life on earth requires light. the term you are looking for botanically then is "shade tolerance".this study may help you search. https://www.sciencedirect.com/topics/agricultural-and-biological-sciences/shade-tolerance

Let's at first take a set of SHORT DAY PLANTS which are distinguished from the other plants using the photoperiodism parameters. Taking one plant at a time and performing starch detection test by keeping the plant under sunlight may be the only possible way to determine which plant is the most efficient at producing maximum amount of food when kept under sunlight for a particular time.
If we go deeper into the molecular level, maybe a cross section of the chloroplasts could provide us with the data of number of Photosystem 2 that are present which get activated at 680nm of light and also the number of electron carries like Ubiquinone. Their abundance can determine the quickness of carrying out photosynthesis.
There are even a separate variety of C4 plants that undergo Crassulacean Acid Metabolism also known as CAM plants found in deserts that undergo photosynthesis at night.
Thus such an experiment would require diverse plants with several parameters to keep in mind and is quite difficult.

Also there is no numeric parameter to determine light tolerance but depending on the environment, botanists have averaged the amount of chloroplasts in plant leaves and thus have set a barrier for an optimum amount of light that a plant requires. When plotted graphically it shows an asymptotic graph with a peak point showing the optimum level. Also, over irradiation of leaves to light can cause bleaching of chloroplasts and damage to leaves.


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Is it possible nowadays to artificially create an organism just by inserting organism's DNA into an artificial environment?
Let's say we have a DNA of a bacteria and we want to recreate the bacteria just from this DNA. Is it possible nowadays to get this DNA and insert it into some artificial solution so that from this DNA a bacteria coulb be grown?

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There may be technical issues that make certain genomes easier to transplant than others, but it can and has been done. Craig Venter's lab used such a transplantation technique to discover what minimum set of genes are required for viability in an engineered bacteria.

Actually what I'm really interested about is a possibility to create an organism just from DNA using just just some artificial solution neccesary for organism's growth etc. Or is it always necessary nowadays to transplant this DNA into some living organism?

What is in your artificial solution? Nuclear proteins? TFs? Ribosomes? ATP? Floating balls of lipid bilayers? By the time you build this artificial solution that has what you need to get the necessary biochemistry going, you would effectively have the constituents of a cell, minus your DNA of interest.

Short answer-NO.
Long answer-NO, too. We are far from having the technology to do such feats of engineering no matter what some ill-informed pretenders say. We have the technology to create artificial genomes which could be integrated into real cells and good progress is made on creating artificial chromosomes, e. g. bodies containing the genetic information needed to sustain an organism, but we are far from being able to artificially create one.
And there is also the problem of infinite regress which no one seems to bother about but it's out there. It's essentially the notion of which component comes first in order to jump start a metabolism - whether you first put the genetic apparatus or the metabolism which is required to support it or you jumpstart them both. It's an issue that still hasn't been resolved yet.
So, NO, we aren't capable of creating artificial life yet and we aren't likely to be capable of creating it in the near future. That's the answer to your question.

I'm not denying the correctness of your answer but it would be nice to have some sources to help people put it into context. Thanks.

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Very perceptive answer.

While this answer contains some correct information, you may want to expand into viruses, where it is certainly sometimes possible to create viruses from the genome alone or using plasmid-based systems (done for a bunch of viruses, including adenovirus, influenza, coronavirus, plant viruses, bunyaviruses etc.)

This answer is incorrect, in addition to being poorly written.


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Why does the SARS-CoV2 virus not remain infectious forever? Or does it?
Given that the majority of biologists do not currently consider viruses to be alive, a virus can never die.  It can, however, get destroyed by long exposures to soapy water, alcohol, and apparently certain frequencies of UV light.
Why is an individual SARS-CoV2 virion not infectious forever?  Or is it?

Would it help to think a little differently? Rubber bands (for example) aren’t alive either, but there are several ways they can be destroyed, including physically pulling them apart or just by having them exposed to air enough. Viruses are the same, conceptually.

@Laurel Yes, that does help!  So is it simply that being exposed to air very slowly destroys SARS-CoV2 (so slow, in fact, that it takes many days)?

@RockPaperLizard Probably best to think of it more like something like radioactive decay... Individual viruses may be destroyed immediately, or only after a long time. You're waiting for some sort of chemical reaction to occur that is sufficient to make each individual virion no longer capable of infecting. When people talk about the virus staying on some surface for 72 hours, they have given some % reduction in the concentration that they are waiting for. Almost all of the virions are inactivated well before the 72 hour marker, just not enough to consider them effectively gone.

@BryanKrause Thanks Bryan.  Your comment helps as well.  When you write "may be destroyed immediately", are you referring to environmental reactions, similar to the ones that take longer to destroy an individual virion?

Think of it like "x% of viruses inactivated each minute", starting from a very large number. Depending on what "x" is, it may take a long time to reach something like 0.0000001% of the initial virus concentration where you might say "it's basically all inactive".

@BryanKrause Thanks.  And now all we need to know is how many virions it takes to get someone sick (which will obviously vary quite a bit from person to person).

Very little is known connecting "# culturable viruses on a surface" and "chance to be infected". The associated experiments aren't really ethically supported for the most important viruses - we're left with just best practices (wash hands, clean surfaces that can be cleaned, distance from people) and general safety margins. Additionally, it's going to be probabilistic so any estimate is going to come with error bars that make it not that useful. Best just stick to the general guidelines, this isn't a problem with a closed form solution.

Would it help to think a little differently? Rubber bands (for example) aren’t alive either, but there are several ways they can be destroyed, including physically pulling them apart or just by having them exposed to air enough. Viruses are the same, conceptually.
Soap works in part by dissolving the layer of fat that keeps the virus together. It also ends up surrounding dirt so that it doesn’t stick to your skin and can be washed away with water. (These mechanisms take some time to work so that’s why people are recommended to wash their hands for 20+ seconds.)
As for when a virus is just on a surface, logically we know that how long a virus remains viable depends on both the air and the surface because the science reports different numbers depending on what the humidity is and what the surface is like. One helpful source notes:

Similar molecules appear to interact more strongly with each other than dissimilar ones. Wood, fabric and skin interact fairly strongly with viruses.
Contrast this with steel, porcelain and at least some plastics, such as Teflon. The surface structure also matters. The flatter the surface, the less the virus will “stick” to the surface. Rougher surfaces can actually pull the virus apart.
The surface of fibers or wood, for instance, can form a lot of hydrogen bonds with the virus.
In contrast, steel, porcelain or Teflon do not form much of a hydrogen bond with the virus. So the virus is not strongly bound to those surfaces and is quite stable.

Thanks Laurel.  So if wood, for example, forms a hydrogen bond with the virion, it has the potential to destroy it in the process?  And conversely steel has no such potential since it does not bond with the virion?

Viruses are made of nucleic acid (DNA or RNA), a few proteins and often lipids (like Corona viruses). they are not alive as they cannot reproduce without host cells but they are delicate and when they lose the ability to reproduce with exposure to the host, the virus is just completely dead...
Its possible to maintain viruses possibly forever by preserving them and freezing them. Just like reproducing - they can't live for prolonged time without help... in this case a human lab tech.


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(Soft) Lay Survey of human natural history
I am looking for an introduction to the natural history of humans. I had originally thought Sapiens until I found out it is more a history and archeology book of dubious scientific accuracy. The Sorts of things I am interested in are: Neanderthal interbreeding, human canine bond, comparison of human with other primates.
If this is off topic, I am sorry. There was a similar question already posted some time ago, but the answers seems outdated.

Can you link to the previous question and note the ways in which it did not sufficiently address your question? Was it only because of time? Those are still some broad topics.

A general overview would be accomplished by a text book, however some of what you are asking about is rather in depth concepts I doubt you will find them covered in detail in the same book. the issue with newer science is it takes a while for it to be collected in a single textbook so you may have to search of each topic individually.  this site may at least help get you started with terminology. https://www2.palomar.edu/anthro/hominid/australo_2.htm


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RFLP Pedigree question
A relatively frequent, completely penetrant recessive disease variety of mutations in the gene. The gene has been recently cloned. Analysis of the region flanking the gene reveals that the population has at three (3) RFLP (this is a type of DNA marker; they are not SNPs so have much larger sizes) alleles in this region. The sizes of the RFLP alleles are 7, 10 or 13 kb in length. Shown here are two small pedigrees of families in which affected individuals are shaded in black. The size of the RFLP alleles each individual carries is shown below the pedigree. enter image description here

Question: If the male child from the left pedigree marries the female child from the right pedigree, What is the probability their child will be a carrier?
I said that there isn't enough information to tell since the parents genotypes are unknown.

I said that there isn't enough information to tell since the parents genotypes are unknown.

It seems like you are misreading the diagrams since you say the parent's genotypes are unknown.  All 8 individuals in the two pedigrees have the same information given for each, appearing in the eight columns directly beneath the eight individual's symbols.


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Egg mass on glass
mid-April, East Texas
Can someone ID the egg mass deposited on our window? It's about the size of a fingerprint.

I may have to try again with photo- thanks for forbearance
Eggs are bright green, mass is oval in shape but each is round and linearly arranged. On glass.

Can you get a picture from the other side of the glass?

Mollusc or insect I suspect. Slug or snail  most likely.


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Do plants take in the same amount of CO2 as they release?
There are many claims in the media that trees remove more carbon dioxide form the atmosphere than they release back into the atmosphere. By what chemical pathway can this occur?
The law that matter is neither created nor destroyed surely applies as shown by the chemical pathway in the photosynthesis and respiration process.
6CO2 + 6H2O + sunlight energy.  -----> C6H12O6 + 6O2
C6H12O6 + 6O2.                  -----> 6H2O + ATP (energy) + 6CO2
Thus the SAME amount of 6CO2 taken in is released, in order for the plant to have formation of the ATP usable energy for plant tissue creation, so photosynthesis cannot happen at a  more rapid rate than respiration. If that happened, then yes, more CO2 is removed then released, but that would leave an unbalanced equation.
I am not arguing the story further down the road of tree tissue and carbon sequestration/storage.

The road to hell is paved with chemical equations.

Alan, check if there is some scientific research which proves that coal actually exists and comes from plants.

Doesn't an oak tree have more mass than an acorn?  Where did that mass come from?

You've made one faulty assumption: that the second reaction is occuring at the same rate as the first.  In fact, plants only burn enough glucose to fuel their activities. Much of the formed glucose is converted into storage forms like cellulose and starch.  In fact, the vast majority of a plant's carbon mass comes ultimately from CO2 which has been converted photosynthetically into carbohydrate forms. (Further reading)
Ultimately, when plants die, those carbon molecules are used as food for other species, such as animal and bacteria.  Ultimately, whether in composted plant material or fecal mater, the carbon is deposited on the ground.  So ultimately it is correct that trees & plants are removing CO2 permanently from the atmosphere.  Although some is being released to the atmosphere catabolically, more is re-absorbed for anabolic processes, and ultimately, that CO2 gets deposited on the ground in more complex carbon forms.

The amount of carbon stored in plants can be measured by carbon mass in it's dry weight. Trees are known for carbon sequestration ability, because they're long-lived, improve local microclimate and water retention and provide a habitat for many species. There are many positive consequences of having more trees, but soil is a much more efficient biological vehicle for carbon sequestration (still trees required).


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Why can't we always create a vaccine against a virus when an ELISA test to detect it is possible?
Before precising my question, here are some facts that I presume to be true:

A vaccine works by injecting the antigens of a virus into the body to train the immune system to recognize the virus and to be prepared to fight it if it shows up.
The ELISA test indirectly recognize the presence of a virus into a blood sample by testing the presence of the antigens of the virus and the antibodies that fight against it.
One of the reasons there are still no vaccine against HIV is because this virus has a very high mutation rate.
The ELISA test is used to detect the presence of HIV.

I have the feeling these facts contradict themselves and I would like to know where I am misleading.
Indeed, if we have an ELISA test for HIV, we should be able to create a vaccine because we know the antigens of the virus and we can inject a harmless version of them into our body, right?
Apparently, the answer to this question is no because the HIV virus has a high mutation rate and the antibodies produced thanks to the vaccine won't be able to fight every mutation of the virus (that's the answer that gave me my former biology teacher in high school). But if the HIV has a high mutation rate, how can we be able to produce an ELISA test for it?

I found the question quite interesting and will to provide a concept and a speculation although I could not answer the question to my own satisfaction (edits to this regard are welcome)
Currently (2020), the advanced form of ELISA tests for HIV are designed to simultaneously detect both the HIV P24 antigen (produced by the virus) and anti-HIV igG and igM antibodies (produced by the body in response to the virus). Refs (CDC: What kinds of tests are available, and how do they work?)(HIV Diagnostic Testing: 30 Years of Evolution)
While it is easy to detect known viral antigens like the p24 capsid protein in a diagnostic, it is not straightforward to use the same antigen as a vaccine and expect the host to mount an immune response that neutralizes the viral infection, although attempts have been ongoing. Possible scenarios could be that the binding strength of the antibody to P24 might be good enough for detection, but not enough for immunity or that recognizing and binding to P24 does not inhibit the infection. Coming to the evolution/mutation question, since both the p24 antigen and a few antibodies are being detected, it is unlikely the virus would mutate so as to evade the ELISA for all the targets.
The first point in Charlie's answer might be getting at this but it did not come through clearly.

Yes. What you said was absolute right. It's a complicated question. Here are some key points:

To begin with, it very very important to understand that ELISA is a well-established experimental set-up, it does not make any sense to make strong correlations between ELISA results and human vaccination outcomes. This is applicable to any research: We cannot try to make direct link between lab work and real-world problems.
To answer your question 'But if the HIV has a high mutation rate, how can we be able to produce an ELISA test for it?'. We now know that there is a type of antibodies called broadly-neutralizing antibodies (short name: bnAbs) that can fight against a wide variety of mutated viruses. About 20% of HIV patients have bnAbs, and it would take them months even years to have bnAbs. What we do in ELISA is detecting HIV with bnAbs that we found from HIV-infected individuals. But that does not mean we can induce bnAbs with vaccines easily. So these are two completely different process: ELISA takes bnAbs we found to detect HIV, we have those antibodies made and we use it in experiments. Vaccine try to elicit bnAbs in all patients, we know some of the patients can produce bnABs, most of them don't, scientists are working on why that's the case and how we can tackle that.

I'm not sure to understand your second point. If only 20% of HIV patients have bnAbs and ELISA only detects HIV with bnAbs, the test should produce a lot of false negatives, right?

@Pierre He is saying HIV has a few conserved epitopes, when your antibodies target them you won't develop AIDS, and once sucessfully isolated + hydroma stuffs such antibodies provide a good way to detect HIV-antigens independently of its immune-escape intra-host acquired mutations. What is strange to me is that since the virus stays for a while into the body shouldn't our B-cells pools eventually always find those conserved epitopes ?

@reuns It's very difficult to find epitopes on HIV. One of the main reasons is that the virus is covered in glycan (sugars). And these glycans are produced by infected human cells-that is to say, we the virus is covered in glycan, it looks like us. Our immune system do not want to attack ourselves. Even if B cell find these epitopes, not every antibody is effective. In many cases, antibodies against conserved epitopes are not very effective.


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Growing Mouth Bacteria in a bowl of sugar water
I want to teach my nephew why brushing in necessary and how sugar in mouth reduced by bacteria to acid.
I plan to put sugar mixed water in bowl and take swab from his mouth and dip in bowl, and test ph using Litmus paper to show him that sugar is converted to acid.
Is it possible to grow mouth acid making bacteria in this solution and will it change pH enough to show in litmus paper?

It's really going to depend on the concentration and type of microbiome... and it'll probably be more complicated than just "put bacteria in sugar water"; the concentration of sugar has to be low enough not to dehydrate the bacteria, you'll also need some salts and nitrogen source, again in low enough concentrations.  The simple answer is probably "try and see," because we don't know the exact paramaters.

I like the concept of this demonstration for teaching science!
As rotaredom's comment pointed out, bacteria does not grow in plain water with sugar. Bacteria require a nitrogen source, trace minerals and vitamins to grow in significant numbers.
I have a few recommendations that you can try, but I attached an extensive guide to kitchen microbiology below.

Growing the microbes in diluted milk (~ 1:10 dilution) + salt (a pinch for half glass) with and without added sugar (1 teaspoon for half a glass) might be a good starting point. Add yeast extract if you have some (not bakers yeast, but this is the killed version of that).

Make sure to boil and cool the milk, the container and other ingredients to keep conditions sterile.

Avoid a cotton swab if you can (as the cotton might not be sterile), I would take some milk solution, swirl it in my mouth and spit it back into the same container.

Also have a sterile culture in the experiment, without the oral microbes for comparison and a great teaching point.

Grow the microbes for 2-4 days with an air permeable cap (the air allows faster growing aerobic organisms, the cap ensures dust does not fall in)
Extensive source: Microbiology at Home: A short non-laboratory manual for enthusiasts and bioartists
PS: I'm studying PhD to be a microbiologist


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What causes the localization of myoglobin in turkey to regions of muscle tissue?
I've read that myoglobin localization is responsible for the darker colour of leg muscles in turkeys. Why does this localization occur in terms of any of cell biology, molecular biology, or biochemistry? I'm not looking for bigger picture explanations at the levels of physiology or evolution, although I understand that they'll be connected to this question.

"Localization" is probably the wrong term, but I think I know what you mean... It more has to do with "expression."  While the exact mechanism to my knowledge is not elucidated, it has to do with the type of motor neuron innvervating the fiber.
This has been demonstrated by studies where they cross-inervated; that is, they took the neurons which usually innervate Type I muscle fibers and innervated Type II muscle fibers with them and vice versa.  The Type I fibers took on fast glycolytic properties, whereas the Type II took on the slow oxidative features (such as higher levels of mitochondria and myoglobin that you're talking about).

Source:
Sherwood L, Kell R. Human Physiology, First Canadian Edition. pp. 282-283.

"Localization" refers to describing, predicting, or determining the location where something is or occurs. It can also refer to the fact that something is located in particular places. I am referring to the description of where myoglobin typically occurs in turkey muscle tissue.

I'm mulling your answer over. That's quite interesting.

I think it qualifies as an answer mainly under cell biology. I'm accepting it.

Yeah it's just at least in cell bio when we talk about "localization" of a proteinusually we're talking about where it's moved to; the point of the distinction that I was making was that it's not that the myglobin is produced ubiquitously and then localized in certain cells; it's expressed at higher levels in certain types of muscle tissues.  Just semantics; sorry.

That is semantics, but it is not just semantics. That is jargon within a specific domain. That jargon applies to this context, so I understand your desire to use it here. However, the existence of applicable jargon in a particular domain doesn't invalidate the use of more generic usages. Jargon is a fine tool, but not the only hammer. There's no universally accepted rule for deciding whether to use generic vs domain-specific language, though opinions abound, so I'm sympathic to your clarification.


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Is there a critical size for a bacteria colony forming?
I am a maths student doing a project based on modelling bacteria and phages. In one of my models the bacteria population reaches a population size of ~450 cells.
Would a colony of bacteria this size be at risk of completely dying out if there was an environmental change (e.g. pH or UV)?
Also, is there such a thing as a critical colony size? e.g. if a colony of a certain type of bacteria falls below this critical size then the probability of a colony forming would be very low.

Welcome to the site!  What type of bacteria? How much of a change? What environment are they in currently?  And pH or UV is two questions; it would be best to [edit] down to just one to make the question answerable.  Thanks!

Can you be more specific about what your goals are in your simulation? We would need to know a lot more about the kind of model you're talking about to know what the significance of a particular number of bacterial cells is. "Colonies" of bacteria are generally artificial and arise in the lab because we grow cells in isolation or near-isolation on nutrient plates under controlled conditions. Such cells are growing as fast as they can; it's not like they need a critical mass of cells to survive.


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Why are two-winged animals much more common than four-winged?
In flying vertebrates, almost all have only two wings (with the exception of Microraptor and its close relatives). This makes some sense because you need some way to walk also, and a wing isn't very good as a leg, hence why bats are so bad at walking. Of course, bats do demonstrate that being able to walk well is not necessary to be a successful clade.
As far as insects are concerned this might seem like an odd question, since most insects technically have four wings. But among the four largest insect orders (which together make up a sizeable majority of insects), Coleoptera, Lepidoptera, Diptera, and Hymenoptera, all of them functionally have two wings. In Diptera and Coleoptera, only one pair of wings is used to fly. In Hymenoptera and Lepidoptera the two pairs are attached and don't move indepedently.
So my question is, why is two-winged flight so much more common than four-winged? If two-wingedness is advantageous, why do other insects retain four-winged flight (most notably Odonata)?

Note you are talking about two very distinct conditions
In vertebrates, 4 "wings" only evolves once in vertebrates (in early birds) and only one set function as wings the others "wings" are control surfaces for low speed stability, they generate insignificant amounts of lift. for large animals like vertebrates you can't fit two sets of functional wings on the same animal. Large wings need a lot of space to flap and you would need to make the torso longer to give enough room for a second set of flapping wings, which would add a lot of weight and defeat the benefits.
In Insects four wings is the default, the groups with two wings got them by transforming one set of wings into something else useful. Wing covers in beetles ,which protect wings from damage, and Halteres in flies which act as a sort of sensory organ to determine position. Two wings are more common numerically becasue those two groups are extremely successful. Basically if you have two of something but one will also work and evolution can turn the other set into something useful then you have a chance to lose one set of that thing. Two wings are more common numerically becasue those two groups are extremely successful. By turning four wings into two those groups ended up with more abilities than their four winged relatives, becasue they did not just lose the wings they turned them into something else.
In insects wings actually evolved from gill covers, insects could have had six wings, why the first set never evolved would be an interesting question. It may be due how HOX genes are expressed in insect segments.
Source

Thanks for your answer! It still doesn't explain why hymenoptera and lepidoptera have 'decided' to get rid of independent wing motion; they did not transform a second pair of wings into something else useful. I'm wondering if there's some unifying reason why two wings is better than four? The same thing seems to hold for airplanes, though I suspect that may be a different reason.

Perhaps this is not the right place to ask this question.

It is the perfect place ot ask it you just need to clarify your question. hymenoptera and lepidoptera still have two wings, they beat together becasue the mechanism insects use to flap the wings can generate more force that way, insect wings are not like bird's the muscles do not pull on the wings dirrectly, the mechanism driving their motion is different. There is not one unifying answer, each different mechanism has a different functional answer.

Thanks. It just seems like an odd coincidence that across (most) insects, dinosaurs, and airplanes, there's been an 'experiment with four wings' phase, but the two-winged forms are more successful in the long run.

There is no four wing phase in dinosaurs, there is a two wing and two rudder phase, If you see a picture of microraptor with the lower "wings" horizontal the artist has broken the creatures legs to get them in that position. there is a whole question about this https://biology.stackexchange.com/questions/62502/any-simulations-of-four-winged-dinosaur-flight-microraptors

I don't think there's any real consensus on how microraptor used the leg wings. But you're right it doesn't seem plausible that they were used in a similar way to the front pair. It's pretty unlikely (but not impossible given the distortion of the fossil; it's difficult to make definitive claims about animals that died 100+ million years ago) that it splayed its legs in flight.

@DarkMalthorp it is actually very easy, the hips are not distorted and therapod hips don't allow much lateral movement, becasue they are not a ball and socket joint but more like a rod and socket creating something more like a hinge. You literally have to break the hip joint to splay the legs. the leg feathers however help with stability in low speed flight, the very kind of flight that will be the most unstable in the early evolution of flight. we see different low speed stabilizers in bats and pterosaurs, but their legs are not free to use either.

Let us continue this discussion in chat.

Four winged insect's ancestors were lucky because they had the sky all to themselves for perhaps 50 million years, giving them valuable time to develop more complex wings which can compete with simpler forms of flight. The first terrestrial insects came 380 million years ago, and the first dragonflies are from 300 million years ago. The high oxygen at the time made all forms of flight easier to develop.
They had to go through various stages of inefficiency which are developmentally expensive. Earlier animals could afford to fly clumsily compared to today's ones because there were less areal hunters to catch them on the wing.
Robot flight tests suggest that four-winged flight is generally less efficient than two-winged, so if another four-winged insect developed independent control of the up and down muscles on both sets of wings, it would require 20 or 50 percent more food to travel the same distance for thousands of generations to compete with the two-winged variants, added to the fact of being easier prey.
Dragonflies can also not fold their wings for protection and burrowing and rely on high energy food sources, so they have a limited habitat today compared to most two-winged insects.

This is far from being the complete explanation (which I don't have). But:
From a molecular standpoint, the symmetry between left and right is achieved often by presence / absence of gene expression of certain developmental genes.
In some cases, these genes could be expressed in a gradient, forming gradual transitions of patterns.
A four winged animal would require a dev gene to be expressed on one axis (generating left and right) but also on another, being expressed in two pulses (two sets of wings). This is much more prone to deleterious mutations, since there are more factors weighing in. Hence, it could be evolutionary more disadvantageous.

This makes logical sense to me but if I understand correctly, it would only explain an actual reduction in the number of wings (like diptera), not a re-purposing of one pair (as in coleoptera), or a linking of two pairs to make a functional single set as seen in hymenoptera and lepidoptera. In vertebrates, the four-winged forms didn't have a different number of limbs from normal tetrapods either.

This is not how wing development works, by this logic any organism with more than a single set of limbs is at a major disadvantage. It is also disproven by insects in which four wings is the default both originating from the same developmental pathway.


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Will moth larvae pupate in response to food deprivation
Context: Trying to exterminate a clothes moth infestation.

Supposing you have a room with clothes moths, or rather, with clothes moth eggs and larvae.
Suppose then, that you remove all of the soft furnishings, all of the clothes, all of the carpet, and you thoroughly clean and vaccuum to remove as much dust and hair as possible.
Would one predict that the remaining larvae would then immediately pupate into moths, in response to this food deprivation?
I know that lots of plants will suddenly flower or fruit if they perceive that they are at risk of dying, in order to reproduce before they die. I believe the moths are essentially just a reproductive phase of the moth, so I'd be unsurprised if they did pupate.
On the other hand, I imagine pupation takes a lot of energy and food reserves (not to mention needing material for the cocoon), so I can imagine that they might be unable to do this?
Which way do it go?
Will moth larvae pupate in response to food deprivation

Specific reason for the question is that, a week after we pulled up the carpets, we've started seeing more and more moths in those rooms. Trying to work out if this is "expected" or not :(

Not officially an expert, but I have been watching clothes moths for years and haven't noticed any small ones, so dont expect early pupation. I would expect small pupae to give small moths (like with houseflies). I do see the hormone traps reduce population, but only with lots of them (2 per small room).


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Why is it that evolution of organisms had oxygen as their life-supporting gas?
On Earth, gaseous N2 is abundant. However, life began by dealing with O2 and CO2.
What can be considered the major reason for life developing in such manner?

Ambient temperature range, oxygen & water at the same time?

Have you ever tried to do chemistry with gaseous nitrogen?

Life did NOT begin with “dealing” with oxygen. It was anaerobic before the great oxygenation. And if you expressed a chemical question in chemical terms instead of using words like “dealing with” you would be nearer to considering for yourself the chemistry and thermodynamics involved.

$\ce{N2}$ may be abundant, but in the environmental conditions typical of Earth today, and back when life appeared, $\ce{N2}$ is nearly inert. That is, $\ce{N2}$ generally doesn't participate in chemical reactions except at higher temperatures or with special catalysts. $\ce{O2}$ on the other hand can participate in many chemical reactions at temperatures and pressures typical for Earth. At a more fundamental level, the reason for the inertness of $\ce{N2}$ is that the electron affinity of $\mathrm{N}$ is much less than the electron affinity of $\mathrm{O}$.
Think of it this way: Q: why don't we build cars out of tissue paper? A: Because the material properties of tissue paper are a poor match to the material requirements of cars.

Why not use $\ce{O2}$? It's used widely at Chemistry SE.

@RodrigodeAzevedo thanks for the suggestion. I've edited the question to fix that.

I was just wondering whether there is a particular reason to use \mathrm instead of \ce if both are supported.

\mathrm is a generic tag for turning off italicization  of symbols. \ce is a tag specifically created for annotating chemical formula, so the choice of tag helps convey the semantics of the the formatting.

Amusingly, I did not even know that \ce worked outside Chemistry SE until 10 minutes ago.

@Rodrigo de Azevedo: And those of us who don't regularly do chemistry wouldn't even know that :-)

@RodrigodeAzevedo   Better to use HTML  tag as it doesn’t change the typeface. Especially as the question shows no consideration of chemical energetics. Why waste time with it anyway?

@David, you seem to have a rather idiosyncratic model of posting style. I've had my posts edited on other exchanges for not using the appropriate MathJax for chemical symbols. As far as I know there is no preferred style guide for this exchange, so users are free to use MathJax or not as their personal preference dictates.

The method used to achieve a certain typographic effect should be unimportant if the result is the same with different techniques.  In the case of subscripts and superscripts the methods available yield different results — HTML maintains the sans serif typeface and size, MathJax results in serif typeface that is different in size. My recommendation is not “personal preference” but standard biochemical usage as found in e.g. J. Biol. Chem. and Biochem. J. The rationale is that there is no need to make such expressions stand out from the text — they are not mathematical displays.


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Is there any free software similar to CellDesigner that allows me to represent large networks of biochemical reactions in the human body?
I continually have to review multiple articles, in multiple journals. These articles present how various enzymes, proteins, lipids, carbohydrates, etc. intervene in the processes that lead to certain pathologies (generally neurodegenerative). I have used Celldesigner and Freeplane, but Freeplane is very general software and CellDesigner provides reduced work spaces. I would like to know if there is any other free software that works for this purpose (I usually work in Linux).

Here is a list of such programs. It is an old post but most of the tools it lists appear to still be functional. I found this by just googling "celldesigner alternatives", which is always a good idea to search first for these things.
I have used cytoscape and it is ok, maybe too general also for your purposes. For very simple purposes I have used KEGG pathway in the past, which is in addition to the others.