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If plants benefit from carbon dioxide, why is car traffic something bad?
This is going to sound really stupid or as a joke, but... Ever since I was a little kid, I have been confused about the following:

Humans need air/oxygen to breathe in order to live.
Plants/trees/bushes/flowers produce this oxygen, and are thus crucial for humans to survive.
Plants/trees/bushes/flowers need "carbon dioxide" to survive, just like humans need oxygen.
Plants/trees/bushes/flowers MAY also need some oxygen/air? (I assume so.)
Cars (traditional ones) output "carbon dioxide"... yet they are... not good for nature?

I don't understand how this fits together. It seems as if nature should absolutely thrive in the middle of highways and nearby, if they get so much nice carbon dioxide from the cars! Yet cars are instinctively seen (also by me) as "evil nature-polluting machines of death". Car exhaust seems to be the opposite of what a plant or tree wants, yet it's full of carbon dioxide, so... why?
Can somebody explain this once and for all?

There are at least two separate answers to your question.  First, with respect to plants needing CO2, they have evolved to deal with the limited amounts of CO2 normally in the atmosphere.  That's really all they need, or "want": adding more doesn't really benefit them.  Think of it this way: you need water to live, right?  And drink a certain amount of it every day.  But drinking large amounts of water can kill you https://en.wikipedia.org/wiki/Water_intoxication and holding you under water for a few minutes certainly will.  (As in the comment above, and even better example would be oxygen: we need it to live, but too much can cause all sorts of problems: https://en.wikipedia.org/wiki/Oxygen_toxicity )   Likewise, plants need nitrates, but applying too much can kill them.  So extra CO2 in the air is of little or no benefit to plants.
The second answer has nothing to do with plants.  It's that atmospheric CO2 traps solar heat, causing the Earth to be warmer than it otherwise would.  Without the extra CO2 from fossil fuels, Earth maintained a comfortable temperature, one that we'd all (and I mean not just humans, but all life) had gotten used to.  Add more CO2, and more solar heat is trapped, making the Earth uncomfortably warm, to the point that many plants & animals can't live where they are, and generally can't migrate.  So you wind up with a lot of dead plants and animals.
Of course there's more going on than this, things that are feedbacks from and side effects of the increased CO2, such as ocean acidification.  If you really want to know more, here's a good starting place: https://history.aip.org/climate/index.htm

Where is your source for extra CO2 being of no benefit? Here's NASA saying the opposite: https://climate.nasa.gov/news/2436/co2-is-making-earth-greenerfor-now/

@Wayne Conrad: Because there is abundant practical evidence - artificial (or organic) fertilizers, irrigation, &c - that plant growth in natural conditions is seldom limited by CO2.  Even when those other factors aren't limiting growth, predicting long-term response isn't a simple matter, e.g. https://science.sciencemag.org/content/360/6386/317 or https://www.newscientist.com/article/dn11655-climate-myths-higher-co2-levels-will-boost-plant-growth-and-food-production/

@jamesqf It would be helpful if you included that supplementing information into your answer, and maybe add some appropriate caveats as theforestecologist suggests.

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

@Wayne Conrad What about some  "extending", not limiting factor:  and does that mean more plants, not just larger ones?

Exhaust gasses from combustion contain many compounds in addition to CO2.
Some of them under the right circumstances‡ can be of limited benefit to some plants, but others such as ozone are damaging to all forms of life.
Other compounds in vehicle exhaust that are known to cause damage to plants are oxides of sulfur and nitrogen — these react with water to form acids and contribute to "acid rain" that lowers soil pH thereby interfering with nutrient uptake and may also directly damage plants1.
Finally, as noted in other answers increasing levels of atmospheric CO2 due in part to vehicle exhaust contributes to climate change that has a global consequences for plants — this however seems beyond the scope of the original question which appears to be about local effects on trees growing "in the middle of highways and nearby".
‡Note: For example, increased CO2 can be growth promoting at least in the short term.
Reference:
1: Oswalt, C. M., & Clatterbuck, W. K. (2005). Impacts of Air Pollution on the Urban Forest. University of Tennessee, Agricultural Extension Service.

Firstly, I don't think it's entirely clear whether the entire premise of the question is correct. I couldn't find any evidence to suggest that plants don't thrive on highways and areas with lots of cars. If anyone has any data on this, I'd be interested in reading it.
Some of the answers here seem to be a bit light on evidence. Let's look at some data on this.
This report shows that there can be around 1.5-2x increase (from the baseline level of around 410ppm to between 600-800ppm) of CO2 levels in areas surrounding highways. This value varies somewhat depending on whether it is peak time or not, but it seems like the median amount is around 600ppm. I'm aware this is only a single study, so it's perhaps not best to generalise too much, but it should give us a broad idea of how much CO2 increase to expect in areas surrounding highways.
In contrast to what jamesqf said, CO2 enrichment does increase the growth rate of plants, under certain conditions. This has been known for quite a while. Mauney et al (1987) state:

Comprehensive reviews of the plant science literature indicate that a
  300 part per million (ppm) increase in atmospheric carbon dioxide
  (CO2) concentration generally increases plant growth by approximately
  30%.

Importantly, the range of increase that you see in areas surrounding highways certainly increases the growth rate of plants. Ainsworth & Rogers (2007) state:

Across a range of FACE experiments, with a variety of plant species,
  growth of plants at elevated CO2 concentrations of 475–600 ppm
  increases leaf photosynthetic rates by an average of 40%

Furthermore, a recent study showed that the human-caused increase in CO2 levels has actually caused a relative greening of the worlds global vegetated area. So this isn't just an effect of ideal conditions in FACE experiments, it also occurs 'in the wild'.
However, it's not quite as simple as increased CO2 -> increased growth. As we can see from the figure above, the levels of CO2 in the highway vary temporally between peak and non-peak times. Fluctuations in CO2 levels actually reduce the growth rate of plants, for various reasons. White et al (2020) state:

..we calculated that yields increased 65% as much in fluctuating
  elevated CO2 of FACE as in constant elevated CO2

So it certainly seems like this might have an effect of reducing plant growth on highway areas.
As other people have alluded to, the other thing to remember is that cars produce a high level of other particulate from the exhaust fumes, which certainly have a large negative impact on the growth of plants. Power et al (2011) state:

A wide range of effects were detected, including growth stimulation
  and inhibition, changes in gas exchange and premature leaf senescence.
  This was complemented by controlled fumigations with NO, NO(2) and
  their mixture, as well as a transect study away from a busy inner
  London road. All evidence suggested that NO(x) was the key phytotoxic
  component of exhaust emissions, and highlights the potential for
  detrimental effects of vehicle emissions on urban ecosystems.

Overall, it seems likely that a combination of fluctuating CO2 levels (rather than constantly high levels) and particulate pollution might cause a reduction in plant growth around highways.

Back in the early days of climate science, there were some scientists who considered the possibility that increased CO2 production would lead to increased plant growth, and that this in turn would result in keeping the oxygen-carbon dioxide balance more or less stable. This was referred to as the "Gaia hypothesis" and basically revolved around viewing the entire ecosphere as a "living organism" that would maintain itself.
To an extent, this does happen.  Increased CO2, by itself, may result in increased plant growth.  So may increased temperature resulting from the increased CO2 trapping the sun's heat (the greenhouse effect).
The problem is that we're producing way too much of it, way too fast.  Even if the atmosphere and climate are becoming more favorable for plant growth, plants can only grow so fast - and it's not fast enough to stop carbon buildup from increasing the planet's temperature to levels that may make things difficult for existing forms of life (including humans).
Also, we're destroying plants, both through direct deforestation and indirect desertification, faster than they can grow even with the more favorable conditions, which doesn't help matters.
So you're not wrong - carbon dioxide production may increase plant growth.  But it also causes problems, and plants can only mitigate those problems - and they can't mitigate them fast enough.

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Ignoring for a moment the other pollutants emitted from car exhaust, increased CO2 levels are warming the planet, through what is called the "greenhouse effect".
Photosynthesis is a set of reactions where CO2, water and sunlight are turned into chemical energy used for plant life.
However, these reactions only work well in a narrow temperature range.
As plants heat up past a certain point, they can't run some photosynthetic reactions as well, or at all.
As the atmosphere heats past a safe range, plants must divert resources to making so-called "heat shock proteins" or HSPs to protect photosynthetic machinery.
If the atmosphere gets too hot, plants suffer irreversible damage, can no longer generate energy to live, and therefore die.
https://bmcplantbiol.biomedcentral.com/articles/10.1186/1471-2229-14-111

You really have a good point, maybe you want to check this paper https://bsapubs.onlinelibrary.wiley.com/doi/full/10.3732/ajb.95.2.165  It looks like C3 plants could thrive in the near future, although C4 species could have an advantage during years with water stress.But temperature wise, in a high CO2 environment C3 plants perform better

It seems as if nature should absolutely thrive in the middle of highways and nearby, if they get so much nice carbon dioxide from the cars!

In fact, some species of plants are likely to thrive from the excess pollution coming from cars, provided they can tolerate the hotter summers and grow quickly enough to take advantage of the higher CO2 levels.  Unfortunately, many of the plants people care about are not going to be the ones that benefit most.

Yet cars are instinctively seen (also by me) as "evil nature-polluting machines of death".

"Nature" colloquially refers to "plants and animals as they are currently".  Pollution doesn't destroy nature, but it does change it, which people tend to perceive as bad because we are prepared for the world around us being a certain way.  For example, more Co2 is likely to be very good for cockroaches and mosquitoes (which thrive in warmer weather), so some of the plants and animals that currently do well will be exchanged for more bugs.  People who have to deal with more roaches and mosquitoes will probably perceive this as bad, even if those insects are still part of nature.

Excellent point about "change" -- the long time scale perspective suggest "change" and not "destruction" its occurring. However, you need to provide citations or other forms of support for the basics points made in your response. Thanks

'Destruction' is only the name we give to rapid changes

Anthropogenic Climate Change is why carbon dioxide, from fossil fuel powered transport in combination with other fossil fuel uses is considered problematic  - i.e. "bad".
With respect to plant health insufficient carbon dioxide is not a problem; even with some plants getting some benefit from raised carbon dioxide concentrations those benefits are outweighed by the harms and costs expected to accrue from climate consequences of profligate fossil fuel burning.
About the climate consequences the US National Academy of Sciences says -

Climate change is increasingly affecting people’s lives. It is having
  significant effects on infrastructure, agriculture, fisheries, public
  health, and the ecosystems that support society. It is also changing
  the environment in ways that affect the distribution, diversity, and
  long-term survival of species of plants, animals, and other forms of
  life on Earth.


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In the PR segment of an ECG, how come there's no current flowing?
I don't really know how to phrase the question, but to put it as clearly as I can, I don't get why it is the P wave "flattens down" when the atria have completely depolarized. I get that the charge is uniform across the atria, but the ventricles are still polarized (and therefore of a different charge compared to the now completely depolarized atria), wouldn't this create a difference in charge and therefore a voltage to produce a current? I think this GIF can help explain my question better:

At frame 12:

I don't understand why there's no current flow and no deflection on the ECG leads despite the charge difference. Rather, why does the GIF deal with the current and charge difference in the atria and ventricles separately? I thought this all might be because of the fibrous cardiac skeleton, which acts as an electrical insulator, but that doesn't make complete sense either; sure it prevent current flow within the heart, but it wouldn't influence current flow outside of it, right?

I'd suggest reading the rest of the Wikipedia article on EKG rather than focusing on the particular cartoon you are using right now, because that cartoon does not depict the dipoles that are measured.
The key interpretation that you are missing is that the signals measured are not voltage differences between intracellular compartments of the heart (like between the atria and ventricles, or between the depolarized and polarized part of one compartment), but a moving dipole created during polarization changes.
As the atria depolarize, there is a wave of negative extracellular charge as positive ions enter cells, creating a dipole: there is more negative charge at the most recently depolarized point than ahead of the wave where cells haven't yet depolarized. This is the signal you measure. If you were to pause this process at any moment, those extracellular charges are free to move and the potential dissipates quickly.
There is too much conductivity in the extracellular space for the dipole to be maintained without the rapid polarization changes that occur when ion channels open. You can think of this as a high-pass filter; the amplitude of the dipole measured would approach zero as the speed is reduced regardless of static differences in intracellular voltage measured against some reference.
This is what happens during the brief "pause" between atrial and ventricular contraction: there is still a dipole, but it is much smaller as it travels through the AV node than in the muscle and would only be measurable from local electrodes. You begin to see the signal again once the ventricles contract.
http://umdberg.pbworks.com/f/Hobbie-EKG-1.pdf may also be useful.

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Research on chicken that cannot feel pain
In was having a conversation about the ethics of vegetarianism, and if it is right to cause pain to other animals.
It is then that I stumbled upon the question, that if, just the way chicken and many other animals have currently been cultured or genetically modified (or by any other means) to have certain desirable qualities (from market and demand perspective) such as the fat content, quality of eggs etc., will it be fine to consume chicken if we also, if possible, raise chicken that do not feel any pain at all (if that is defined, or can we define that?).
I realise that this is not philosophy stackexchange, so I would not ask about the ethics of it.
What I want to ask here is this: is such research taking place (anywhere on earth) to develop breeds of chicken that do not feel pain, if yes I would be thankful to know at least the basics, and if not, do you think it is possible in the near future or what possible approach would you contemplate?

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Inability to feel pain seems likely to make an animal accident-prone.

I used to raise chickens (among lots of other animals.) Chicks peck at anything that stands out, they can't help it. They don't do it to be cruel. If another chick didn't get out of the way when pecked, it would get a bloody or bald spot on it, which would attract more pecks, and further injury, etc. Eventually these chicks die of infection. I've seen it happen a lot to a particular kind of chick (called broilers) bred to grow quickly to market size. Unfortunately, they were also dumber than a box of rocks, and didn't get out of the way. Since I didn't debeak chicks...

...the broilers had more than a 50% mortality rate when raised with normal chicks. It was heartbreaking, and I had to isolate the broiler chicks, and never had the heart to eat them though they grew to be very large. They were also very docile, so easy prey for foxes, coyotes, etc. But my point in all this is... pain matters a lot to survival. I doubt a chick without pain would have much chance to survive to adulthood.

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Is it possible to artificially induce a 40°C fever in a controlled and safe manner?
In search for any possible new treatments for COVID-19, I am of the understanding that the SARS-nCoV-2 virus may suffer deterioration at high temperatures and high humidity, to perhaps weaken it sufficiently for your immune system to be able to handle it.
Is there any research done on artificially inducing a (let's say) 40°C fever, in a controlled manner, such that brain function will not be endangered?
(Are there any fundamental biological functions that would prevent this possibility?)

Possibly Related Questions:

Should we induce fever to assist healing?
How does fever physically work?
Paper shows 2 hours of high humidity and hot temperatures kills corona virus, does this stop the spread of the virus?
What are the environmental conditions for 2019-nCoV to survive?

References:
[1] https://www.cancer.gov/about-cancer/treatment/types/surgery/hyperthermia-fact-sheet
[2] https://en.wikipedia.org/wiki/Hyperthermia_therapy
[3] https://en.wikipedia.org/wiki/Thermoregulation
[4] Janeways Immunobiology (book)

SE Biology is concerned with the mechanisms of biological processes, and questions are generally answered by people with biological rather than medical or epidemiological expertise. It is possible, therefore, that some questions about coronaviruses relating to the recent 2019-nCoV outbreak may not receive a satisfactory answer. You may therefore wish to consult this list of reputable external sources of such information.

In my opinion this question is off-topic. Ostensibly it is asking for information on physiological or medical research, and in this respect it is not asking for an answer to a biological question. However the reality is that it is a question asking for discussion on a proposal for a treatment for an infectious disease. As such it falls in the category of questions of the type "I have this great idea, do you think it's right?", which can only have subjective answers. As the "great idea" it propounds is a medical treatment, it is particularly inappropriate on this list and at this time.

@David Ok, so what do you propose I should do? Close the question?

Yes I think that would be best.

In search for any possible new treatments for COVID-19, I am of the understanding that the SARS-nCoV-2 virus may suffer deterioration at high temperatures and high humidity

If you are referring to the linked question, that is for virus in air on a dry surface.  It is a test of how long the virus can survive outside of a host before it is desiccated and destroyed by the environment.  It is not relevant to viral particles inside of an organism.

Are there any fundamental biological functions that would prevent this possibility?

There is little evidence that elevated body temperature has much effect on duration of infection with most common viral diseases. This is why antipyretic drugs are commonly recommended for people with viral infections.


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Why does constant current in electrophoresis mean that the molecule moves at the same rate?
Two part question:
Part 1:
I have always learned that when running a SDS-PAGE current is what decideds how fast the macro molecules migrate.
However, if the force excerted on a molecule is equal to charge times electric field.

Then wouldn't the speed at which the protein migrates depend more on voltage then current? As the the electric field is a measure of Voltage across an area.
Also, does this change based on the type of electrophoresis? (specifically, Agarose/DNA, and native page)
Part 2:
How do you calculate the time it would take for a molecule to reach the end of a gel based on the length of the gel and either the voltage or current?

Related

Voltage is proportional to current, so it depends on both equally.  Constant current is safer though, since as the resistance drops, so does the power dumped into the circuit.

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text:
Is the backward positioning of photoreceptors bad design?
(Several questions have been asked about this topic but most are quite old and there has been at least one study since then that has attempted to answer this in a new way)
Since photoreceptors are placed at the back of nerve cells in vertebrates, these nerves have to then bundle up before passing to the brain, leading to a blind spot. This video (from a usually reliable channel) from 2:30-4:00 says that its bad design and is just something the initial eyes in vertebrates fixed on, and was too difficult to correct later.
But this report of a study from 2015 says that this arrangement helps vertebrates see colours more easily during daytime, and is not a bad design.
Even if this design does help in seeing colours better, the same effect could have been achieved through other means without having to create a blind spot, no?
Can this be called a bad design or not?

Properly speaking, you should not use the word "design" when talking about evolution. All you can describe are more or less fit variations. A variation that is advantageous in one context can be detrimental in another.
That being said, I assume what you are asking is whether the eyes could be better, as if an engineer would design them from scratch. The answer is "probably yes". The backward wiring of the photoreceptors is an issue that the brain has mostly been able to work around, but it is obvious that forward-facing photoreceptors would be easier to work with. There are multiple issues, one is the blindspot as you identified. Another one is the diffraction of the light by the ganglion cells fibers. Part the light is adsorbed too, so because of the non-homogeneous thickness of the macula there are color distortions near the center of the visual field. But again, it is not impossible that having a forward-facing retina would be more detrimental in some environment, although I fail to think of a case where a backward retina would be better.
As for the sources you cite, I watched only part of the video but it was very spot on. The science daily article however is very misleading. Frankly, the quoted scientist doesn't seem to have a very good grasp of evolution. Though the actual paper is more nuanced. Basically it is possible, as suggested by the authors, that some mechanism mitigates the scattering of light by the retina. That does not mean that the retina is backward because of that. Claiming as one of the authors did that they have "explained why the retina is built backwards" is very, very, bad logic. With forward-facing photoreceptors you wouldn't even have to have such a mechanism. And as pointed out by the video you linked, cephalopod's retinae are not backward.

One big downside of forward facing photoreceptors is that that design requires either a larger eyeball or a stronger lens. I'd say that it outweighs both the blind spot and the occlusion by other structures (which can be subtracted out because it's constant in time)

@JohnDvorak Good point. The thickness of the retina would also need to be more homogenous.


text:
Expression of eukaryotic ribosomal DNA
The Wikipedia page for rDNA says "Ribosomal DNA (rDNA) is a DNA sequence that codes for ribosomal RNA" Also, the figure next to it says "The gene segment of eukaryotic rDNA contains 18S, 5.8S, and 28S tracts and forms a tandem repetitive cluster". So, it gave me the impression that rDNA codes for both rRNA and the structural proteins of ribosome. Is that right?

Wrong. Read about ribosomal protein genes.

Thanks David! Could you tell me, what exactly is meant by "The gene segment of eukaryotic rDNA contains 18S, 5.8S, and 28S tracts and forms a tandem repetitive cluster; the 5S rDNA is coded separately. NTS, nontranscribed spacer, ETS, external transcribed spacer, ITS, internal transcribed spacers 1 and 2, numbered from 5' end."  in the picture (https://en.wikipedia.org/wiki/Ribosomal_DNA#/media/File:Eucaryot_rdna.png)

As well as messenger RNA (mRNA) that encodes protein, there are a variety of RNAs that have structural or regulatory roles and do not code for protein. Ribosomal RNAs (rRNA) are one such structural RNA. Like mRNA, rRNA (and other stable RNAs) are  specified by genes in the chromosomal DNA, although the details of their transcription (the RNA polymerase employed and the nature of the promotors) may vary.
The mature eukaryotic ribosome contains three species of rRNA that are analogous to those in prokaryotes — 18S (cf. 16S), 28S (cf. 23S) and 5S (sizes for mammals). However there is an additional 5.8S species in eukaryotes. The questions addressed in the article are: 1. What genes and what transcripts give rise to these mature RNA species? and 2. Is there a single gene for each species or multiple repeated genes? A third, implicit, question is whether the situation in eukaryotes is similar to that in eukaryotes.
The answer to question 2 is given in the phrase “forms a tandem repetitive cluster” — there are multiple copies of the genes for 18S, 28S and 5.8S rRNA, clustered together one after another. These genes are separated (‘spaced apart’) by regions of the genome that are not transcribed, and are termed non-transcribed spacers (NTS).
(There are also multiple copies of the 5S rRNA gene, although these are only clustered in some species.)
The answer to the first question is that the 18S, 28S and 5.8S rRNA are transcribed from a single gene and are initially present in a single transcript. This is processed by ribonucleases to generate the three mature species. If one compares the sequences of the mature species with that of the gene/transcript one can identify portions of the initial rRNA transcript that are not present in any of the three mature species. These are termed transcribed spacers. The one at the 5′ end of the transcript is termed the external transcribed spacer (ETS), and those that are between the three mature species are termed  internal transcribed spacer (ITS).

The situation in prokaryotes differs from eukaryotes in so far as the 5S rRNA gene is part of the gene/transcript containing the 16S and 23S rRNAs, lying at the 3′ end of this. This is mentioned in the Wikipedia entry for Ribosomal RNA, rather than that for ribosomal DNA, quoted in the question, and illustrated in the figure below taken from the teaching web pages of Ross Hardison at Penn State University. Notice the transfer RNA gene in the transcript between the portions resulting in the mature 16S and 23S rRNAs.

Thank Dav! You have been very helpful to me. Thank you so much!

"rRNA are synthesized in a different pathway. In the nucleolus, the rRNAs combine with ribosomal proteins to form the large and small subunits of the ribosome. Ribosomal proteins are synthesized in the cytoplasm and transported to the nucleus for subassembly in the nucleolus. They autoassemble in a long complicated maturation process which ends in the cytoplasm (ER)". https://www.nature.com/articles/35030006 says there's more rRNA than protein in the ribosome, so there are a lot of copies of those few transcripts. Did they succeed in producing ribosomes in-vitro from the separated ingredients?

@reuns — As I understand it you are asking either one or two supplementary questions. In answer to the question in your final sentence. Nomura reconstituted bacterial ribosomes in 1968 (if I remember rightly) and showed that resistance (or sensitivity — I forget) to streptomycin was a property of one specific protein (S12). People I knew were trying unsuccessfully to do the same thing for eukaryotes in the early 70s, but I imagine (and seem to remember) that was subsequently achieved. As assembly in vivo occurs on the rRNA precursors, the reassembly in vitro is somewhat artificial.

Tks, also I realize what I said was wrong (for prokaryote) the 30s subunit contains only one single stranded rRNA (secondary structures make it locally double stranded) of 1500 nucleotides each containing about 20 non-hydrogen atoms gives the 30000 rRNA atoms mentioned in the nature article. Thus (for the small subunit) it is about assembling 1 rRNA and 21 proteins which is doable and has been achieved since 40 years. This explains why the map of the 30s is described in term of 5' central and 3' parts


text:
How many kingdoms are there actually?
I am wanting to learn (memorise) some of the tree of life; the classification of organisms. So I have come across a lot of kingdoms in my research. Basically, I don’t want to waste my time learning the wrong thing, so my question is this. Is there an official or most recent system of classification, some authority in organism classification that we look to? After kingdoms it seems pretty clear, the phyla in (say Animalia) seem pretty defined and uncontraversial.
These are all of the ‘kingdoms’ I have found while researching. Some are called kingdoms in one source and not another. I know that some overlap others. This is just to throw every possible example out there.
Animalia, Apusozoa, Archae, Archaebacteria, Archezoa, Bacteria, Biliphyta, Chromista, Chromophyta, Ciliofungi, Cryptophyta, Eufungi, Euglenozoa, Excavata, Filastera, Fungi, Monera, Nucleariida, Plantae, Proteoarchaeota, Protista, Protozoa, Rhizaria, True bacteria, Viridiplantae
I don’t ask that you go through them and explain them. Only what the actual system of classificating organisms is. On that note. As far as I’m aware, there’s two types of domain systems. Two are Eukaryota, Archae/-bacteria, Bacteria. Another is Eukaryota, prokaryota. A clarification on this too would be appreciated.

All of the hierarchical classification schemes are somewhat arbitrary. There is a real tree (with some complicated attachments due to horizontal gene transfer), but the labels placed on different levels of the tree are made up and subject to opinion and argument. The kingdoms are probably the most poorly defined within that classification because as a group they are not monophyletic at all.

Welcome to Biology.SE! As @BryanKrause says, there is no "correct" answer since these are classifications made assuming a simple branching topology that can not completely encompass the complexity associated with living organisms. The wikipedia article on this and the many linked articles are a good place to start learning about this subject. ——— As for domains, "prokaryota" is invalid since it is not monophyletic.

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

Why do you wish to memorize this? Science involves understanding, not recall of “facts”.

@David as you can see I am not a biologist. I lurk more in the realm of mathematics, and so naturally, systems of organisation interest me, so why not that system which organises all living organisms. It's mostly for trivia because I think it's interesting; I don't intend to use these 'facts' in my occupation when I'm older.


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how the coronavirus was distinguished?
I have read a lot about the outbreak of the coronavirus, I know that in january scientists had already sequenced the viral genome.
How was the virus identified prior to the sequencing
Given that viruses are not like germs that you can see and distinguish readily in microscope, how could scientists know that there was something new about the new disease and how could they purify the pathogen that cause that disease without knowing what it is and without knowing its genetic code?
Where can I find information about procedures that are used to identify new viral pathogens?
Given that there is a group of people with suspicious desease, what are the laboratory procedures used to eliminate known pathogens and how you discover that you have a novel virus without knowing its genetic sequence (and without the ability to extract it - as far as I know you can not isolate virus particle with tweezers...).
Thank you!

Welcome to Biology.SE! Please take the [tour] and then go through the help pages starting with [Ask] questions effectively on this site and [edit] your question accordingly. In particular, you seem to be asking for someone to summarize an entire field, which may not be practical on this site. ——— We also 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). Thanks!

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

This is basic epidemiology. When medical professionals notice that a group of people with some characteristic in common, are being seen for a similar disease, they ask if there's a connection. In this case, several people in Wuhan were diagnosed with severe pneumonia, and the doctors noticed that they worked in the same location.

Three adult patients presented with severe pneumonia and were admitted to a hospital in Wuhan on December 27, 2019. ... Her occupation was retailer in the seafood wholesale market. ... He had been a frequent visitor to the seafood wholesale market.

--A Novel Coronavirus from Patients with Pneumonia in China, 2019
You're more likely to follow up when the disease is unusual or severe, and when the connecting factor is unusual or suspicious. In this case, the severe pneumonia was presumably unexpected, and live animal markets always have potential for disease transmission.
(In fact, it's quite possible that the virus had been circulating in the region for weeks before this cluster was noticed, and that previous cases had not been surprising enough to trigger the research needed to identify a new virus; though it's also likely that the medical personnel in Wuhan had noticed that there were an usually high number of pneumonia cases and were already looking for a connection.)
See also the answers to How did scientists discover HIV?. Old-fashioned epidemiology is always critical.
The same article explains how the virus was sequenced:

Bronchoalveolar-lavage fluid samples were collected in sterile cups to which virus transport medium was added. ... RNA extracted from bronchoalveolar-lavage fluid and culture supernatants was used as a template to clone and sequence the genome. We used a combination of Illumina sequencing and nanopore sequencing to characterize the virus genome.

And isolated:

... supernatant from bronchoalveolar-lavage fluid samples was inoculated onto the apical surface of the cell cultures. ...  After three passages, apical samples and human airway epithelial cells were prepared for transmission electron microscopy. ...

So briefly, they took patient samples, grew them on cultured cells, used electron microscopy to check the kind of virus. They sequenced fluid (not cells, since the virus would be secreted into the fluid, making it a relatively pure source of virus RNA) and then sequenced using a standard high-throughput sequencing approach; knowing the likely kind of virus would make this easier but isn't essential. There would have been lots of human RNA in the sequence, but it's easy to bioinformatically separate that out and limit your analysis to the viral sequences. The virus isolate was also not essential for the identification; knowing the sequence is the critical information today. But having a virus isolate certainly makes all the subsequent work much easier.
This is pretty standard modern molecular biology, not an esoteric skill.

it doesn't answer my question. i didn't ask about that stage. i'm asking after you understand that there is a group of people with suspicious desease, what are the laboratory procedures used to eliminate known pathogenes and how you discover that you have a novel virus without knowing it's genetic sequence (and without the ability to extract it- as far as i know you can not isolate virus particle with twizzers...).

The article I linked also explained the isolation in detail. I've edited it into the answer. These are standard modern molecular biology techniques and most reasonably modern infectious disease labs would be able to do them.

thank you............!

@ iayork    'RNA extracted from bronchoalveolar-lavage fluid and culture supernatants was used as a template to clone and sequence the genome' i still don't understand how could they know wich of the templates is that of the suspected virus. also, when extracting RNA from tissue you get a lot of different sequences, many of them belong to the patient's own genome or to other unharming viruses and microbes. how can you know which primer is the one you are looking for? . (i've learned MB of the cell, still i don't know how to approach this issue)  thank you!

Not much human RNA in the fluid, but the virus gets secreted there. In any case, it’s easy to bioinformatically drop out the human sequences in your computer after the fact, leaving just the virus.


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How does high-intensity aerobic exercise affect the brain?
I have been reading articles claiming that serotonin, endorphins and BDNF are produced during exercise, but they never mention the intensity or duration of exercise for this to happen.
To not make this question too broad, I want to narrow it down to, lets say, a 4-5k run over 20 minutes. Also, I want to restrict it to the body's response during these 20 minutes.
How will this affect the brain? Which chemicals do the body produce/release into the blood stream that could have an effect on the brain? And, how much?
I am asking because I am always curious about the mechanisms underlying the effects of exercise on the brain and because it's always difficult to find information regarding results of exercise; Googling mostly results in content marketing articles (like this one for Buffer).

In this article The Effects of Acute Exercise on Mood, Cognition, Neurophysiology, and Neurochemical Pathways: A Review (Brain Plasticity, 2017), there's a comprehensive table The Time Course of Behavioral, Functional, Physiological, and Neurochemical Effects of Acute Exercise (scroll to Fig 1 and zoom it) that shows the duration and intensity of exercise needed for the effective release of cortisol, neurotrophins (BDNF, IGF-1), neurotransmitters (dopamine, norepinephrine, serotonin, acetylcholine, GABA and gltamate) and endogenous opioids.
Examples of effects of exercise on the cognitive function and mood:

Prefrontal-dependent cognitive function (learning, memory): 50 min exercise at 85% of age-predicted mean heart rate
Enhancement of positive mood: low to high intensity exercise 7-70 min
Decrease in negative mood: 60-120 min exercise at ~50% intensity

Cortisol:

In humans, acute exercise stimulates the HPA axis in an
  intensity-dependent fashion, with increases in cortisol occurring
  after a threshold amount of exercise that equates to a duration of 10
  minutes or more at approximately 60% of VO2 max or greater...After
  exercise cessation, peripheral cortisol levels peak around 30 minutes
  and remain elevated for up to two hours.
...cortisol strongly influences learning and memory...The extent
  to which cortisol influences learning and memory processes depends on
  several factors including the intensity of cortisol elevation. For
  example, moderate increases in cortisol enhance working memory...Cortisol elevation over a certain threshold, however, serves to impair memory...
acute exercise also helps mitigate the debilitating effects of stress.

Brain derived neurotrophic factor (BDNF):
Moderate exercise for 30 minutes can release BDNF.

...studies have shown a positive association between acute
  exercise-induced peripheral BDNF levels and short-term memory as
  well as motor skill memory.

But, this does not work in everyone and not in all circumstances...
Dopamine:

Twelve, healthy, regular exercisers underwent PET scans after either
  rest or 30 minutes of treadmill running at 85% of age-predicted MHR.
  Surprisingly, dopamine was not found to increase after acute exercise
  in these humans.

Serotonin:

Acute exercise significantly increased plasma serotonin, with a
  positive linear correlation found between serotonin concentration and
  exercise intensity.
As serotonin regulates mood, emotion, sleep, and appetite, and
  dopamine regulates motivation memory, reward, and attention, the
  central fatigue hypothesis claims that the interaction between these
  two neurotransmitters contributes to exercise-induced fatigue, with a
  high serotonin to dopamine ratio supporting a low activity, exhausted state and a low ratio supporting a high activity, activated
  state.

The effects of exercise-induced increase of norepinephrine and acetylcholine on cognitive function are not well known.
Endogenous opioids (ß-endorphins, enkephalins and dynorphins) and endocannabinoids:

Neuromodulators are involved in a variety of processes including pain
  modulation, reward, response to stress, and autonomic control.
In humans, acute exercise causes significant increases in peripheral
  levels of endogenous opioids; this effect is intensity-dependent,
  corresponds to acute exercise-induced changes in HPA axis hormones,
  and is linked to improvements in mood.
Though the endogenous opioids have received much attention in terms of
  their involvement in the “runner’s high”, scientists are beginning to
  understand that endocannabinoids may be equally or perhaps more
  involved.

Other sources:
Effects of physical exercise on anxiety, depression...(Clinical Psychology Review, 2001):

Acutely, emotional effects of exercise remain confusing, both positive
  and negative effects being reported.

...or as Alex Corb, PhD says in Boosting Your Serotonin Activity (Psychology Today):

Interestingly, if you try to do too much exercise, or feel forced into
  doing it, it may not have the right effect. Recognizing that you are
  choosing to exercise changes its neurochemical effect. That may be a
  result of your ancient instincts — the difference between running
  because you're hunting something, and running because it's hunting
  you.

How to increase serotonin in the human brain without drugs (Journal of Psychiatry & Neuroscience, 2007):

Exercise improves mood in subclinical populations as well as in
  patients. The most consistent effect is seen when regular exercisers
  undertake aerobic exercise at a level with which they are familiar.


text:
Are there any animals that are unable to hear the human voice?
Humans and animals have different hearing ranges. The frequency range of a human, for example, is stated with 20 Hz to 20 kHz, whereas the fundamental voice frequency is stated with 125 Hz for men, 250 for women and 440 for children.
Now if I understand correctly, the hearing range of bats, for example, is commonly stated with 1 kHz to 200 kHz (depending on species). The hearing range of mice is stated with 1 kHz to 70 kHz.
Are there (apart from those with no sense of hearing at all) any animals that are unable to hear human voices at all?
(Edited in reaction to the first and the second comment below. Humans can obviously realise speech with energy at much higher frequencies. My examples are in this respect misleading.)

In your background information you may be misinterpreting the meaning of fundamental frequency; human speech includes substantial energy at much higher frequencies than the ones you mention, centered around about 1 kHz on a log scale.

There are plenty of animals that don't have a sense of hearing. E.g. I don't think sponges or jellyfish have a sense of hearing

Thank you, Mr Krause, for your remark. I have indeed misinterpreted the meaning of fundamental frequency and insofar given misleading examples. I do realise that humans are able to realise speech at much higher frequencies than at fundamental level. My original question, however, if there are animals that  do have a sense of hearing and yet are unable to hear the human voice, remains. Thank you,

Are there (apart from those with no sense of hearing at all) any
  animals that are unable to hear human voices at all?

I don't know of any examples off the top of my head, but let's think about this systematically.
The voiced speech of a typical adult male will have a fundamental frequency from 85 to 180 Hz, and that of a typical adult female from 165 to 255 Hz.
These are fundamental tones, and DO NOT include overtones (harmonics) of higher frequencies, that are actually responsible for the timbre of the voice, i.e. its characteristic sound and full content sonic content.
Here is a Fourier transformation of an audio clip of a female voice (a plot of frequency vs. amplitude, whereby the original recording was broken down into its constituent sine waves).

As you can see, the vocal cords produce overtones up to - and beyond - 7.5kHz. These overtones theoretically go to infinity in frequency, but are very negligibly quiet past around 10kHz in our case. Certainly very low in terms of decibels (though do not confuse real decibels with the -70dB sensitivity on the graph; with audio processing gear, 0dB is at which the signal is maximally saturated, or 'clips'). Let's assume 10kHz is the upper limit for normal female speech.
Keep in mind this does NOT mean that one could not perhaps sing a high note, and produce overtones past 10kHz - this is in fact doable. But let's stick with regular speech in our case.
Below you'll find the hearing ranges of some animals (source).

You'll find that all animals listed (save one) can hear some significant range of a regular (female) human voice. The little brown bat would not be able to hear the upper harmonics of a typical female speaker, given that they speak in a monotone.
Lastly, please keep in mind the difference between decibels ('loudness') and frequency (ability to sense a pitch). Some of the extreme high overtones are very quiet, so even if an animal would be able to sense them, they may not have a sensitive enough ear to pick up how quiet these sounds would be.
And really lastly, remember that sound produces vibrations and resonates through objects that sound waves hit. These resonate at different frequencies, so your voice can be sensed indirectly too through these resonating frequencies.

I hate to upvote an answer to what I consider a poor question, but I congratulate you on the evidence you have brought to bear on this.


text:
Can the apparent drop in insect population be explained by local insects evolving to avoid traps?
In this widely reported Plos One article, it is stated that, after roughly 3 decades of placing Malaise traps in a set of predetermined locations (counting and replacing them regularly), a sharp decline (roughly 75%) of insect population is observed. The idea is that the amount of insects caught in the traps is a proportionate representation of the insect population.
This seems to be a very important publication. It is getting reported in many popular articles as the most compelling evidence for a massive recent decline in insect biomass.
Maybe I didn't read the article thoroughly enough, but I saw no mention of the possibility that the local population (around where the traps are set) are adapting to avoid the traps. Since getting caught in a Malaise trap is lethal, genes that promote the behavior of avoiding those traps would thrive, in a local population of flies, at a higher proportion than their competitors. And since flies reproduce very quickly, 27 years seems (intuitively, to me) like a lot of time for this new local selection pressure, created by the experimenters, to make notable changes in a local fly population--particularly, their tendency to avoid Malaise traps.
Could the result of the linked article be explained by local flies adapting to the new selection pressure of Malaise traps?
When I first read about the methods with which the insect population drop was measured, this was the first possibility that came to my mind. But I can't find anywhere where this possibility is discussed. Could that be because it's so ridiculous that it's not even worth considering?

Welcome to Biology.SE! I would guess that the selective pressure exerted by these traps is too small to have a significant effect — do you know how many insects are being killed relative to the entire population? In addition, do you have any reason to think that flying insects have an isolated local population? ——— You may also wish to take the [tour] and then go through the help pages starting with [Ask] questions effectively on this site. Thanks!

@tyersome Yes, thanks. Intuitively I feel like the effect should be so small that it's likely negligible. However, if I understand correctly, gene with even a 0.001% replication advantage, given enough generations, can eventually dominate a population. And 27 years is a tremendous number of generations for flies. I want to know if the dynamics were considered for this particular case.

From your own PlosOne link comes proof that the selection pressure was very weak:
"Most locations (59%, n = 37) were sampled in only one year, 20 locations in two years, five locations in three years, and one in four years, yielding in total 96 unique location-year combinations of measurements of seasonal total flying insect biomass."
"We collected in total 1503 trap samples, with an average of 16 (4–35) successive catches per location-year combination"
"Between 1989 and 2016, a total of 53.54kg of invertebrates have been collected and stored, over a total trap exposure period of 16908 days, within an average of 176 exposure days per location-year combination."
Wikipedia says about houseflies: "12 generations may occur per year"
https://en.wikipedia.org/wiki/Housefly#Life_cycle
27 years gives 444 generations. That is not a lot of time for evolution, especially with such a weak selection pressure.

There are many other lines of evidence over many decades, using many techniques, all showing declines in insect populations.

Climate-driven declines in arthropod abundance restructure a rainforest food web
Worldwide decline of the entomofauna: A review of its drivers
Where have all the insects gone?
As Insect Populations Decline, Scientists Are Trying to Understand Why
The Great Insect Dying: Vanishing act in Europe and North America
Defaunation in the Anthropocene
What’s Causing the Sharp Decline in Insects, and Why It Matters

Coming up with excuses for the one study misses the forest for the trees.

Thanks, but this does not answer the question. My question does not address whether insects are really declining or not, only whether this particular method of measuring change in insect population is susceptible to adaptation as a confounder. (The bold text is my question, but I can see how my title can be interpreted more broadly. Perhaps I should edit that.)


text:
Which test can be used to diagnose typhoid fever
The only thing I found was the widal test, which is no longer an acceptable clinical method. I can't find much information about this anywhere else other than the test needs to analyze samples of blood, poo, and pee. Is there a specific name for this test?

Welcome to Biology.SE! Please take the [tour] and then go through the help pages starting with [Ask] questions effectively on this site and [edit] your question accordingly. In particular, it is good to check multiple sources before posting — have you read the wikipedia article on typhoid? Thanks!

I have voted this question as off-topic for SE Biology as it is merely asking about current clinical practice rather than about the biology underlying a medical condition or test. It might be on-topic on SE Medical Sciences.


text:
What could the etymology of Phallodriline be?
I'm reading about a series of gutless worms described in several papers as phallodrilines. A search in the World Register of Marine Species shows that there is a subfamily called "Phallodrilinae", but then, in at least one paper this term is used to collectively describe gutless worms in several taxa including Oligochaeta, Annelida, and Clitellata. Since they're also described as club-headed I'm assuming that "Phallo-" is from the Latin for penis, but what would be the rest?

I'm voting to close this question as off-topic because it seems to be entirely about etymology rather than biology.

Phallus in Latin means penis, while drilus is the New Latin word for Greek

δρῖλος (drîlos)

which means both worm or erect penis.
Here you can check some sources corroborating my claim:
Merriam Webster dictionary
Wiktionary: δρῖλος (drîlos) means verpus
Liddel & Scott Lexicon
Drîlos meaning penis in Greek

-o- linking vowel indicates Greek. -i- is Latin, unless the second word starts with a vowel (many -ectomy words for example). This is irrespective of declension or gender. Weird I know.
In fact, Latin phallus is from φαλλός.
The second part is worm δρῖλος (drilos). Actually it can also mean penis, but let's gloss over that...


text:
How are cells that have died replaced by new ones?
I'd like to have a clearer picture how cells that have died are replaced by new ones.
I assume the following:

Normally, when a cell dies it will be replaced by a new one of the same type.
It will be replaced by the division of another cell (of the same or another type). One copy remains where it is and keeps its type (for later use) and the other one possibly travels to its target location (where the died one has lived) and possibly changes its type (during travel or after arrival).

My questions are:

Are these assumptions essentially correct? Or are they overly simplified?
What are possible distances between the regenerating dividing cell and the target location? I assume some static cells will be replaced in situ, possibly skin cells. Others may be regenerated far away, especially floating cells, like blood cells.
If the distance is large: How does the regenerating cell know it has to divide? And how does the regenerated copy know where to travel to?
When one of the copies of the regenerating cell starts to travel,why doesn't the other?
Are there cases where the regenerating cell is already of the same type as the cell that has died – and so are its two copies?
What about the (programmed) lifetimes of the regenerating cells?

I hope these questions - which would give me one consistent picture - can be answered in one comprehensive answer.


text:
How do precordial leads measure electrical changes in the heart?
In precordial leads the electrodes from limbs are connected to a common point via resistors. What is the potential at the common point?

For those who post without using spelling checks I would suggest a change of heart.

Welcome to Biology.SE! Please take the [tour] and then go through the help pages starting with [Ask] questions effectively on this site and [edit] your question accordingly. In particular, the "title" of your question doesn't seem to match the "body". ——— We also 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). Thanks!


text:
How to generate electrical current from biological decomposition
I'm working on a project to generate and store small amounts of electrical current by means of decaying organic matter and would like to know:
a) Is it possible to generate electrical current from biological decomposition ("decay of organic matter") i.e as a result of the naturally occurring chemical reactions that result from decay?
b) If so, how can this be demonstrated in a lab?
I've found this article on the subject so far and am looking for more accessible information on the topic:
https://www.livescience.com/63569-gut-bacteria-produces-electricity.html

Welcome to Biology.SE! Please take the [tour] and then go through the help pages starting with [Ask] questions effectively on this site and [edit] your question accordingly. In particular, please clarify and focus your question — the article you linked to (and the original research article) seems to answer part a) of your question. If you have some reason to doubt that result please elaborate on why in your post. If not, then convert part a) into a statement (and reference the original paper as evidence). Note: you can probably answer b) by reading the Methods of that paper. Thanks!

What I was looking for is called a "Microbial Fuel Cell":
https://en.wikipedia.org/wiki/Microbial_fuel_cell


text:
What is the size (diameter) of the SARS-CoV-2 virus?
You can easily find a lot of pictures of the SARS-CoV-2 virus. But although it should be trivial for an electron microscope to measure the size, I am not able to find accurate size information.
What is the size (diameter) of the SARS-CoV-2 virus?
(Why does some virus particles seem to have a different size?)

http://virology-online.com/viruses/CORZA4.htm.

Although your question is straightforward, it would be great if you could explain why this information is useful to you.

@WYSIWYG As a researcher I'm sure you can think of at least 5 reasons, but we can probably invent another 100. But I find your request irrelevant to the question, especially in the light as 2 people have already voted for closing it. So please contact me elsewhere in case you'd like to know more.

@not2qubit It is not for my personal query. Supporting the question with a rationale helps other readers understand the post better. Since our aim here is not simply help people with their specific queries but make a repository of useful information, it is always good to have some background in the posts.

It would be far more interesting to know on what grounds people are close-voting (more or less) every question I have on this SE? Apparently the common courtesy of at least explaining why they down-vote or close-vote seem completely lacking here... The perfect way to alienate just about every new user you have here.

Electron micrographs of negative-stained 2019-nCoV particles were generally spherical with some pleomorphism (Figure 3). Diameter varied from about 60 to 140 nm. Virus particles had quite distinctive spikes, about 9 to 12 nm, and gave virions the appearance of a solar corona.

--A Novel Coronavirus from Patients with Pneumonia in China, 2019
Figure 3 from that article:

Does a virus have a well defined shape? links to your answer, any thoughts?


text:
Insect Identification (badly damaged corpse)

The photo is of the insect in question in a strainer. The body of the insect is just over half an inch long. I see a separated wing cover and leg in the photo as well.
My location is New Hampshire, USA. Given that it is February (middle of winter), I don't think it was sourced locally.
I believe that this came from a packaged item that would have been sealed in San Diego, CA or possibly in Asheville, NC. The packaging likely occurred no earlier than June or July of last year. The packaging would have occurred indoors in a manufacturing-type setting.
After coming out of the packaging, this individual was submerged in liquid on a stir plate for 36 hours, so it took quite a beating.

Welcome to Biology.SE! It might be helpful if you [edit]ed your post to include what kind of product the insect was packaged with. ——— You may also want to the [tour] and then go through the help pages starting with [Ask] questions effectively on this site. Thanks!


text:
How and when does the regeneration of cells that have died start?
I assume that the replacement of cells that have died (or been removed by any means) doesn't work on a single cell level but starts only when some critical number of cells have died.
My question is: How is this signaled (to the regenerating cells), and how is the critical number encoded, i.e. the signal threshold at which regeneration starts?

Whatever the answers may be, keep in mind this is a broad question and an answer will not apply to all tissues. Take an epithelium such as the gut lining or the dermis. It may help for you to think rather in a dynamic way ("stem cells in the crypt respond to cues to speed up or slow down the rate of cell replenishment") as opposed to a static way ("of 10 cells, 2 die; this crosses the repair threshold, so 2 cells divide to restore cell count of 10").

@SPr: Thanks for the enlightening comment and the instructive picture you point me to - I wasn't aware of "stem cells in the crypt" (what a great name by the way!) Nevertheless: What are those cues the stem cells respond to?

I'm no expert on this, but it is known that stem cells proliferate in response to a variety of mechanical, biological, and chemical cues/signals. They may respond to signals released by compromised cells, to wound healing cues from platelets for instance, to apoptotic bodies, to stretching or exposure to the atmosphere, to paracrine, immune or endocrine signaling, etc. And it's quite tissue specific. Hope that helps.


text:
Can plasmodial slime molds be infected by virus?
According to the definition, plasmodial slime mold consist of a "single cell" with thousands of nuclei. How would such a unique type of cell response to viral infection (if any)? Google search yield nothing.

since all known cells are vulnerable to viruses I'm gonna guess yes. and slime molds are only "a single cell" in the same sense fungi are which also have multi-nucleated cells.

Why do you think having multiple nuclei would have an effect on viral infection? The motivation for your question is unclear to me.


text:
Oakland California spider in home
Found this critter this morning on a stack of clothes.  About the diameter of a penny and in my haste to rehome it, took only this photo.  The belly was golden brown.


text:
Are facial 'cleansing' products 'effective' on human skin, and if so, what is their mechanism of action?
All major supermarkets and beauty stores stock some form of facial cleansing products. They come in the form of scrubs, gels, and lotions which vary in application (from in shower, to apply daily without rinsing). Many of these are not marketed towards clearing acne or other legitimate dermatological problems. The claims these products make tend to include: reduction of dry/oily skin, neutralizing skin PH levels, and clearing pores. I am unsure if any of these terms are reflective of a real problem, or if the products can even even help said issues.
Therefore, this is a three-part question:

Do facial cleansing products actually do what they claim?
If so, what is their mechanism of action (i.e., how do the ingredients work)?
If not, what do the ingredients in the product actually do to human skin?

Examples of such products and associated claims:

Deep Clean® Invigorating Foaming Scrub by Neutrogena
Dr. Alkaitis Organic Purifying Facial Cleanser
L'Occitane Aqua Reotier Gel Cleanser

Example ingredients from the Neutrogena product above:

Water, Glycerin, Sodium Laureth Sulfate, Cellulose, Lauryl Glucoside, Acrylates/C10-30 Alkyl Acrylate Crosspolymer, Microcrystalline Cellulose, Phenoxyethanol, Fragrance, Synthetic Wax, Methylparaben, Sodium Hydroxide, Menthol, Disodium EDTA, Polyquaternium-7, Sodium Benzotriazolyl Butylphenol Sulfonate, Ultramarines, Blue 1

This question is not looking to me to be much of a biology question - I see nothing that asks about biology. There are other sites like Skeptics.SE and maybe MedicalSciences.SE but be wary of each of their requirements for a good question.

This is a medical question (so for MedicalSciencesSE), but I encourage you to first try to find some info from some dermatological website, such as https://dermnetnz.org/ and include it into your question. You can also try to identify active ingredients, like Sodium Laureth Sulfate, and check how they work.

Welcome Michael. Sorry about the following rant, but I think this question should indeed be migrated as indicated above, but in its current form it cannot be, as it contains three quite independent questions, that are under-researched in my opinion. In other words, each respective question in itself might be too broad. I would advise you to go to Medical Sciences and post a new post over there and take a minute to familiarize yourself with their conventions.

I'm voting to close this question as off-topic because it should be migrated to MedSci.SE but cannot be in its current form as there are 3 questions that are very broad as stand-alones in themselves. This question needs work.

Thank you all, happy to have this closed and I will migrate to appropriate location.  Cheers again for your time. I will note comment regarding three questions, though I do feel that they are interlinked with the original. As I honestly know nothing, I can't really ask "how they work" if they don't work, right?

@Jan thank you for the link! Much appreciated.

You can elegantly merge all questions into one, for example: Are such cleansing products more beneficial for the skin health (reduction of dry/oily skin, neutralizing skin PH levels, clearing pores) than regular soap?

Do facial cleansing products actually do what they claim?

This dermatologist-tested cleansing gel formula lathers into a bubbly foam removing surface dirt, oil and makeup, while energizing exfoliators sweep away dead skin cells.

So essentially, they are claiming that it is a foaming soap.
Sodium Laureth Sulfate is a detergent, Lauryl glucoside is a surfactant, so it is a good bet that the product is effective as soap. There are a bunch of other compounds that modify how it forms films, so it probably also foams.
If so, what is their mechanism of action (i.e., how do the ingredients work)?
Similar to any other soap.  They make non-water soluble things on the surface of you skin (such as oil, make up, dead skin cells, etc) more water soluble so that it dissolves when you wash your face.
Some of the other you linked also have moisturizers, so they probably put another oil back in the place of the ones you removed to keep the skin from getting too dry.

I am unsure if any of these terms are reflective of a real problem, or if the products can even even help said issues.

Or do they work better than normal soap of comparable strength?  Probably not much, although having them labeled as use for your face is nice in that you have a reasonable idea that it won't be too harsh or irritating, whereas if you tried dish soap on your face that might not go so well.


text:
Whether de novo mutation can be inherited or not?
Think about the following scenario: A child is diagnosed as having long QT syndrome, an autosomal dominant disease. However, neither of his parents is affected. This may be due to a new mutation in the embryo, which would explain the son having the disease with normal parents. Next, this de novo mutation could be inherited to off-spring of the child? or not?
And there are additional questions. Why do so many genetic tests performed by blood samples represent all germline mutations? Except for cell free DNA, blood cells are not germline cells. Therefore, the mutation found in the blood sample test may be a huge somatic mutation (except blood cancer). For example, for mutations that occurred early in embryo development, many cells may have been affected, and I think this might be in the form of somatic mosaicism. Doesn't it mean that it's a germline mutation if it's found at 50% or 100%?
I asked you a little more, is there only a family test (segregation test) that checks to see if it's a germline mutation?
Thank you so much in advance.
Please answer these long question, because no one answer me about this question.
If you answer me, I 'll always love you somewhere in the earth.

Thank you very much!! And I love you forever :)
And you say, in other words, de novo mutations can occur in postzygotic embryos or by germline mutations in parents.
Then I want to go further and conclude. In this case, an autosomal dominant disorder was detected as a heterozygote on a blood test. If it occurs in the embryo after conjugation, two possibilities are conceivable.
It could happens a heterozygous allele in the whole cell of a postzygotic embryo, Or can occur in one of the cells as a homozygous mutation when there are only two cells in the early embryo. In the latter case, autosomal dominant mutation would be lethal, so the child is likely not lived.
So in conclusion, if I thought that the whole cell of the child had the heterozygous mutation of the long QT syndrome, it was probably the result of the parent's germline mutation.
Am I thinkin right?

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De novo mutations can be inherited if they occur in the germline cells, those responsible for making the sperm or the egg. If you have a de novo mutation in a blood cell or a skin cell, this doesn't pass on to the next generation. But when you test the blood for mutations, it can also mean that the same mutation is present in the germline! However, if the parents are not sufferers of the dominant disease, it means this mutation is not present in their somatic (non-germline) cells. It's likely that the mutation occurred de novo in either the parent's germline during their lifetime (during the production of their sex cells in adulthood).
If your parent has a mutation in their germline, and it is passed on to you, the zygote is formed from both your parents (half of your alleles are from the mutated parent) and this zygote creates ALL of you, including your blood cells and your skin cells. This is why we can test your blood to guess what must have been the case in your germline. Of course, you may have accumulated mutations independently in the germline in the meantime, or accumulated mutations independently in the blood cells! So it's not completely the case that testing blood will tell you about the state of the germline. But you must understand that ALL of you is created from a single cell, the zygote, so at this point there is a 'bottleneck' that forces all somatic and germline cells to share the same genetic makeup.
Also, please consider that humans are diploid, i.e. have one copy from the mother and one copy from the father. And that these recombine and only one copy goes into the sex cell. This may help you think about your problem.
I trust this will help you better understand your questions.


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What type of insect is this found near Mountain View California?

This was taken in a hotel room in the Mountain View area of California. Size wise, it was pretty small, perhaps somewhere around an inch from left to right (not including antennae). My first instinct was cockroach, but, on further inspection, it doesn't look like a German or a field cockroach, as it doesn't seem to have wings. Is anyone familiar with this insect?

It looks pretty difficult to identify, it's been crushed beyond recognition.

That specimen is pretty squished, but I'm guessing it's a cave cricket or spider cricket (order Orthoptera; family Rhaphidophoridae).  They're very common invaders of cool damp places like basements or air conditioning units.  Harmless, but can be quite startling, as most species can jump several feet in one leap.

This would likely be a nymph, not an adult, right? I don't know too much about these types of things, but it was quite small (0.5-1.0 in).

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Assuming Alan is right about the ID (which would be problematic in any case, due to Chris' probable reaction to seeing the subject--I'm assuming the OP also did it in) the specimen may well be an adult (ALL Rhaphidophorid crickets are wingless at that stage); with a few notable exceptions (see for example Tropidischia xanthostoma on bugguide) most species of this family need to be identified from intact adult males, and much unpublished work has been done (for a preview, see the article here, the author of which has since died).


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Is it possible to cultivate cheek epithelial cells in a non-CO2 incubator?
CO2 is important for maintaining constant pH in cell culture. Unfortunately, I do not have access to such incubator and buying a new one is expensive. I found a cheap incubator online, but it doesn't support CO2. I'd like to ask if I can cultivate cheek epithelial cells in such incubator and if it won't negatively affect my cell culture. Another option is building a small CO2 generator inside the incubator. I made some calculations - I know how much CO2 I need to generate, how many grams and mL of solutions I need, moreover the build-up pressure is so small, it should not negatively affect the incubator.

Are you familiar with CO2-independent growth media? (I don't know anything about culture of that cell population specifically, though)

Thank you very much. I am not familiar with CO2-independent growth media, but I will take a look. I planned to buy a cheap DMEM from eBay. I hope, there are some inexpensive media you mentioned, or at least a method to convert DMEM to such medium.

L-15 media does not require a CO2 atmosphere and according to Sigma-Aldrich this media is suitable for primary explants of adult human tissues.

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How does new species come into existence?
The only reason for the creation of new species that I found from the internet is geographical isolation. Are there any more reasons?

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

A paper from Müller et al. proposes a molecular marker called a CBC, differences in which can be used to call two different species, even when closely related: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1950759/

In this study we are looking for a molecular classifier that might indicate that two organisms belong to different species. We are interested in an indicator hypothesis that is easy to work upon and additionally yields a certain probability that two organisms belong to distinct species. Compensatory base changes (CBCs) in the internal transcribed spacer 2 region (ITS2) of the nuclear rRNA cistron have been suggested as such a classifier.

Some mutation event that creates sufficiently different CBCs in a viable offspring capable of further reproduction, i.e., survives natural selection, would therefore lead to speciation, by this measure.

So, natural selection is another type of speciation. I understand.

Natural selection acts on organisms. Some organisms have deleterious mutations. Some have neutral mutations. Some have (more rarely) beneficial mutations. If mutants survive or thrive and (most importantly) reproduce, and if they carry sufficient and specific genetic changes, then those mutants could lead to what this method would term a new species.

This seems like a very specific answer to a very general question... I see it's been accepted but I'm worried that it's a bit misleading.

If it is misleading, you're welcome to provide another answer.

Drive-by downvoting is of no help to improving Stack Exchange, nor this subsite, generally. Clean up your act.


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Why are probionts not considered cellular life?
I am currently studying Prescott's Microbiology, 10th edition, by Willey, Sherwood, and Woolverton. Chapter 1.2 Microbes Have Evolved and Diversified for Billions of Years presents the following figure:

The authors then ask the question: Why are the probionts pictures above not considered cellular life?
I'm unsure of why the probionts are not considered to be cellular life. If I'm not mistaken, the probionts contained ribozymes, no? This means that they have the capacity to catalyse their own reproduction. And, according to the figure, later probionts also consisted of proteins, so I'm presuming that catalysis and reproduction were not issues here.
I would greatly appreciate it if people would please take the time to clarify this.

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This https://biology.stackexchange.com/a/9455/57068 answered my question.


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What are these tiny insects?
I live in Italy (Emilia Romagna), and my house, seasonally in spring, is full of these guys, someone knows their name and if they could represent a problem?
They are very tiny slightly less than 0,5 cm including the antennae.

It could be Anthrenus verbasci.
These insects are not dangerous, but they can damage carpets, clothing and furniture.


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Why is the coremata of Creatonotos gangis huge?
This Australian moth has been some kind of curse image online due to its scent organs (coremata). It is inflated to attract mates. However, why does the coremata have to be inflated for it to work, and why does it have to be so big?


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Identify this tree?
I found this tree in Crete, Greece close to the sea, planted next to a building. Since I haven't seen this tree anywhere else in the island, I suppose it was planted by someone. Here are some pictures of it.

Based on the distinctive leaf shape and placement of the fruit along the stem that appears to be a papaya.
If so then the plant should "bleed" latex (a milky white fluid) when damaged. You can test this by breaking off a small piece leaf.

Image credit: By Max.kit - Own work, CC BY-SA 4.0, https://commons.wikimedia.org/w/index.php?curid=54547062

Indeed they seem identical. I will break a small piece of leaf tomorrow and I will let you know and accept your answer as correct! Comparing the plant with your photo, mine seem to not be doing so well. Could it be the cold? The temperature varies between 9 and 17 degrees

Glad I could help! Your plant does look quite damaged, but that could be due to many things including: cold, water stress, nutrient deficiencies, diseases, or pests. ——— If you want to ask a question about that I recommend [gardening.se].


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Violation of Conservation of energy In food chain?
Food chains use a unidirectional transfer of energy. Plants absorb energy from the sun,  then the energy goes on to next tropic level and so on. But in this system, energy source is the Sun.
When any organism dies, it’s decomposition doesn’t contribute energy back to the sun (as the nuclear process in the sun keeps on generating energy).
So my question is - doesn’t it violate the law of conservation of energy? As energy is not flowing back to the sun? Here Sun is the ultimate source of energy as it just keeps on creating energy, so energy isn’t conserved?

The Sun doesn't create energy; it converts energy from one form to another - in particular, it makes light. The physical details need not concern us here: what matters is that the Sun's fuel supply is gradually depleted (over billions of years), producing light. What interests biologists is that photosynthesis harnesses some of this light energy, and each trophic level receives, on average, about 10% of the one below it.

I agree with you, But if we look at a food chain, Sun is a source of energy. At the end of the chain the energy doesn't go back to the sun. That is the reason for my question...

@neefg Conservation doesn't require energy to go back to where it started. If you use a hob to boil water, the oven never gets back the thermal energy.


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What does myelin insulate against, exactly?
I am aware of the saltatory conduction model, nodes of Ranvier and all that, and that myelin lets electrical signals "jump". What does not add up to me entirely is what the myelin sheath insulates against, why it improves conduction through axon. If the cell membrane is already impermeable to ions, why does a "thicker membrane" improve signal conduction? There are nearly infinite memes on the internet about action potentials through axons, have not really seen any answer this though. Some vaguely mention "less leakage", but isn't the cell membrane preventing that to begin with?

Here's an answer I think is fit to answer your question. It gives you a better conception of how myelin does its job of insulation.

Ions have an electrical charge which generates an electrical field that decreases in strength with distance from the ion. The cell membrane of the axon is not thick enough to stop ions on either side from being attracted to one another and interacting. The electric fields of these ions are what myelin 'insulates against'. This answer to a related question provides some good diagrams and in-depth discussion of how increasing the distance between the oppositely charged ions helps nerve function.

@Hodgkin Can you look at the two related questions linked in comments by S Pr and timeskull? I think your question should be closed as a duplicate of one or the other.

So, myelin increases the distance to the positive ions on the outside of the axon membrane, preventing them from repelling the positive sodium ions that travel down the internodal segment by electrotonic conduction, overall decreasing resistance to sodium ion current?

If that is the answer, then technically it isn't really insulating (as insulation does not insulate against electric fields?), but, just increasing distance (with non-charged matter, the myelin)? insulation in wires prevents leakage of electrons, doesn't it? isn't the metaphor, if so, misleading?

A capacitor involves plates holding charge separated by an insulator - adding more insulator increases the separation. Adding a non-insulator would not. There is also increased resistance overall. So no, I don't think it's misleading nor an analogy, though it's important to realize that biological electrical systems only approximate the perfect/ideal mathematical circuit components (even more so than non-biological versions).

I don't think your statement about positive ions repulsing is correct, either. Just think about it as the amount of charge necessary to change the membrane voltage is less.

The dielectric in a capacitor is insulating, good point. If not by decreased repulsion from the positively charged ions on the other side of the myelin dielectric, then how does the decreased capacitance in the internodal segment improve propagation of the sodium ions?

(what I meant with misleading, it seems to me that insulation around a copper wire is used to prevent leakage, not to decrease capacitance, since the space around the wire isn't electrically charged whereas extracellular space is. better to liken it to a capacitor then, like you did. I got that analogy, which was not an analogy because it is what it is, but maybe you get what I mean)


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Can coronavirus contaminate public water systems?
It's been reported recently that people are panic-buying stuff as the coronavirus epidemic worsens. I've even noticed that the local grocery store is low on hand sanitizer, paper towels, and bottled water.
I did some reading and traced links back to the DHS's ready.gov website, and it recommended preparing a 2-week supply of food, water, medicine, and hygiene products for ISOLATION, though I expect if you're sick you're supposed to plan a trip to the hospital. Most of that makes sense to me. The exception is the supply of water. We have public water systems that send drinkable water to us, so why do we need to prepare a stash?
I tried finding an answer online, but I couldn't. The only guess I have is that coronavirus can contaminate the public water system, and it's not guaranteed water treatment will work. Who here has the know-how on waterborne viruses and water treatment to address this speculation?

What if one person at the water plant gets sick, and the place is closed down and the other workers quarantined until decontamination is carried out? NB: I know noting about water plants, but no, the water system won't get "infected".

SE Biology is concerned with the mechanisms of biological processes, and questions are generally answered by people with biological rather than medical or epidemiological expertise. Although I understand your concern about the coronavirus outbreak, your question is not about the biology of the disease and is clearly off-topic here. I advise you to consult more appropriate reputable sources of information, some of which are listed here.

do you know how I can close this as off-topic? I can't delete it because the site says it has an answer

Try medicalsciences.SE

Viruses can survive a few days in water, i.e. SARS can survive 22 days in lab grade reagent water and 7 days in pasteurized sewage. That is the time the virus takes to be at 99% of it's original concentration. (from "survival of surrogate coronavirus in water").
Viruses can also spread via swimming pools, i.e. hepatitus A and norovirus have been associated with swimming pools. (from "a review of waterborne viral deseases associated with swimming pools").
Boiling water will kill viruses. Children have very little reaction to the virus when they carry it, so it's likely that they act as a transmitter more than water does. I'm not worried about it at all by the way, just do what the doctors advise.

I f you deleted your answer the OP would be able to delete his question which he now recognizes is off-topic.

Perhaps transfer it to the medicalsciences.stackexchange.com

@com.prehensible
"Children have very little reaction to the virus when they carry it" - that's of interest to me as I wonder if it has been the basis of vaccine and treatment therapies research for other parts of the population. Please share further information if you have it. Thank you !

search for "juveniles immune coronavirus" "covid child immunity" you'll find some info although it is a complete mystery, nobody knows even what the T-cells for the new virus are and it's unkown why the effects are so variable.


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How are logarithmic trendline equations used to determine antibody concentrations in ELISA?
For example, say you have plotted a standard curve and managed to obtain a logarithimic trendline equation like:  y = mln(x) - b
And you are working with data that includes:
a) standards,their concentrations and absorbance readings (taken twice - with mean absorbance and blank absorbance also calculated)
b)samples (and their absorbance readings) that you want to know the concentration of
c) all the samples have been diluted two fold
Would you simply just rearrange the equation y = mln(x) - c  to:
x = (y + c) / mln
and input y value as being the mean absorbance readings of the samples you want the concentration of?
Are there any further steps after this? Or any I have missed out?
Is there anything I need to do with the dilution factor?
Do I have to do mean absorbance - mean blank, to get the correct absorbance readings to input as y or are the mean absorbance readings themselves sufficient?
Thank you

You can't write x = (y+c) / mln since ln is not a constant, rather it is a function on x. So, instead write ln(x) = (y + c) / m.

If by ln you mean the natural logarithm, then no, you can't rearrange the equation in that way. Try this:
$$m\cdot \ln(x) - c = y\\
\ln(x) = y + c\\
\ln(x) = \frac{y+c}{m}\\
\exp(\ln(x)) = \exp\left(\frac{y+c}{m}\right)\\
x = \exp\left(\frac{y+c}{m}\right)
$$

Yes, ln is for natural logarithm. Thank you, I will try to work it out using this equation.

@user1136 I'm not sure what new information you've added to this answer, nor do I understand what issue you have with what I have written above. The original question was answered simply by pointing out a mistake in the original poster's algebra.


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In Genetic Engineering, why are we limited to existing creatures when it comes to creating a new species?
So, I don't know much about Biology. Haven't studied it since high school. So please excuse me if my science isn't proper. I'll do my best.
Let's say for example you wanted to make a fire breathing Komodo dragon. Well, from what I understand, it's quite impossible to do because there are no creatures that breathe fire. So you wouldn't be able to gather the needed DNA information for breathing fire.
However, if you wanted to give a Komodo dragon wings, well this would be possible, because there are many winged creatures in this world, so the genetic information you need is available.
What I don't understand is, why couldn't you create or manifest this genetic information artificially in a lab? What stops us from doing that? Say for example, fire breathing?
I'm not particularly interested in the utility behind fire breathing dragons. I'm just using it as an example for my question. Any other features could be added in it's place.

Obligatory not a biologist, I studied physics.
In a very basic way, and ignoring the limits of carbon chemistry, it's all a question of understanding.
If you imagine DNA, and genetics as a whole akin to a language, we're currently barely able to read it, let alone write.
We know the letters of the genetic alphabet, at this point (Adenine, Thymine, Guanine and Cytosine, along with Uracil for RNA), and we're starting understand how to make a few words (genes), but we're still quite a ways away from mastery of the genetic language.
Part of the problem is that some traits have simple mechanisms that go from gene to expression, like how skin colour is largely based on the amount of melatonin in your skin-cells, and how eye colour largely hinges on one or two genes. However, many things are not that simple, from things like autism to adult height, to cancer, most parts of an animal don't hinge on a single gene. This also means that, in your example, we're nowhere close to making a komodo dragon grow wings.
To summarize, we've only barely figured out the genetic alphabet, along with a couple words, but we're nowhere near being able to write whole sentences, nor make up words from scratch.

Be careful when talking about stuff that you obviously don't know. Especially pigmentation and its regulation is a complicated field, although in the end the amount and ratio of the melanin (not melatonin!) is what makes the difference. Getting there is another story.


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What fraction of embryos fail to be born? And why that high?
In the book Developmental Biology by Scott F. Gilbert and Michael J. Barresi, it says:

Most human embryos die before being born. You survived.

So how come is that true???
And what percentage of pregnant women lose their unborn child(ren)?

How can we possibly know without knowing with certainty that a woman is pregnant? Many are lost only days after implantation.

What attempt have you made to answer this question on your own?

Is the fastet sperm always the best?

It's a tougher question than it looks; estimates vary pretty widely https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5443340/#__sec2title


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Relation of root length to plant size
I am thinking of making an aeroponics system.
But after i finished my primary design I though to myself how deep should I make the container for the roots of my plants? Since I want to make my system applicable to a range of plants image from microgreens to lettuce. I was thinking how can I determine the size of the roots of the desired plants? I there a way to determine this from the size of the plant or not?
This would be important since if the container is too small the spriklers my get covered my the roots of some plants. And if the container is too big some roots my not get enough water. Next to this a more space efficient container would be better (So it also looks a bit nice)
I am a complete newbie to this so please let me know if any clarification is needed :) And if this is even the right place to ask.

Root length is something that plants change in response to their environment.

Ok, so let's say the environment for the roots is very optimal would that result in longer or shorter roots?

Compare, for example, root system depth for trees such as oaks vs the Welwitschia plant of southern Africa...


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A question about microbes growing media
I was told in my microbiology course that blood agar can be put in GasPak system (anearobic) to grow strict anaerobes, but why would someone use blood-dependent bacteria in this experiment as these blood-dependent bacteria will be aerobes or at least facultative

Maybe they wish to select against aerobes in a mixed species sample? The blood is just for nutrients.

You can put any media in a GasPak or other anaerobic system depending the type of anaerobic growth you are looking for. Sometimes blood is simply added to media to meet nutritional requirements of an organism. I use Columbia Blood agar often as a general purpose anaerobic medium. In a collection of 100+ obligate anaerobes I am working with, around half grow well on columbia agar with 5% sheeps blood, and many of those will not grow on Columbia without this blood amendment. As an added bonus, I can easily spot certain common contaminants growing on my plates by their hemolysis paterns.

Blood agar is prepared by heating the blood so that there will be lysis of RBC. Blood agar is mostly used to grow pathogenic organisms such as Haemophilus influenzae and Neisseria gonorrhoeae which cannot grow on other media.Neisseria gonorrhoeae can grow in the absence of oxygen. Haemophilus influenzae which is a facultative anaerobe also can carry out anaerobic respiration when there is no oxygen.Blood agar is very important to grow fastidious organisms, i.e the organism which is capable to lyse the RBC.

I think you are describing chocolate agar. https://en.wikipedia.org/wiki/Chocolate_agar