text:
How does a Coronavirus "test kit" work?
A number of countries are using test kits for detecting new cases of nCoV (2019-Coronavirus) and apparently China is running low.
What exactly is in a nCoV "Test Kit" — How does it work?
(Surely they also differ, so in which way do they differ?)

The CDC has made available online its nCoV test kit. Briefly,the kit contains primers and probes for real-time reverse-transcriptase PCR, as well as instructions for appropriate use and (critically) controls and guidelines to avoid false positives and negatives. Kits from different countries may use slightly different primers and probes, though since they are all working from the same sequences and the same principles they should be broadly quite similar.
Explaining how quantitative PCR works and the details of the primers and probes is out of the scope of this SE. A layman's introduction was written by John Timmer at Ars Technica.

According to instructions, the testable specimen include: Respiratory (nasopharyngea, loropharyngeal, broncheoalveolar, tracheal, sputum) and (blood) serum. Can it also be used on urine/fecal  specimen?

Can it also be used on urine/fecal specimen? On the one hand, if you use the kit outside its guidelines, the accuracy, sensitivity, specificity, etc will not be defined. That said, in general conditions for qPCR on most clinical specimens are well understood, and specialists will probably be able to predict conditions that are compatible with the primers. So the answer is probably, It's not recommended for routine lab testing, but specialists with a solid technical understanding will undoubtedly be able to adapt it.

For others like myself who don't know: PCR - Polymerase chain reaction, a technique used to amplify, or make many copies of, a specific target region of DNA.

I don't think you'd expect to find much trace of a respiratory virus in stool or urine.

There are reports that it’s been found in feces, raising the possibility of fecal/oral spread. Unlikely, perhaps, but dismissing it based on weak theoretical grounds seems unwise.

Yes, it an live a long time in stool and urine, please see the links in my nCov Environement question.

SARS was found in stool samples and is thought to be airborne from defecating in a squat position. This may have been an important route of transmission during the SARS outbreak.

"is thought to be" - By whom? Random internet people, or peer-reviewed articles? Frankly this claim looks like racist and ill-informed speculation, and there is far too much of that already on the internet; the last thing SE needs is more of it.

@iayork As little as we all like it, we're operating in a very challenged time at the moment. Many questions and comments are directly taken from non-peer-reviewed research or cutting edge information, research and private communication forums. I'm sure speculation will be dealt with better in a few months as research and pandemic fallout will become more clear.

@not2qubit I'm pretty sure iayork and Matthew Martin were talking about the old SARS outbreak, not the COVID-19 outbreak

There are actually 3+ types of test kits widely used to diagnose diseases caused by viruses. We can check for the nucleic acid of the virus, the antigen of the virus that would cause an immune response or the antibody produced during the immune response of the patient. Since we've already got the whole sequence of the nCoV, the test kits normally used this time (at least in China) fall into the nucleic acid class.
To diagnose a patient with this type of test kit, the patient's nasopharyngeal swab, sputum or alveolar lavage fluid would firstly be collected to get a sample of the virus. Some reagents would then be used to extract the nucleic acid in it. After a reverse-transcription which would produce a DNA sequence based on the original single-stranded RNA gene of the virus, a PCR would be performed to amplify it to a large enough amount to eliminate the interference of other genetic materials in the sample (e.g. human DNA, genes of some normally existing bacteria and/or viruses). Here is where the nucleic acid detection kit would take place: the kit contains several characteristic genes serving as a guideline of the PCR, and it would have two primers that flank the target regions for each gene. The kit would also check if the amplification process goes well: it contains fluorescence molecules whose intensity would increase exponentially with the number of amplification (if target fragment exists in the original sample).
The whole set of the testing process is called qPCR (quantitative polymerase chain reaction, or real-time polymerase chain reaction) and it requires highly precise thermal control and real-time fluorescence measurement. The labs where those qPCR instruments are in also need to be high-standard cleanrooms with negative air pressure in order to ensure that samples would not be contaminated by previously amplified DNA products. Unfortunately, most hospital labs in China are not qualified enough to perform tests of this level and that's why it takes so long to truly diagnose a patient with nCoV, even if tons of test kits are already sent to the infected area.
Recently a new method called POCT rapid detection is being tested and it is said that it takes only 15 min to get the result. This method takes a colloidal gold-based immunochromatographic assay to detect the nCoV antibody produced by the patient. Going through the strip, the material tested would pass through a layer of the colloidal gold marker that binds to the antibody, a detection line that contains the corresponding antigen, and a control line that would change colour once it detects any liquid that contains the colloidal gold. This method feels kind of like a pregnancy test, where two lines are bad (i.e. antibodies is detected in the sample as they bind with antigens) and one line is good. It's much faster than the nucleic acid test and it's easier to apply, but the problem is that you can get false positives or false negatives due to the different amounts of antibodies produced by patients. It can be used as a supplementary method for nucleic acid detection, but for clinical use we may want to be more careful with it.
Hope this answers your questions!

Excellent addition to accepted answer! Welcome to Biology SE!

Can you provide a link describing the POCT method, because it's an ungooglable  general term for Point of Care Test, which I don't think is what you intended.

@not2qubit - not quite excellent, as it is not sourced in any way.

@AliceD I know what you mean, but I think we need to give people a little bit of slack for having to source something that have just very recently become available and possibly not even official or marketed yet. (Also some test kits have already been shown to be very poor with only 60% accuracy etc.)

Apparently they are called Point of Care Test as found in this very nice summary:
Recent advances in the detection of respiratory virus infection in humans.

@AliceD My bad, it's my very first answer on bio SE and I didn't quite know how things work here. Thanks for pointing that out!

There are several proposed tests for 2019-2020 novel coronavirus responsible for the Wuhan outbreak. The main techniques these are based on are:

PCR or qPCR targeted amplification

CRISPR-Cas9 genome editing

PCR-based tests are the current standard for diagnosis of viral infections (as these are faster than protein staining and can be made widely available as a kit). Most tests in use are based on PCR targeting sequences unique to novel coronavirus from the publicly release viral genome sequence. These protocols are recommended by the CDC and kits are commercially available or in development from Novacyt SA, or Liferiver Bio-Tech, or Altona Diagnostics. Before kits were available, various companies such as GeneSig offered primer design or primers specific to 2019-nCov which can be performed with standard PCR or qPCR kits. Bio-Rad has been cleared by the FDA to provide a test using Droplet Digital PCR (ddPCR).
PCR-based tests have the advantage that anyone with experience with standard molecular biology techniques or clinical testing can perform them, they do not need specific expertise in microscopy or pathology. Controls are important but there are still issues with low specificity with these kind of tests. For example, PCR tests for influenza type A (a similar virus) have high relatively false-positive rate for a clinical test. Considering the prevalence of the disease, these should only be used to triage people showing symptoms for further diagnosis. Results should be interpreted carefully. It is difficult to design specific PCR-based tests for viruses as they can mutate quickly (as 2019-nCov has been shown to do), especially in emerging epidemic. Note that as an RNA virus "reverse transcription" is required before PCR can be performed. These tests take several hours and it can take days to get results if a lab has many samples to process.
A proposed alternative is tests based on CRISPR. Several startups are working on this including Mammoth Biosciences in San Francisco and Sherlock Biosciences in Cambridge, Massachusetts. However, further testing is required to demonstrate the performance of these tests and none have been FDA approved yet. The advantages of this approach is that the test could be performed faster during an outbreak or epidemic. This is an emerging technology that has not been thoroughly tested.
Updates
Recently, another testing technique has been announced (in English and Japanese) by Drs Hayashizaki and Usui at the RIKEN institute. This proposed testing technique uses the Smart-Amp2 technology which has been commercially released. This technique is based on cycles of amplification similar to PCR but has the advantages of being more cost effective and able to perform the test as fast as 30 minutes.
We should also bear in mind that these tests are all subject to false positive and false negative results. Many current media reports do not acknowledge this limitation. Any reports based on a single case deserve skepticism due to the inaccurate nature of some of these tests. For example, the State of New York was not using the CDC recommended test in February 2020 due to problems that they’ve identified with it.
Research is ongoing to ensure accuracy. In January 2021, the H.U. Group Research institute reported concerns with detecting mutant variants using the Japan National Institute of Infectious Diseases (NIID) primers and adopted the USA CDC recommendations at the time.
Disclaimer: while I was affiliated with RIKEN when SmartAmp2 was published and have since joined the H.U. Group Research Institute, I was not involved in the development of either technology.
Note: at the time of writing, antigen and antibody tests were not yet available.

https://www.synthego.com/blog/sherlock-crispr-diagnostics#Unlocked suggests that crispr-cas13 (not cas9) is just replacing the fluorescent probe. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5961727/ says the theoretical advantage is that a cas9 based probe needs much smaller concentrations

Less PCR cycles required? Running many cycles can take hours. Of course sample preparation and the RT step will take time as well. I’m not sure but this is the benefit claimed by the companies proposing CRISPR-based tests. I doubt it’s cheaper.

For nCov the sequence amplified by WHO' primers is 100 nucleotides long, they recommand 45 cycles of 45s. Now maybe for more common viruses they need longer sequences ?


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Question on kilobase - packaging of genomic material in viruses
I have been looking up some information of SARS. Wikipedia says it is 29.7kb in length while 1kb is around 300nm. However, the microscope image on wiki shows the virus size <100nm. It doesn't make sense mathematically so that think I missed some knowledge. I hope this question qualifies to be posted on stackexchange. Thanks in advance.

This value is only true for linear DNA. However, DNA in cells is not linear, it is folded, which makes it ways more compact (otherwise the DNA in our own cells would be around 2 meters long).
See the figure from reference 1 for a schematic view how this works in higher cells:

The table below (from reference 2, either klick on the picture or the link below for a bigger version) shows how the length of a piece of DNA is influenced by packaging:

There is another caveat in this question, Corona viruses (as the SARS virus) are singlestranded RNA viruses. The RNA of viruses contains packaging signal sequences, where special proteins bind, before the virus is assembled around the bound genetic information. See reference 3 for a general overview and reference 4 for the packaging of the SARS virus in special.

DNA Packaging: Nucleosomes and Chromatin
DNA, chromatin and genome numbers
Genome packaging in viruses.
Assembly of severe acute respiratory syndrome coronavirus RNA
packaging signal into virus-like particles is nucleocapsid
dependent.

source: Stack Exchange

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

sort: votes


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Immunity to one's own microbiome
It seems that a human bite can be very dangerous, because of the myriads of bacterial species found in saliva.  This leads to several questions that, perhaps, may have the same single answer.  But, I'll boil it down to a single question per the comment.
Is there a mechanism by which the body "tames" their own oral bacteria that could otherwise be dangerous pathogens, so that the bacteria don't cause pathology but also don't arouse a typical immune response or inflammation?
No doubt this question has been explored often, but I haven't been able to find a clear answer.

This is a good questions, but it is difficult to answer in brief.  To point toward an answer, consider that many members of the oral microbiome are considered pathobionts, meaning that they are symbiotic in their native niche but pathogenic in other contexts.

Upon reading the article to which you provided a link, it seems that the interactions between different species in the oral bacterial community may be important for keeping potentially pathogenic members of that community in check -- but the article doesn't indicate how that occurs.  I know for example that bacteria can modify the pH of a medium and thereby control bacteria or yeasts that require a specific range of pH.  But in a complex community like the mouth, a change that inhibits some pathogens might well benefit other pathogens.  Are there lots of independent factors analogous to pH?

Please limit yourself to one question per post. Take a close look at your linked reference to see if it answers any of the questions for you. That might help you narrow things down.

One way to identify mechanisms by which the body tames the microbes in the mouth is to observe what happens when those mechanisms are impaired:

Deviation from symbiosis among the bacterial community
  leads to “dysbiosis”, a state of community disturbance. Dysbiosis
  occurs due to many confounding factors that predispose a shift in the
  composition and relative abundance of microbial communities.
  (Dentistry Journal)

1) Immunity
Normal innate, cellular and humoral immunity helps to prevent oral flora from causing infections.
a) When the immunity is impaired due to a disease (HIV/AIDS, cancer...) or long-term treatment with antibiotics, steroids, immunosuppressants or chemotherapeutics, a part of normal flora, such as the yeast Candida, can overgrow and cause oral thrush.

Host defense against infections with Candida spp. depends on rapid
  activation of an acute inflammatory response by innate immunity,
  followed by an incremental stimulation of specific immune responses
  mediated by T-cells (cellular immunity) or B-cells (humoral immunity). (Immunology of oral candidiasis, J Pharm Bioallied Sci.)

Picture 1: Oral candidiasis (source: Wikipedia, creative commons license)
b) Impaired immunity can result in osteomyelitis of the mandible, caused, for example, by the Actinomyces bacteria:

Systemic factors such as diabetes mellitus, agranulocytosis, leukemia,
  severe anemia, malnutrition, or alcohol abuse affect immune
  surveillance and lead to impairing the osteomyelitis
Actinomycotic druses and filaments were detected from the sequestrum
  of the fracture site (Rapidly Progressing Osteomyelitis of the
  Mandible, Case Reports in Dentistry)

2) Saliva
Saliva helps to prevent mouth infections by flushing microbes into the gut and by the antimicrobial substances.

Among such protective factors, the flushing effect of saliva flow is
  the most important one...(Antimicrobial function of human
  saliva--how important is it for oral health?, Acta Odontol
  Scand.)
Importantly, saliva is crucial for defense against microbial species,
  as it is rich in antimicrobial compounds such as hydrogen peroxide,
  lactoferrin, and lysozymes...disruptions in saliva secretion increase the frequency of oral
  conditions such as oral candidiasis, gum disease, and tooth decay
  (caries), as well as respiratory tract infections (The power of
  saliva: Antimicrobial and beyond, PLoS)

Impaired saliva excretion due to a disease (salivary stones, Sjögren's syndrome, untreated diabetes, radiation injury) or drugs (antihypertensives, antidepressants, tranquilizers, diuretics, antihistamines...) can result in dry mouth (xerostomia), which increases the risk of oral thrush and other mouth infections.
3) Lack of substrate for microbial overgrowth
Clean healthy mouth does not contain enough food for microbial overgrowth.
On the other hand, in untreated diabetes mellitus, the abundance of glucose in the saliva promotes the overgrowth of the yeast Candida (oral thrush):

A dry mouth coupled with a higher amount of glucose in the saliva can
  also make for favourable conditions for thrush.
  (Diabetes.co.uk)

Mouth full of food debris due to poor hygiene can promote bacterial overgrowth:

Periodontitis is caused by certain bacteria (known as periodontal
  bacteria) and by the local inflammation triggered by those bacteria.
  Although these periodontal bacteria are naturally present in the
  mouth, they are only harmful when the conditions are right for them to
  increase dramatically in numbers. This happens when a layer of
  bacteria and food debris, known as plaque, builds up and is left
  undisturbed on the teeth...(What is periodontitis, European
  Federation of Periodontology)

The bacteria from normal oral flora often involved in periodontitis: Porphyromonas and Streptococcus (Lumenlearning.com).
4) pH
The normal pH in the mouth is 6.2-7.6 (Journal of Indian Society of Periodontology). When it falls under certain value known as critical pH (~5.5), acids derived from bacterial fermentation of dietary sugars start to dissolve tooth enamel and cause caries. The bacterium Streptococcus mutans is a part of normal oral flora, but is commonly involved in caries (Lumenlearning.com).
5) Low susceptibility of mouth mucosa for certain microbial toxins
Certain microbes, such as Staphyloccocus aureus, which are a part of normal mouth flora do not likely cause infections in the mouth, even when they appear in the mouth in much greater amounts, for example, in food poisoning and even if these microbes can cause severe diarrhea (Centers of Disease Control and Prevention). This is because the mouth mucosa is not susceptible for the toxins secreted by these bacteria, while the stomach or intestinal mucosa is.

This answer is definitely useful, but not quite satisfying.  #1(a) indicates that the immune system is active in manipulating the ratios of oral flora without necessarily eliminating any particular species.  #2 points out that saliva flow constrains the ratios according to the relative abilities of species to find safe niches to avoid being washed out.  #3 indicates that the ratios of different available nutrients affect the growth ratios of different species that depend on specific nutrients.  #4 mentions pH, which can be considered analogous to temperature and will affect species ratios

@S.McGrew What did you expect? There are surely more mechanisms and more specifics, but I don't think I need to cover just about everything. My intention was to show there are certain mechanisms that allow the oral flora to exist without being harmful.

according to species' preferred pH range.  #5 points out that different bacterial species have different inherent ability to break down specific tissues in the body.   All of this supports the idea that oral flora form an ecosystem in which the various member species regulate each others' growth via the usual competition, cooperation, and other such interactions, and that the body "simply" imposes constraints that tend to shape the overall microbial ecosystem.

I would like a better understanding of how and why those constraints work, and how the microflora interact, and what the modes and conditions of stability are.  Links to research on that topic would be welcome!

I personally find it impossible to say why something works when it works normally. Because it just works. For me, the only way to say how it works is to observe mechanism when they are disrupted and conclude from that how they normally work. To go into more specifics, I would need to know what goal, beyond just knowing some facts, are you trying to reach. There were interesting sub-questions in your original question, but that appeared to be broad. You may want to open some of those as separate questions.

re "What did you expect?", I think what I'm looking for is specific mechanisms by which the body regulates a whole community of hundreds of species of microbes.  Or, specific mechanisms by which the body manages to get along with a given pathogen without mounting an immune response to it.  I'm an engineer, not a biologist, and want to know how things work at a fundamental level.  Can't quite bring myself to be satisfied with "it just works" - though I understand that some things (especially in biology) are far from being figured out yet to the level I'm hoping for.

@S.McGrew, "taming" oral microbiome by lack of food for microbes, immune response (cellular and humoral) and antimicrobial agents in saliva are specific mechanisms. I believe that making a more specific answer makes sense when the question is also more specific, in which case we all know what actual goal we are solving.

It's an interesting question.
More interestingly there are a number of articles and a lot of studies are going on to prove that by manipulating oral microbiota, Caries or Periodontal diseases can be prevented.
At this I want to point out as the OP has asked about the body's way of 'taming' the flora, I will share the references of the studies in which the oral flora was manipulated not by body's own mechanism but externally. And this resulted in prevention of oral diseases commonly seen.
This answer is an add on knowledge which I will share, I know not the exact answer since how the oral cavity by itself provides immunity has been satisfactorily answered by @Jan.

Probiotic
therapy or -
bacteriotherapy’ (Rajendhran and Gunasek-
aran, 2010) has the potential to naturally cure and
prevent disease at its early stages by incorporating
beneficial bacteria that can reestablish an ecological
balance or enhance the biodiversity of a microflora. For
example, research showed that individuals with high
amounts of Capnocytophaga ochracea had lower
amounts of P. gingivalis and displayed no periodontal
disease progression. Individuals with low C. ochracea
did exhibit disease progression. In probiotic treatment, a
patient found to have elevated levels of P. gingivalis
could be given C. ochracea probiotics to reestablish a
healthy equilibrium before any periodontal disease
generates.

Here is the article

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


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Does melanin protect against nuclear radiation?
It is known that melanin protects against UV radiation.
But say a nuclear bomb dropped somewhere would more people of dark complexion survive the radiation burns because the melanin would protect them?
Or as another example, suppose there was a meltdown and someone had to swim into the reactor to pull out the core, would it be best to send the light skinned or dark skinned person to ensure maximum chance of survival? All other things being equal.

The absorption of gamma and x-ray radiation by skin is negligible, so the amount of melanin present is irrelevant. Stopping high energy photons requires a lot of mass, not a few microns of melanin.
Edit:
I think a citation that x-rays and gamma rays go through skin is unnecessary (they'd be useless for imaging bones otherwise), but NIST has tabulated values for different tissues as a function of photon energy if anyone wants to double check:
https://physics.nist.gov/PhysRefData/XrayMassCoef/ComTab/tissue.html
As expected, x-rays have absorption path lengths on the order of centimeters to meters in soft tissues, which is why you can use them to image through skin.

interesting. There was an article about a mould that was inside a nuclear reactor, and they said it survived because it had high levels of melanin

@zooby Were you thinking of this? https://en.m.wikipedia.org/wiki/Radiotrophic_fungus

@LifeInTheTrees What is wrong? It seems like you agree with my point that high energy radiation penetrates deep into skin due to low absorption.

Yes sorry I misread the first statement, i'll delete it, i upvoted previously. There is a difference caused by melanin at least for beta radiation.

Maybe not much of an immediate advantage, but evolutionarily, I mean...according to the article below, the melanin in frogs with darker skin was enough to sway natural selection and drastically reduce the population of green frogs while the population of black frogs flourished
https://www.livescience.com/black-frogs-evolution-chernobyl?utm_source=facebook&utm_medium=news_tab

An answer should stand of it own and not consist of a link. References are for for further reading. Please edit your answer accordingly.

Ken Mac is correct, melanin has an effect and you should also consider fatty people to be the heroes of your scenario.
Melanin can cause more surface burns compared to a person with light skin and good fat coverage.
Here's a study that states that black people complain of skin problems more often during radiation chemotherapy.
also this research:
Human and animal heterogeneity in terms of skin tissue distribution and impact on radiation dose distribution:
In humans, subcutaneous skin thickness and body fat vary as a function of age, sex and ethnicity. Fat tissue thickness can lead to wound variability, especially in the case of beta radiation, and the presence of MSCs in the adipose tissue could alter the response. Therefore, care must be used in selecting a model that minimizes these variables.
In pig and mouse models, there can be different healing rates based on what part of the skin is irradiated. For example, in the pig, thicker dorsal skin heals differently than the thinner ventral skin. Mice also have similar skin location differences, in that radiation-induced damage can be very different in that of leg skin compared with that of ear skin.
Proximity of the radiation exposure to bone can play a role in the extent of damage.
Effect of skin melanization in view of possible differential radiation responses due to higher levels of melanin, as well as challenges involved in scoring erythema in pigmented skin:
Concerning the use of a pig such as the Duroc, which is more heavily melanized, differential sensitivity to high-energy radiation may be observed due to the presence of melanin.
The physics forum would know, the radiation types are so variable. Older style atomic bombs had flash burn from the explosion and the fallout from the sky aftewards, i.e. in bomb tests near the Marshall islands.
Marshall islands research.


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If a gene is missing from an operon that structures a protein, then would that protein not be made properly?
From my understanding, operon is a series of genes that are regulated by a single promotor. In many cases genes in an operon form subunits of a protein.
I obtained a genome in my study and looked for genes that constitutes part of a metabolic pathway, and ended up finding that one of the genes in an operon was missing.
Does that imply the protein made from those genes in the operon will not be made properly or other genes will compensate for the loss?

From my understanding, operon is a series of genes that are regulated by a single promotor. In many cases genes in an operon form subunits of a protein.

Genes in an operon can code for protein subunits, but they can also code for separate proteins. Often an operon will have a few genes responsible for one core function, with other accessory genes that may help regulate or enhance that function is some way. Sometime genes are fused, combining multiple subunits into a single gene. In other cases, subunits can have related functions in the absence of other units.
For example, The ArsAB complex uses ATP to pump arsenic from bacterial cells, conferring resistance. But many bacterial Ars operons lack the arsA gene. Minus this subunit, the ArsB transporter still functions to efflux arsenic from the cell, just less efficiently, harnessing the proton motive force instead of burning ATP.

... ended up finding that one of the genes in an operon was missing.
Does that imply the protein made from those genes in the operon will not be made properly or other genes will compensate for the loss?

If the gene is truly missing, it's can't be transcribed, and the subsequent protein can't be made, but the remaining genes will probably still work. I would start by asking what the operon's function is, and then consider whether the missing gene is essential for that function (hint: If it's missing and the rest of the operon is still there, it's probably not essential). If it is essential, then consider whether it's truly missing. Are there other open reading frames in the operon that could encode something with similar function? Could the organism have multiple copies of the same operon (possibly found on a plasmid)?


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identifying OTU interactions / hubs
I would like to know how can i run a network analysis for identifying major OTUs hubs. I wish to build a network of co-occurring OTUs found in different soils samples.
I've started going through the VEGAN R package but i'm not sure it's what i'm looking for.
any recommendations network analysis packages ?
thank you!

Can you better define "major OTU hubs"?  Are you attempting to build a network of co-occurring OTUs and observe groupings?  Please revise your question.

can you tell us what your starting data look like? raw reads? count tables?

I am going to assume you have a count table that you are starting with. Every tool you decide to use is going to have its own respective instructions so let me get you pointed in a direction to find one that works for you.
I wrote a simple R package for my lab awhile back but there are much better ways to put together Co-occurrence networks (in no particular order):

SparCC
CoNet
MENA
Spiec-Easi
MDiNE

Now speaking specifically about "hubs", "connectors", and other keystone organisms, I would recommend reading more about what they are and how they were developed. Again, I have a brief summary here but the original "hub" came from a paper on bee pollination networks


text:
Can virus survive dessication (and come back functional after rewetting)?
I am thinking of ideas for disinfection that can be done by the average person. So, this is one question I have: Can a material/surface be effectively disinfected (I am more interested in virus) by drying using low/medium heat + wind (or any other less thermally-intensive means)? Would the virus be only temporarily inactivated and is able to come back functional?

Viruses that are protected by a protein shell (non-enveloped) like adenoviruses, rotaviruses, and hepatitis A virus can survive dessication for a while. This paper showed adenovirus remained clinically infectious after 28 days on smooth surfaces, and this paper found around 1% of human rotavirus and hepatitis A virus survived after 60 days.
Other viruses might survive dessication even longer, these are just the ones I looked into.
Regarding rewetting, any test for virus survival will re-wet the virus.

No exactly related to surfaces, but in terms of killing viruses via heat, a study from a few years ago looked at the time required for inactivation of various Alphaviruses in blood serum samples at 56°C, finding that it could take anywhere from 20 min to 2 hrs [1]
If you're looking for ways that the average person can disinfect surfaces, some fairly common consumer disinfectants are actually already capable of killing certain types of viruses (e.g. Dettol claim that some of their products kill influenza, coronavirus, RSV, etc. [2])
[1] Park, S.L., Huang, Y.-J.S., Hsu, W.-W., Hettenbach, S.M., Higgs, S., and Vanlandingham, D.L. (2016). Virus-specific thermostability and heat inactivation profiles of alphaviruses. Journal of Virological Methods 234, 152–155. https://doi.org/10.1016/j.jviromet.2016.04.004
[2] https://www.dettol.com.ng/products-old/see-all-products/


text:
How much does one stem cell cost?
I am interested in scaled price on 1 stem cell, only for educational purposes. I couldn't find any information about pure price on stem cell, only whole procedure price. So if anyone know, I'll be very appreciated.

I'll hazard a rather educated guess that nobody on the planet sells single stem cells. The problem is that single cells usually do not do well on their own and normally you order them in bulk or isolate a population yourself; there will be loss in each cell recovery step in your procedure, and one is hardly enough for any step, ever. Maybe a (fertilized) zygote... and those rapidly develop out of the one-cell stage and cannot really be easily stored. I'm sure some may exist, but are probably not commercially sold. On this basis I hope you understand that the question should rather be closed.

I'm voting to close this question as off-topic because it is not about Biology in terms of SE Biology.

@David So, where can I ask it?


text:
Will all bacteria become resistant against all antibiotics in the long term?
(I asked the same at medicalsciences beta, but I expect a quite different perspective on it here)
This is about bacteria that can infect humans, and their multi-resistance.
The evolution of bacteria to be resistant against antibiotics is certainly a trait that is helpful for the bacteria, and there is not much evolutionary pressure to loose it.
We will always hope that the next best antibiotic will help against a given infection, giving the bacteria a chance to get immune against the next as soon as we lost the battle for the previous one.
Does that deterministically add up to all bacteria being resistent against all antibiotics in some point in time?
Or is there reason to assume that we can find new antibiotics fast enough to outrun bacteria evolution? I assume it's not, because evolution will not stop, and there is a finite number of antibiotics, I would expect.
(Or is there reason to believe that we become extinct before all bacteria become resistant, so we do not need to worry about bacteria?)

The problem about finding new antibiotics is primarily cost not time. Namely, a new antibiotic will not generate much revenue as it is a reserve drug, so is mostly reserved to academic endeavors. Also, resistance comes at a cost. E. coli resistant to streptomycin is adapted to it and grows poorly without it (dependent). So a bug resistant to dozens upon dozens of drugs will be less fit. Also, for some topical compounds resistance is highly improbable (chlorhexidine (stuff in corsodyl), iodine etc.)

@MatteoFerla That looks like a pretty solid answer!

Regarding the close vote as opinion based: I do not think it is, the answer in the comment above is evidence for it. (That answer may be controversial, but it is about facts, not opinions.)

and there is not much evolutionary pressure to loose it

The energetic cost of replicating antibiotic resistance genes in the absence of antibiotic selection is not trivial, and varies depending on the environment and genetic background of the strain.1  Beyond simple metabolic costs, there is some recent research that suggests that carriage of resistance genes in the absence of antibiotic selection leads to more frequent DNA breaks, adding a mutational burden to resistant strains.2
It may also be the case that expression of a resistance gene by one cell affords a protective phenotype to neighboring cells.  Consider β-lactams, the most common class of antibiotics.  Resistance to β-lactams is often achieved by secretion of β-lactamases, so genetic heterogeneity of a bacterial population can be maintained with respect to β-lactamase gene carriage as long as the cells with the gene are producing sufficient enzyme to protect their susceptible neighbors.

Or is there reason to assume that we can find new antibiotics fast enough to outrun bacteria evolution? I assume it's not, because evolution will not stop, and there is a finite number of antibiotics, I would expect.

Then why not use evolution to our advantage?  Phage therapy is a field that has been around for decades, but there has been a resurgence of interest as the frequency of infections by multidrug-resistant pathogens increases.  Because phages parasitize bacteria, the effective sequence space for phage evolution is as large as the sequence space for bacterial evolution, and equally fast.  Phage therapy has been highlighted recently for its ability to eliminate infections that are recalcitrant to antibiotic treatment.3  Interestingly, phage selection can be used in conjunction with antibiotic treatment to re-sensitize resistant bacteria to antibiotics.4

Durão P, Balbontín R, Gordo I. Evolutionary Mechanisms Shaping the Maintenance of Antibiotic Resistance. Trends Microbiol. 2018 Aug;26(8):677-691.
Balbontín R, Frazão N, Gordo I. DNA breaks-mediated cost reveals RNase HI as a new target for selectively eliminating antibiotic resistance. bioRxiv. 2020.
Dedrick RM, Guerrero-Bustamante CA, Garlena RA, Russell DA, Ford K, Harris K, Gilmour KC, Soothill J, Jacobs-Sera D, Schooley RT, Hatfull GF, Spencer H. Engineered bacteriophages for treatment of a patient with a disseminated drug-resistant Mycobacterium abscessus. Nat Med. 2019 May;25(5):730-733.
Chan BK, Sistrom M, Wertz JE, Kortright KE, Narayan D, Turner PE. Phage selection restores antibiotic sensitivity in MDR Pseudomonas aeruginosa. Sci Rep. 2016;6:26717.

As mentioned, antibiotic resistance is actually quite expensive. Bacteria that fail to discard it when antibiotics are not present will be wiped out by competition from other bacteria that devote more resources to reproduction.
One major source of antibiotic resistance is the 'multidrug efflux pump' which transports harmful chemicals outside the cell. You can imagine how it costs energy to run a pump. These pumps also protect the cell from other harmful molecules such as heavy metals and organic pollutants, so making them more specialized for antibiotics will increase vulnerability to other toxins.
Looking at the question more broadly, if bacteria could become universally resistant, it would have happened already. Remember that the most famous antibiotic, penicillin, was discovered because a fungus invaded and killed bacteria being cultured in a petri dish. The microbiological world is a brutal war that has raged constantly for billions of years between bacteria, phage, fungi, other bacteria, etc. Antibiotics and the resistance to them have been around much longer than humans, let alone modern medicine. If we don't take that into account, it seems like medically important pathogens have developed new defences in a very short time, so we overestimate their ability to adapt to new threats.


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Can storing food in a de-pressurized container result in anaerobic bacteria growth?
I was looking for a way to store for longer some products which go bad quickly. I found a stainless steel container made with a hermetic lid that you can remove air through (using a pump) so you create a vacuum of sorts (I don't know to what level can the internal air pressure be reduced). The issue is whether storing food which isn't specially sterilized, such as vegetables or spices, can result in the growth of pathogens such as Clostridium botulinum? What I originally looked to buy such a container for is soy lecithin, as I read these go bad very quickly even if stored in a cool, dry place as advised.

Any sealed container can become anaerobic relatively quickly if there are oxygen consuming organisms inside (which there probably are if it's not sterilized). So, growth of anaerobes should always be a concern when using a sealed container for food storage, and proper temperatures for such storage should be considered.
A container like the one you describe would probably be good for extending the shelf life of dry foods that are sensitive to oxidation (coffee, spices, or your soy lecithin powder), and might even help stave off aerobic spoilage organisms (like molds), but it probably won't do anything to prevent growth of anaerobes like C. bolulinum or C. perfringins.

So it can increase the probability of anaerobic growth? It seems the usual aerobic spoilage is not potentially lethal, but stuff like botulism is.

I'm not sure that it would actually increase the anaerobic growth, but it probably won't help prevent it. The trouble there is that anaerobic spoilage can be less obvious than, say, mold growing on your food. Might be why C. perfringens is among the leading causes of food poisoning. Good news is that botulinum and perfringens don't grow well at colder temps, so keeping food in the fridge or freezer, when possible, is a good way to prevent them from growing.

Thanks. Though, I think within the freezer at -20 Celsius no bacteria or mold should develop anyway whether there's vacuum or not. Within the fridge (3–4 Celsius) be, how effectively can it prevent such anaerobic growth? The non-freezing temperatures probably don't halt it completely, so if the stored product is something that takes months to finish, what might happen?


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Why do many humans, including myself, find cats so cute?
After all, they are descendants of big, dangerous lions and other wild cats, which doubtlessly have eaten many humans in the past, and probably continue to do so in some places even today.
Yet we for some reason find these tame, small versions of the "real deal" very cute. Even though they are still usually very arrogant, selfish, sadistic and whatnot, even when not physically posing a threat to humans.
Actually, I find even lions and leopards and pumas and cheetahs and tigers to look "cute", even though I wouldn't try to pet one for obvious reasons. I like the idea of truly dangerous cats not eating me and acting like "guard cats", but I wouldn't risk it even though there have been such cases where a human got accepted by lions who could kill him in an instant, yet don't.
I hate "eight-legged freaks" (spiders), yet I cuddle all the time with a four-legged beast which is much bigger. I would never stop washing my hands if I ever so much as touched a spider, but I can drill in my face into the fur of my cat and can't get enough of petting him and giving him expensive cat food and letting him in and out from the balcony door, etc.
It doesn't make sense to me. What is it about these furry animals with tails that is so appealing to many of us? It seems so natural for there to be a fluffy cat in here, sleeping/relaxing most of the time, but really, it's just a slightly-less-wild mini version of a lion, and who knows what he'd actually do if he were "full-size"? Probably eat me for closing the kitchen door on him...

Cute?  "…three proper Men out of five will always throw things at a Cat whenever they meet him" Rudyard Kipling.

You might turn the question around, and ask why you (and many other humans) have an irrational dislike of "eight-legged freaks" :-)

It's a very good and interesting question in general, but it's a difficult fit as a Stack Exchange question. It is possible that a more scientifically-written version of this question might be on-topic in Psychology & Neuroscience SE It can probably be on-topic here as well but it only takes five cat-dislikers to close it (humor).

@jamesqf or why cats have irrational dislike of cucumbers and skinny eggplants (search YouTube) (random example)

Cuteness is a subjective term to designate a psychological response to neotenic features (i.e. features that delay or slow in their growth) of the body mostly associated with young animals. These are features where the body parts are proportionally exaggerated compared to other body parts and the adult stage. It make the young individual attractive to the human observer - and most likely to animal observers as well - which is the psychological response. This response is an evolutionary adaption to assist in caring for offspring by inciting nurturing behavior in the parent(s), a hypothesis first proposed by Konrad Lorenz (1943, 1 ; but see also 2). Since other animals display neoteny, the physiological response can be transspecific (i.e. across species).

I like your answer very much. Care to add a reference to better complete your answer? I think this one actually testing Lorentz's idea of Kindchenschema ought to suffice! And as a bonus I suggest explaining the jargon terms (neoteny and transspecific) so that laypersons can understand the entirety of what you put so well. Those are very alien words to non-specialists.

@ S Pr, thanks! I hope sufficiently honored your request.

No, thank you. Good work :)

some recent research has hypothesized that felines, especially cats, evolved cuteness. Cats, unlike other animals domesticated themselves. Crescent, wild cats adapted to living with humans, hunting rodents in grain stores and abandoning their aggressive wild-born behaviors, which led to today's house cats. Also according to another research, the more something resembles a human baby, the cuter we think it is. It’s believed that when an animal has the same dimensions and features of a baby, it hijacks a neurological response to care and protect the creature. Moreover, the way kittens meow at us, it is very similar to how a human infant might cry. They modify their sound when seeking food, adding a higher-frequency element that exploits our sensitivity to infant wails and thus making it harder to ignore.

This doesn't really explain why many humans also find many other furry animals, especially young ones, to be "cute".  Sure, dogs might likewise have evolved (or been bred for) "cuteness", but this doesn't explain horses, ferrets, lambs & kids (that is, young goats), even bear cubs.  Indeed, the fur-cuteness link has sometimes caused me to wonder how human infants manage to survive.  Poor little things, having to go through life with no fur, no tail, no floppy ears... :-)

This is very interesting. I think you should add the citation to the research.


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How to start learning disease profiling?
I am student of Biological Sciences and interested to learn profiling in order to characterize the state of organisms (especially diseases). You know that there are different types of profiling like, Genome, Proteome, Metabolic and many more.
I am confused from where should I learn in order to understand principles of profiling.
Kindly, guide me.
Thank you!

Are you asking about various classifications of diseases?

Sort of! But characterizing diseases with molecular profiling. Likewise, all skin cancers are not equal but through profiling, we can classify.

I am focusing more on profiling. It's technique.

There are many results for the search "disease profiling." You can try this and ask what remains unclear.

Are there any books related to it?

Okay! I'll try.


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What is the developmental and health outcome of an XY individual with an SRY addition on their X chromosome?
I know that "XX male" syndrome occurs through various means, including the addition of an SRY gene in one of the X chromosomes. The developmental and health outcomes of such individuals can be problematic. But what about a person with an X chromosome with an SRY addition, along with a Y chromosome?
It seems that it would be similar to XYY syndrome, but without the over-expression of anything but the SRY gene. Would it even be obvious, from a visual point of view or fertility point of view, that a person has the extra SRY gene?
I know that rodents aren't humans, but it does appear that there are species that have naturally acquired multiple copies of the SRY gene.


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help identifying marine item found on beach
Need help identifying this hard waxy egg like item found on beach in Destin, FL (USA).  It feels waxy and semi hard. Also smells like squid or real fishy. it is also semi transparent with dark tan looking tie on inside

Larger versions of pictures shown below:

Please [edit] your post to include the approximate size and any additional relevant info. Thanks.

You've found a swim bladder. Swim bladders are largely made from collagen, so when they're dried out on beaches they feel tough and rigid.
Swim bladders differ in shape between species. As an example, the swim bladders of oyster toadfish are similarly-shaped to the one you have found, but that general shape isn't uncommon, so it could have come from many other species.


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Reflex muscular activity in three months old fetus

At the end of the third month, reflex activity can be evoked in
  aborted fetuses, indicating muscular activity

This quote is from Langman's Medical Embriology.
Have I misunderstood it or it is really talking about muscular reflexes in aborted fetuses?
Do we have any video proof or something like that?
How does it happen and why?
Why do we need a muscular reflex during prenatal life?


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Is genetic equivalence a universal truism or are there exceptions?
Someone who I have been discussing scientific topics for some time came around to the notion that, on a biological level, the seed of a plant is not the same organism as the mature stage of the plant. When I brought up the theory of genetic equivalence he completely shut down and refused to go further. He then told me to pose the question here so here I am. To be concise "is an acorn a tree".

Is an acorn a tree?
It all depends on your definition of identity. What makes two things being the same things to you? There is no "fundamental biological definition of identity". Therefore a sentence like

[..] on a biological level, the seed of a plant is not the same organism as the mature stage of the plant

This sentence has no meaning as it wrongly assume that there is some kind of fundamental biological definition of identity but there is no such thing. Scientists are not dictators stating how things must be defined. Scientists use terms that they define that help them describe the world. Anyone is free to come up with its own definition and work with it.
Let's consider two possible questions that are better defined
Is the genetic material found in a tree cell the same as the one that was found in the acorn before it became a grown-up tree?
Yes for most cells you would consider and yes again but except for somatic mutations and shortening of telomeres.
Is an acorn the same weight as a tree
No!
So, really it all depends upon what your definition of identity is.


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Hippos in infrared
Watching Netflix's "Night on Earth", I discovered that Hippos, or at least some Hippos, have quite a weird appearance in infrared. They seem to be covered by IR bright spots all over their body, possibly excluding their heads.
Something similar can be seen in this video on YT starting around 0:12. The following picture is a screenshot from that video:

What's the reason for this weird pattern? Why are some spots on a hippo's skin warmer than the rest?

EDIT in response to a comment by @jamesfq:
As far as I can tell, these images were taken without the use of IR illumination. The crew in the video linked above were apparently using a repurposed military thermal imager by Selex. As far as I know, these operate without any additional illumination.

EDIT II:
@Harun suggested that this might be related to hippo sweat, which looks a bit like blood. But the images I could find (the one below is from here) do not seem to suggest that it forms spots comparable to those in the IR image. But maybe the secretion spreads around the glands it comes from and looks quite different in the IR. It also looks like they sweat on the head, which has a much more uniform appearance in the IR than the body. Of course these are all just single images, maybe not representative.

I don't remember the explanation, but there's a good description in this documentary: Inside nature's Giants:Hippo

@Harun Thanks, will try to get my hands on this.

As a comment in lieu of a speculative answer below: I can also imagine the spots are depositions from insects or secretions from glands of the hippo. I've heard of secretions that have a sunscreening function, i.e. appear black in UV. They could also attract or repel UV-sensitive insects that commonly spend time around these animals; this is not uncommon with coloration visible only in UV (e.g. dark spots that plants harbor to attract). Just expanding on the speculation... I have no good suggestion as to why there would be spots in the IR spectrum!

@SPr Hmm, that's interesting. I hadn't thought about secretions, only about this being a property of the skin itself.
No luck finding the documentary mentioned above yet...

It would help to know just how the IR photos were taken.  Are they using night vision cameras that project their own infrared light (in which case the might be just spots of different IR "colors"), or are they using the hippos' own thermal radiation?

At thermal IR wavelengths most materials have similar high emissivity especially anything organic, which suggests that the variations are more likely related to temperature than to different materials on the surface. So I'd venture a guess that it's increased blood flow near the surface, possibly due to bug bites, but it's just a guess. But what's still bothering me is that the ground is black. I'd expect the ground to be warmer and therefore brighter than the sky and trees.

Sorry I can't turn this explanation into an answer, this page seems to have it: https://www.scientificamerican.com/article/do-hippopotamuses-actuall/

@uhoh Good question regarding the ground. I asked on physics SE: https://physics.stackexchange.com/q/529616/35915

@Harun Interesting point, I remember seeing this in the zoo when I was a kid. But the secretion does not seem to form spots the size of those seen in the picture. At least in the images I could find.

@user35915 The size of the brighter spots can be misleading. If they're secretion from glands in the skin, they will spread at least a little and can be warmer than the surface of the body.

@Harun Good point, will include it in the edit.

There is research to support the idea that these are areas used by the animal to regulate its body temperature.
Citation: Schneider, Marion & Kolter, Lydia & Zoo, Cologne & Germany, & De, (2003). Visualisation of Body Surfaces Specialized for Heat Loss by Infrared Thermography. J. Exp. Biol. Quart. J. Exp. Physiol. Medicine Comp. Biochem. Physiol. A J. Anim. Science. 2068. 1727-1738.
As the researchers found using a thermal camera and imaging software, there are distinct spots that can be observed in the hippo. the authors of the above mentioned paper infer that these higher temperature areas coincide with areas of rich blood flow and high nerve innervation, used to regulate blood flow and thus body temperature.
The authors also note that similar mechanisms are present in marine animals, such as seals.

Our findings demonstrate for the first time that the hippopotamus is able to open thermal windows. They appear in all body surfaces and vary in number, size and shape. Earlier histological examinations of hippopotamuses revealed a network of blood vessels deep within the dermis, and a thin epidermis, richly applied with nerve endings [3], suggesting an underlying thermoregulatory mechanism through nerval vasomotor control of the skin through connected arteriovenous anastomoses. These are referred to as specialized cutaneous vascular structures, densely innervated by sympathetic nerve fibres which permit local regulation of blood flow [4]. Arteriovenous anastomoses have been identified as thermoregulatory structures in the skin of seals [5] and presumably represent the underlying structures for thermal windows in the hippopotamus. Elephant, rhinoceros and hippopotamus are large herbivores, live in the same climatic region, and have almost hairless skin. Elephants show a great capacity for heat loss in the ears [6]. Contrary to the rhinoceros, the hippopotamus lack sweat glands but exhibits large sub dermal glands distributed over the body which release a red secret.

Nice, thank you. I couldn't find the full text. If you have access to it, could you clarify the connection between these areas and the red Hippo sweat? It's mentioned in the last sentence of the abstract, but I don't quite get the connection. Are the glands for the "sweat" also the thermal windows or are they distinct?

Also: my girlfriend reminded me that there is also footage of a seal in Night on Earth that shows the same spots, as is mentioned in the abstract. I had forgotten about that.

Nice answer, but the reference appears to be garbled — it includes a partial email address and multiple journal abbreviations all lumped together. It would be great if you could edit that so that it is easier to find the actual paper (all I could find was a Research Gate link, which appears to be where the incorrect reference information came from ...).

Here is a link to the abstract for the paper cited, there is also a link to download the whole paper on the below web page: https://www.researchgate.net/publication/228879361_Visualisation_of_Body_Surfaces_Specialized_for_Heat_Loss_by_Infrared_Thermography

@MatthewMartin It seems that researchgate is your primary source. Not many people have an account in researchgate. Does this paper have a doi or pubmed link (check the first page of the article)? The citation is not clear as tyersome already mentioned.

Following from Matthew Martin's citations, we can infer what kind of temperature management the "biological thermal windows" are for, as they travel through 4-5 inches of fat and leather:
If the hippos dwell in 25'C to 30'C water for much of the day and night, they can waste energy warming up, energy which can be spent on growing, rearing young, defending territory.
As changes in vascular perfusion are not energetically demanding, thermal windows broaden the temperature range in which endothermic organisms can regulate body temperature with minimum costs (the thermoneutral zone), particularly by extending its upper limit. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4843926/
Hippo's have spent millions of years as a water dwelling clade, their closest living relatives being dolphins, whales and porpoises. So the hippos are equipped with radiator-valves can let them stay warm in water for many hours and stay cool on the riverbank.


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How much blood do we have when the heart first starts to beat?
How much blood do we have when the heart beats for the first time?
It should be between the third and fourth week of embryonic life.

Note: there is a heart "beat" but no pumping at 3-4 weeks. The blood vessels and chambers of the heart have not developed. The "beat" is just electrical activity in cells that will eventually become part of the heart.

From your comment I guess we don't even have blood at 4 weeks


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What Kind of Bug is This
I found this bug in southern Florida in February. It was approximately 1cm long or less, fully extended.  What type of bug is this?

Please [edit] your post to include an approximate size of the specimen. Also, if you have additional information about where you found it or clearer photos, you should update to include that info as well.

It's probably the larval state of a tortoise beetle, or a closely related beetle. They are known to build a "faecal shield" at the end of their tail, sometimes including shed exoskeleton and any debris that sticks to it. They hold this shield over their bodies for defensive purposes that aren't fully  understood.
Lacewing larva look somewhat similar and also cover themselves with debris, but their legs are longer and their head and mandibles look quite different.
Here's an image of a thistle tortoise beetle larva:

Amazing detective work, looks just like it! Thanks so much!


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Where can I obtain Sputnik virophage samples?
I'm working on a project where I'm trying to use virophages as viral vectors in introducing CRISPR-Cas proteins into other viruses. I was wondering where I might be able to find replication-defective Sputnik virophages or other virophages for this kind of experiment?


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will a plant grow faster if it is exposed to concentrated sunlight?
I know that plant grow faster depending on the hours of sunlight it has, but what happens if i put a giant mirror focusing light to the plant?.
Will the growth rate be limited by the damage the sunlight produces, or will it be limited by the speed of the photosythesis?

The Wikipedia page on photoinhibition has a good explanation of the relationship between light intensity, photosystem damage, and photosynthetic potential.

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). In addition, this is an unanswerable question without knowing the type of plant and the light levels before and after concentration (different species tolerate different level of light).  ——— 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!

In nature, there is often ample sunlight available to plants. From this NIH page:

However, even at the maximum light intensity encountered by photosynthetic organisms (tropical noontime sun, ≈1.2 × 1020 photons/m2/s), each reaction-center chlorophyll a absorbs about one photon per second, which is not enough to support photosynthesis sufficient for the needs of the plant. To increase the efficiency of photosynthesis, especially at more typical light intensities, organisms utilize additional light-absorbing pigments.

In other words, plants are not entirely photosynthetically efficient and do not typically use all of the light available to them. From Wikipedia:

Photosynthesis increases linearly with light intensity at low intensity, but at higher intensity this is no longer the case (see Photosynthesis-irradiance curve). Above about 10,000 lux or ~100 watts/square meter the rate no longer increases. Thus, most plants can only utilize ~10% of full mid-day sunlight intensity.

Up until a point more light will accelerate plant growth. Beyond that it will stop helping and then become damaging. The optimal level of light to give commercially valuable plants has been studied extensively, and varies substantially between plants.
This concept is formalized in the daily light integral, the number of moles of photons per square meter per day a plant optimally needs, and the photoperiod which is the number of hours per day that light should be distributed over. You can look up values for different plants.


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How sharp are the borders between Brodmann areas?
How does the border between two Brodmann areas look like in Nissl stains? How large is the transition zone where one cannot tell to which of the two areas a neuron belongs to? How many neurons are ambiguous compared to the number of unambiguous ones, roughly? 1%, 5%, 10%?
Is the inner connectivity of a Brodmann area greater than its connectivity with a neighbouring area across the border? Can this be seen in Nissl stains? Or is short-range inner-cortical connectivity somehow homogenuous over adjacent Brodmann areas?

Hi Hans, this might be the sort of question that's best answered yourself by looking at some labeled Nissl sections, or by reading about criteria used to determine areas.

@BryanKrause: I'll try, but I'm afraid my view is too unexperienced. Could you  give me a reference explaining the criteria to determine areas?

I tried searching Google Images for "brodmann nissl" (but no quotes); one example led me to https://webvision.med.utah.edu/book/part-ix-brain-visual-areas/the-primary-visual-cortex/ (figure 9 on that page). Figure 1 here: http://www.nibb.ac.jp/brish/Gallery/cortexE.html also looks like a place to get started in looking at the layers. Note that there is a huge variety in the discriminability of Brodmann areas (and one reason there are so many different parcellations of cortex): some are really easy, others require an anatomist's trained eye and I can't tell them apart myself.

I think you'll get a better picture by going through some examples to get a sense for yourself, rather than trying to quantify it.

@BryanKrause: Figure 9 is great and gives me a better sense: It's about "distinctness of appearance" (in this case of layer 4 which is also present in V2 but not so distinct as in V1). What can be seen also: The border is only sharp in layer 4 (and here, it is astonishingly sharp) but its sharpness does not extend to the other layers: there it becomes diffuse.

@BryanKrause: With "so many different parcellations" you mean "by so many different authors"?

Let us continue this discussion in chat.


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Rescuing a virus from naked (c)DNA
Reading the articles it seems that for several human virus strains, synthesizing the full-length genome then electroporating into vero cells and incubating a few days gave birth to living viruses that can infect people as well as the original do (thus offering an easy way to add some mutation and make chimeric virus)
Am I correct and what are the few facts to know about this ? For example influenza would need more efforts, transfecting either seven separated plasmids, or the full genome plus infecting with a living virus producing the influenza RNA polymerase.


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Are there nuclei with "real" interneurons?
In Kandel's "Principles of Neural Sciences" in the chapter about the anatomical organization of the brain one reads (p. 323, 4th ed.):

»Although a variety of [relay] neurons are involved at each stage in information processing, these neurons generally fall into two functional classes: principal (or projection) neurons and local interneurons. The axons of principal neurons convey information to the next stage in the system. Interneurons may receive inputs from the same sources as the principal cells, but they contact only local cells involved in the same processing stage [(relay)].«

This means: All neurons of a "relay" (= functional unit) receive external input, but only some give external output. I wonder if there are examples of functional units (nuclei, cortical areas, etc.) with significant numbers of

interneurons receiving input only from local cells
principal neurons receiving input only from local cells

If there were, there would also be distinguished input neurons, receiving external input but not giving external output.

I don't think assigning those classes the adjective "real" makes any sense. Additionally, in an ANN, there aren't any interneurons if we think about it like the brain. Otherwise almost the entire CNS is interneurons, except for the motoneurons and sensory neurons themselves.

@BryanKrause: Of course, the entire CNS is interneurons (except motor, endocrine, and sensory neurons), but I asked for smaller populations of neurons like nuclei and cortical areas. And why shouldn't a layered ANN have interneurons?

I think I wasn't very clear. What I meant is that the definition of what an "interneuron" is varies with systems, and ANNs and the brain are not organized very similarly. One could just as much consider a hidden layer of an ANN to be a collection of neurons that project to another layer. It's fine to call them interneurons in an ANN context, I'd just be hesitant to carry that definition over to analogies.

@BryanKrause: I dropped the ominous adjective "real" because it adds nothing to my question and was responsible for some confusion, as I am afraid. Now the question should be rather clear-cut - or isn't it still? Also, mentioning ANNs didn't add anything essential to my question, so I dropped it, too.

I think that's better. I feel like it's missing some motivation as-is, but maybe someone will come along with an answer. You're likely to find cases like this in the periphery/sensory organs, but I'm kind of missing the "why" of why this matters.

@BryanKrause: I could imagine that functional units with "real" interneurons and "proper" input and output neurons might do different kinds of "computations" or have different "modes" of computation than those without them. But this would have to be shown, e.g. by corresponding ANNs.

I see. I think that in most cases brains are simply much more complicated than that; there are too many good reasons to keep, for example, an efferent copy of an output signal (making the output neurons...improper). Probably the retina is a relatively complex structure that fits at least some of your requirements, but computationally it is quite boring compared to other brain areas.

Let us continue this discussion in chat.


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Species Identification : What insect is this?
I noticed this insect in the end of last December on the window of my room in Pune, India. There are at least 15 such insects on this window and 12 on another. None of these have moved even a millimeter since I first noticed them. They don't move even when the window is lightly banged. They are almost 1 to 1.5 cm in length and their tails have two ends. They are almost transparent.
Imgs:

I know that it is a Mayfly (Ephemperoptera), but I am not familiar with the mayfly families in India. The reduced wings on this individual are unusual.

More properly, this was a mayfly; it is a castoff exoskeleton from either a last-instar naiad or a subimago; many mayfly groups have only two caudal filaments as seen here, so while that detail will help in the eventual identification, it cannot be used on its own.


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Is there more biomass on earth today than there was in the past?
Is there more, (or less) matter on earth sequestered as a part of biological systems than there was at any(arbitrary) time in the past?
Edit:
I realise I don't have a specific question, and was looking for a lesson of sorts on what is the footprint of life and will the new not come if the old doesn't die and dissolve(biologically atleast).
If you could suggest me good sources to study this, that would be great.

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All the coal, limestone, and other bio-deposited stuff on Earth attests to the fact that past life has left behind a giant, cumulative mass of modified matter.  Even components of our atmosphere would be part of that mass.  Some of all that gets recycled by living organisms, and some gets modified by geological processes so that it may be hard to distinguish from "non-biomodified" matter.

@S.McGrew I am not talking about bio-modified matter as much as matter which forms the bodies etc. of living organisms.

Then that would include limestone, coal, & peat.  Marble is metamorphosed limestone.

I would guess there was more in the past during warmer periods.  For example, imagine if Antarctica was covered in lush jungle rather than ice, then all else equal, there'd have been more biomass back then.  But  I don't think all else would have been equal, as it seems warmer temperatures promote more developed ecosystems in general, so all the rest of the continents would likely have had more biomass.  And of course, with tectonic drift, there were likely times when the large desert areas like the Sahara would have been in different areas with more rainfall and more biomass.  Plus, certainly during past periods of dramatic volcanic activity, all of the nutrients landing in the ocean would have led to much more phytoplankton which would have supported more ocean biomass as well.  Currently, many parts of the ocean simply can't support that much life since there aren't any nutrients in the water.


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Does parasitism, one of Bacteria's lifestyle?
The parasite is an organism that lives in or on a host. It depends on its host for survival.
Bacteria lives in decaying organic matter, within human organism (colon, oral cavity). It can be a saprophyte or commensal.
Does the parasitism, one of bacteria's lifestyle ?

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In particular, your definition of parasite better fits "symbiont", which suggests you might benefit from doing some reading of introductory material. 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. Finally, textbooks with a good level of detail are also freely available online e.g. from NCBI.

If you are asking whether some bacteria are parasites, then absolutely yes. I think this is absolutely clear and evident to any and all biologists and would require no discussion. I could expand with some examples, but they would not be very representative of the incredible diversity of parasitic bacteria.
Parasitism
Many bacteria parasitize and live selfishly on hosts. Among them are obligate and facultative parasites. Many become parasitic if there are changes on their host (e.g. think pH in your oral cavity). These are endless. And to expand on this ecological discussion, I think another related and interesting relationship in nature exists which is not technically parasitic but falls into a similar category...
Commensalism
Yet many other bacteria are symbiotic commensals, i.e. do not benefit nor harm the host. As commensals, they have various commensal relationships with the host:

chemical commensals

(exploit the available chemistry of the host),

inquilinism

where the bacteria will live in the host's prepared environment (think ant hills or termite mounds or bird nests; or sewers, air vents, the list is endless especially for human environments)

metabiosis

(when the aprasite depends on the environment previously prepared by another organism; think how bacteria may parasitize fungi on the ground, which digest dead plant matter; the fungi deploy antibiotics to prevent this kind of parasitism, and we've used these defences for our own medicine... penicillin is from fungi!), and

phoresy.


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Changes in DNA and forensic cases
If DNA changes over time, how is it that forensic DNA gathered decades ago can be matched to a person today for solving crimes?

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@Dirigible ?? DNA profiling is not based on sequencing at least until 2010, it is doing a fingerprint of the reaction product of a PCR+electrophoresis with specially designed primers targeting microsatellites https://www.yourgenome.org/facts/what-is-a-dna-fingerprint


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A question concerning the strength of synapses
Synaptic strength can be defined

»as the average amount of current or voltage excursion produced in the postsynaptic neuron by an action potential in the presynaptic neuron«

Synaptic strengths and their changes depend on many factors and mechanisms, from LTP and LTD to STDP and STF and STD. Possibly, also neuromodulators should belong to this list – but maybe they shouldn't.
Assuming that synaptic strength is a well-defined quantity even when the synapse is at rest, the strength of a synapse is a continuous or non-continuous function over time, that ideally can be plotted.
Now I wonder whether there have been recordings and/or simulations of the synaptic strength of a single synapse as such a function over time - and how the plot would look like at different time scales: long term trends superimposed by shorter and shorter fluctuations?

What you are describing is exactly how long-term potentiation/LTP (or depression/LTD, for that matter) is measured electrophysiologically.
Here's an example from a 1988 review by Nicoll et al:

Nicoll, R. A., Kauer, J. A., & Malenka, R. C. (1988). The current excitement in long term potentiation. Neuron, 1(2), 97-103.
The x-axis is time in minutes, the y-axis is a measure of synaptic strength: the slope of the local field potential response to simulation of a particular pathway. You could also measure an EPSP internally, measure voltage with a voltage-sensitive dye, etc.
At the point marked "tetanus", a long train of pulses is delivered that is known to cause LTP. Afterwards, you see an increase in synaptic strength that is maintained for many minutes.
It's also possible to perform these experiments over longer time scales, with different paradigms, in the presence of various drugs that influence LTP, etc. Different protocols will give different durations of LTP.
These sorts of plots are ubiquitous in the LTP/LTD research field, so if you read any papers in that area you are likely to come across many similar presentations.

Thanks a lot, but what about larger time-scales, from days and months to years and decades? And what about smaller time-scales, down to seconds and milliseconds (why not)? Or will the concept of synaptic strength loose sense on the millisecond level?

@Hans-PeterStricker At a millisecond level you would be thinking about short-term plasticity rather than synaptic strength. At very long time scales the answer is far too much "it depends" to be contained in a stack exchange answer.

But what is plasticity the plasticity of if not of synaptic strength? The other way around: What's the difference between plasticity and synaptic strength?

@Hans-PeterStricker I suppose in a sense you could consider it a measure of synaptic strength, but it isn't a mechanism typically employed in artificial networks, where "synaptic strength" is used as a concept. Read up on "short-term plasticity" and contrast it with what you know about long-term plasticity - they are really quite distinct biologically.

May I note that by definition "synaptic strength" is a purely physical concept (it's all about voltages and currents) - the underlying biological mechanism don't really matter (in my understanding and in the context of my question).

@Hans-PeterStricker In a biological system, there is no way to measure synaptic strength by any one number the way you can in an artificial one without adding further information to that definition.

Let us continue this discussion in chat.


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How are lipid-coated mRNA-based vaccines transported into cells for expression?
In CNN's video Scientist says Coronavirus vaccine could be ready by 2021 after about 00:25 'Robin Shattock, the Head of Mucosal Infection and Immunity at Imperial College London' says:

We were able to access the sequence that was published by Chinese scientists and made globally available, which was a tremendous thing to do. And we went from that sequence to identifying part of the sequence that encodes for the surface proteins of the virus. And we’re using that sequence to manufacture our vaccine.
We’re using a particular approach where we make a synthetic vaccine based on RNA, so essentially it’s essentially genetic code, we package that in essentially a lipid droplet, and use that to inject in a muscle; it expresses that protein, and the body recognizes that as foreign and it makes protective antibodies.

I'm assuming that the RNA mentioned is mRNA, and so once it reaches the cytoplasm of the vaccine recipients muscle cells it will be expressed and somehow returned to the cells' membrane where it will be recognized as foreign by passing lymphocytes.
Questions:

Is this basically correct as far as it goes?
If so, what causes the lipid droplet to fuse with muscle (or other) cells in the first place?

From what I read transfection of DNA vaccines are based either on electroporation or viral vector

@reuns There is a whole world of nonviral transfection reagents that do not depend on electroporation. They typically include cationic polymers, lipids, and peptides.

@user137 It says you'd want a few of the mRNA lipid-PEG coated particles to become endosome in dendritic cells where (after release and translation by ribosome) the protein is taken by the MHC pathway for presentation on cell's surface. Then (because particles provoked an inflammation?) the surface MHC-antigen is processed by the immune system for acquisition of new antibodies. Is it the real-life scenario you are thinking to ? The possibility of replacing the mRNA by a replication competent RNA virus encoding it is briefly mentioned.

@reuns I've just asked Do both DNA and mRNA-based vaccines sometimes require electrical pulses to work?

@user137 ditto.

“Essentially Genetic Code?” No, No, No. A thousand times No. Educate a public that understands the difference between a current and a voltage, and don’t discredit one of the major scientific achievements of the 20th century. Or does he really not know what the genetic code is?

I can't give an authoritative answer on this because my PhD work was based on mRNA delivery using peptides instead of lipids, but many of the concepts are the same. I also don't have time to provide proper citations, but this is probably too much for a comment.
Anyway, mRNA is a very fragile molecule, it can be broken down extremely quickly in the blood by serum nucleases. Therefore we must protect the mRNA by mixing it with some other chemical, in this case a mixture of positively charged lipids. The positively charged lipids are attracted to the negatively charged phosphate backbone of the mRNA, and form a nanoparticle trapping the mRNA inside and hiding it from the nucleases. The lipids are often, but not always, PEGylated, which means that a molecule of polyethylene glycol (PEG) is attached to the lipid. The PEG groups form a layer on the outer surface of the nanoparticle that helps prevent protein binding.
These mRNA lipid nanoparticles are then injected into a patient. This will probably be an intramuscular injection so that the particles are most likely to be taken up by muscle cells. The exact mechanism explaining why lipid nanoparticles are attracted to cells isn't entirely clear, but it's likely a combination of electrostatic attraction between the positively charged nanoparticle and the negatively charged cell membrane and proteins that bind to the nanoparticle and are then recognized by receptors on the cell surface.
After the particle is taken up by a cell it is usually trapped inside a membrane-bound structure called an endosome. As the endosome matures it is acidified, and as the pH drops from about 7 to about 5.5 the nanoparticle is disrupted. The lipids that made up the nanoparticle can merge with the lipids that make up the endosomal membrane, disrupting that membrane and breaking open the endosome, allowing the mRNA to escape into the cytoplasm.
Once in the cytoplasm the mRNA will find a ribosome and produce protein. Just like you said, the protein in this case will be membrane bound and expressed on the outer surface of the cells for eventual immune recognition.


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Additive property of taste
It might be a dumb question to ask, but I find it confusing.
Is the perception of taste additive?
Or to be more precise, can two tasty food items combine to give a more delicious product?
For me, this sounds logical. I believe that the sense of taste is due to some chemical reactions in our mouths, which in turn fire up our taste receptors to give some specific signals to the brain. So when two tasty foods combine, there would be more signals that are identified as 'Tasty' by the brain. That should give the food combination a stronger taste than its constituents.
But I found some contradicting examples.

I like to drink tea and coffee. But once, when I accidentally mixed a cup of tea with coffee, it wasn't tasty at all.
I have seen some specific 'COMBINATIONS' of foods that taste better than their constituents.

What does this mean? More likely, my understanding of taste perception is flawed.  If it is, then what is the real working mechanism of taste?

What we think we are "tasting" is usually a combination of taste and smell. I assume you are asking about the broader experience which involves both? In that case it's pretty complicated. 1, 2, 3 If you like mixing things and you're asking only about taste by the tongue, then try eating anything citrus with a bit of miracle fruit!

Maybe this would be a good question for https://cooking.stackexchange.com/.

taste is itself a combination of smell and "taste" an apple and an onion taste the same without your sense of smell.

I would classify the neurological phenomenon of "taste" or "tastyness" as an emergent property (1), and therefore synergistic (i.e. not adequately explained simply by additive effects). For example, when something "tastes like chicken" that's a synergistic sensory pattern in your brain involving the specific ratios of the 5 basic tastes(2) on your tongue, along with your sense of smell, and the sensation of the food's texture in your mouth (is it moist, dry, viscus, etc). This helps explain why simply combining two tasty flavors (coffee+tea) does not necessarily yield something twice as tasty, and also why foods which might not be tasty on their own, can be tasty in the right combination (e.g. potatoes+onions+salt+oil+heat makes tasty hashbrowns, but none of those foods are especially tasty on their own).
Taste preference (tastyness) also involves a certain amount of neurological learning, which is partially why often people don't like the taste of something like coffee when they are young, but learn to enjoy it as they find it elicits a response from the reward centers of the brain.
In summary, "tastyness" is most likely an emergent and synergistic property of a system of complex sensory and neurological interactions, and not simply an additive.

Long answer from a non-biologist.
I was dreaming about explaining coffee flavors as an n-dimensional space spanned by the discrete detectable flavors/aromas present in a cup. In this model, a single flavor state is comprised of one distinct association (e.g. "blueberries") and amplitude (e.g. "a lot" or "not at all"), which mechanistically must comprise a certain molecule and chemical state.
In this model, a fictional ground truth exists for a given cup, which would correspond with a delta distribution on the 1D projection of a single flavor. The perceived flavor is convolved with various aberrations: grind size distribution causing over/under extraction (sample-specific, an alteration of underlying chemical states); a smoker whose sensory apparatus are perturbed (detector-specific).
Getting to the point, from a chemical sensing perspective, it seems that you could treat flavor as additive if the discrete molecules comprising it are non-interacting. That's at least two fold: (1) no molecular interactions, e.g. chelation of a salt; and (2) no sensory interactions of chemical constituents underpinning a flavor.
At least one common case in cooking comes immediately to mind: a pinch of salt heightens the perceived sweetness of a recipe, which would invalidate clause 2 above.
Summing up, it seems the answer is non-trivial. Perhaps the underlying molecular/chemical states are additive, but our human sensory apparatus is severely non-linear in its detection scheme.

The last sentence is the correct interpretation. Nerve density is different for different receptors and senses over different parts of our body. I'm not a neruro guy, but I would hazard a guess that we have more receptors for salt and sugar than we do for say bitter as we need salt, but can survive some bitter or short term exposure to a lot of bitter toxins.


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How exactly can a drug affecting squalene epoxidase affect the methylation cycle, necessitating the use of 5-MTHF?
I found a case report in which the authors say that Terbinafine might have possibly affected the methylation cycle in a patient, necessitating the prescription of 5-methylfolate to correct the imbalance. I tried googling to find some description that would include the interaction of ergosterol synthesis and methylation cycle, and found nothing.
Maybe I was not googling the right words.
I can't seem to find how exactly we can affect the methylation cycle by affecting squalene epoxidase (the target of terbinafine, the drug used by the patient in the case report).
The article quoted is titled Antifolates and MTHFR (Trachtman and Pagano, 2015)

This might be a better fit in Biology.

@CareyGregory - feel free to move the question to Biology, I wouldn't mind ))

Preamble
I have tried to follow the logic of the rationalization of the clinical case described in the report of Trachtman and Pagano, but have failed. I suspect from the quality of their biochemical illustration (arrows leading from compounds to enzymes, and talk about ends of cycles) that they do not have a clear idea themselves. However, having done the literature search, let me set out the picture as I see it, in the hope that this may enable someone else to see a connection I may have missed.
Anti-fungals inhibit the erosterol biosynthesis pathway in fungi
As the poster states, anti-fungals such as terbinafine do act by inhibiting the synthesis of ergosterol, which is a cell-membrane steroid, unique to yeast. Of relevance to this analysis, there is a methylation reaction in this pathway, that lies after the target of terbinafine, squalene epoxidase:

Methylation step in ergosterol synthesis (from Uniprot)
Inhibition of ergosterol synthesis can affect S-adenosyl methionine in yeast
The only experiments that I can find linking ergosterol synthesis with the methylation cycle in yeast do not involve anti-fungals. Rather, they involve yeast with mutations in the genes encoding enzymes of ergosterol synthesis. In a study performed by Shobayashi et al. (2006), mutants of the gene, Erg6, encoding the methyltransferase, resulted in the accumulation of S-adenosyl methionione (SAM). Clearly there are other methylation reactions in the cell which utilize SAM, but this suggests that the ergosterol synthesis pathway is so active in yeast that its disruption affects the concentrations of intermediates of the methylation cycle.
What is the relevance of this to methylation in humans?
Although the situation described above confirms a connection between the methylation cycle and ergosterol intermediates in yeast, as mentioned in the original clinical report, it is difficult to see how it relates to human metabolism. This is because, although squalene epoxidase does exist in man, the ergosterol synthesis pathway and the methylation step catalysed by the methyltransferase (the erg6 gene product) do not. In any case, inhibition of a methylation step would result in an increase in SAM, whereas just the opposite appears to be the case in the patient.
Final observations
The clinical report is of one patient with a mutation (MTHFR) in the methylene tetrahydrofolate reductase gene, which would reduce his ability to regenerate the methionine and S-adenosyl methionine needed for methylation. L-methylfolate greatly reduced his symptoms. Nevertheless, this report is for a single patient, whereas “The gene mutation known as the MTHFR affects approximately 45% of the US population”. If MTHFR were the only factor involved in this case one would expect other reports of adverse reaction to terbinafine. In the apparent absence of such reports one suspects that in this patient the affect of terbinafine — whatever it may be — involves some other, yet undiscovered metabolic interaction.