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Why is 70% ethanol preferred for aseptic techniques?
Are other concentrations (say 80%) less effective,or is this just for convenient manufacturing? Is the concentration chosen only because it is less volatile than 100 percent ethanol and hence safer?

70% ethanol is the minimum concentration when used in a lab setting for aseptic technique. You don't want to go lower, because it will not kill the microorganisms you are trying to kill.
However the solution requires water to be effective at doing its job. The 30% water is necessary to provide sufficient polarity to the solution.
EDIT

A rough indication of a solvent's polarity is a quantity called the dielectric constant. The dielectric constant is a measure of the solvent's ability to insulate opposite charges (or separate ions) from each other...
Water is the most effective solvent for promoting ionization, but most organic compounds do not dissolve appreciably in water. They usually dissolve, however, in alcohols, and quite often mixed solvents are used. Methanol - water and ethanol - water are common mixed solvents for nucleophilic substitution reactions.

Dielectric Constants

Water - 80
Methanol - 33
Ethanol - 24

-Organic Chemistry 11E T.W. Graham Solomons et.al.

Note
Dexter's answer provides experimental evidence for why 70% ethanol is used. My answer is based on my experience and understanding and the concentration that I have used in the lab. I would add that 70% was likely chosen as a balance between cost and effectiveness. If you are a little off on mixing the solution from 95% Ethanol stock, then you are still at a bactericidal level, where as if you err at 60% concentration, you could start to let a few bacteria survive.

70% ethanol is still flammable and should be handled with care. The issue with ethanol greater than 98% pure is that the only way to distill the last 2% of water out is to add benzene, and benzene is a known carcinogen. There will always be trace amounts of benzene in 100% reagent grade ethanol.

I thought ethanol to be pretty polar? More importantly,  I thought higher percentages EtOH caused microorganisms to dehydrate, killing the cells, but conserving the viable spores of spore-bearing bugs?

DAMN IT @AliceD... you actually went there and you made me drag out the Organic Chemistry text book... I am hating you right now! ;-)

I disagree about cost and effectiveness point. That is not correct. Main reason to add water is to denature protein faster. You can still kill bacteria with crude ethanol but with different amount of exposure time.

@Dexter That comment refers to the choice between using 60%, 70% all the way up to 95%, as the data you provided showed that 60% to 95% by volume had the same efficacy at killing all of the S. pyogenes. You don't go for 60% because mixing errors can make it less effective. 70% has the same bactericidal activity as 95%, but by cutting with water, you get equal efficacy at lower cost.

Yes, that data is for one species. But point of showing that table was not to comment on percentage dilution but to show that other dilutions can also be used with different exposure time. Cost effective point make sense if below 70% ethanol is very less effective. In that case, we could have used 60% or 50% instead.

It is not very clear to me how dielectric constant has a role in the potency of the disinfectant.

I read recently that absolute ethanol might just cause severe dehydration, and that would preserve the bacterial cells in a bacteriostatic condition, not letting the alcohol enter.

@WYSIWYG the dielectric edit was to address AliceD's comment about the polarity of ethanol and why adding water increases polarity.

@AMR How does polarity contribute to the disinfectant efficacy?

@WYSIWYG That is probably worth its own separate question.

General disinfectants
You need two things for good aseptic agent or disinfectant,

It should be able to kill most of microbes (Spectrum)
It should do it in short time (Speed)

Many chemical disinfectants including ethanol are non-specific antimicrobial. Their predominant mode of action is by protein coagulation or by denaturation. This results in disruption of cytoplasmic integrity, cell lysis etc. Protein coagulation occures at optimum alcohol concentration. In presence of water proteins are denatured fast compare to without water. Alcohol induced coagulation occurs at cell wall involving various plasma proteins.
Ethanol
Ethanol is highly efficient in killing non-sporulating bacteria and mycobacteria but inefficient against bacterial spores. Ethanol is effective bacteriostatic at 10% (Vol/Vol). It is bacteriocidal at concentration above 30% depending on species, exposure time and water content. Following images taken from (Seymour 2001) shows how it is effective within given parameters for one specific species. ("+" sign indicates growth of test organism, "-" sign indicates no growth of test organism )

In 1950, people have standardized set of parameters which are most efficient for killing wide spectrum of microbes with very short duration. Hence ethanol can be used in different concentration but you have to fine tune exposure time accordingly (You can see in above figure, that 50% and 100% can still act as a bactericide, they are less efficient than 60%-95% and require longer to kill all of the S. pyogenes.). 70% ethanol helps in killing wide spectrum of microbes with very less time.

I think that you need to explain how to interpret the figure you added. What do the pluses and minuses indicate. Does in mean that S. pyogenes survives in 50% for 20s but all are dead by 30s? Do the minuses mean that all bacterium were dead at that time point?

Original paper says "+" sign indicates growth of test organism, "-" sign indicates no growth of test organism while "+/-" sign indicates growth in some test and failed in another

Okay, so then I am not sure how you draw the conclusion that you make in the italicized parentheses. 50% and 100% show some growth given a certain time course (Must have used the concentration, then significantly diluted to stop, spun down the bacteria and plated), where there was no growth seen at any of the time points for 60% to 95%. I think the correct interpretation is that at 50%, the concentration is low enough that S. pyogenes can survive about 20s and still grow while they are actually able to survive better in 100% ethanol (60s), due to it being a lower polarity solution.

I concluded in parentheses for reason it is effective with very small exposure time. And I doubt you can comment on it's polarity. Reason you add water is to make protein denature faster. Again the concentration and exposure time you have to standardize accordingly.

You are saying 50% and 100% are more efficient that 70%, but that is not what the figure shows. Plus in this instance is bad because it means that they when they plate bacteria exposed to 50% for 20 seconds, colonies formed, and at 100% they were getting bacterial colonies even when the bacteria was exposed for 1 minute. From 60 to 95% you see no growth, even when the bacteria were only exposed for 10 seconds, therefore those concentrations are the most effective. You are interpreting that chart incorrectly, assuming that what you said about + and - is correct.

1- How would adding water denature proteins faster? You would need detergents to do that. If anything water would maintain the protein conformation as the hydrophobic regions on the inside would  stay on the inside. 2- Solvency is based almost entirely on polarity. That is why salts don't melt in oil, though some ionic compounds won't even dissolve in water, and you need nonpolar solvents such as hexane to dissolve nonpolar organic compounds. Lipopolysaccharides are amphipathic molecules, you need the water to solvate the polar parts and the alcohol to dissolve the less polar parts.

The water helps alcohol enter the cell.If all the water is removed( as would be the case if absolute ethanol was used),the cell is completely dehydrated- making it hard for the ethanol to permeate and denature plasma proteins.


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Why would a bacterial population show initial growth when it is in unfavorable growth conditions?

This figure shows the anaerobe E. faecalis grown in aerobic conditions, E. coli grown in restricted conditions that are not specified. Why do they show an increase in abundance initially? The black line is growth rate and to me I would think neither would grow at all.

E. faecalis is an aerotolerant anaerobe. It can't use oxygen but it doesn't harm it.

E. faecalis is an aerotolerant anaerobe, while E. coli is a facultative anaerobe therefore if in a non-aerobic environment it can switch to anaerobic respiration. E.coli is also capable of fermentation.
Here is an article for on the various respiratory pathways of E.coli: http://www.sciencedirect.com/science/article/pii/S0005272897000340
One other reasons why cells may grow in a nutrient poor medium is that many types of bacteria have programmed cell death that ultimately is for the better of the entire bacterial population. When nutrients get low some cells commit "suicide" and release nutrients to surrounding bacteria. Just an extra thought.

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How do you interpret this microbiology/ bacteriology research figure?

This is a figure from a research article that I am to do a senior presentation for. It is showing  bacterial replication of an enteric bacteria population. The researchers hypothesize that the number of regions near the replication origin will be the highest point (peak) on the graph and the terminus region will be the lowest point because there are least copies of this region in a dividing species. The determine that the ratio of the peak to the trough will reflect the growth rate of the species. That all being said, I don't understand their use of color. The peak has several different colors that do not seem to match any of the examples on the right. Wondering if anyone can help me decipher this? Thanks!

The short answer is that it looks like the colors are meant to represent different, partial copies of the bacterial genome in the process of being synthesized.
When bacteria replicate, they initiate replication at the origins of their chromosomes.  In fact, these origins can be replicated multiple times before it gets to the "end" of the bacterial chromosome (terminus). Looks like the stacking on the right figure shows this, with the colors just aiding in differentiating the partially replicated chromosomes. The coverage plot on the left shows how this might look based on read coverage from deep sequencing (again the colors just show different, partially replicated, chromosomes).

I think the figure has the answer. "High copy number near the origin". This is depicted in the graph by the spike at x = 4Mbp. The graph also shows that the number of reads is lowest at a point opposite the ori (2Mbp).
Mbp stands for Mega-base pairs, or 1 million nucleotides. Mbp in the graph refers to a point on the chromosome, with 4Mbp being at '12 oclock', the origin of replication(ori), and 2Mbp being at '6 oclock' opposite the ori. The researchers are measuring the number of DNA fragments(y-axis) that map to a certain position on the chromosome (x-axis). I am slightly color blind, but it seems to me that the colors generally match up. Also note that the reads that fall within the lower-most bracket on the right side of the x-axis span the entire x-axis. This is because these fragments map completely to the chromosome, and indeed they are labelled 'original genome'.
Hope that helps.

First, it would help if you could provide any more information on the figure (how it was made, is it data based or representative of a model?)
Given that there is little to go on, I can offer my two bits - and I hope it will help you get thinking about it - but ...
It appears to me that these data are a snapshot of the replicating bacterial genomes isolated from many cells at a given timepoint. The right side of the figure shows a model of the (circular) genome in black with a number of smaller fragments of the genome caught partway through the replication process. The left side shows the same fragments stretched out in a linear representation.
The green fragment is the largest as it is nearly finished copying. Other colors show different sized fragments at different points in the copying process. It sounds like the graph is meant to relate the number of different sized fragments to growth rate (assuming you measure fragments from the same number of cells).
So, what does this tell you? (I think it would be helpful for you to think this out yourself form here and determine if you believe this is a good measure or not.)

Would you agree that "genomic location" (x axis title) shows that they are splitting the circular chromosome into 4 regions?

Bryant, I don't think they mean to break it into regions. The X - axis is a measurement (in mega-base pairs = millions of bases) according to an arbitrary start point. Replication begins at the origin and extends in both directions. Note the point of symmetry for each of the fragments around the origin.

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Which class of animals constitute the largest biomass?
I found here that species-wise it is cow. But, collectively, insects may exceed even mammals. So, which class of animals constitutes the largest biomass?

Prokaryotes still rule the world. Bacterial and Archaeal biomass far exceeds any other class of living organism.

But prokaryotes are no animals.

according ot this, arthropods. https://www.weforum.org/agenda/2021/08/total-biomass-weight-species-earth the big kicker is krill, there is a LOT of rill in the ocean.

Following from MarchHo's comment, I have not been able to find class-specific (in the formal sense) estimates, but if you meant 'class' in an informal sense, the following may be useful.
A nice infographic covering the relative biomass of all land mammals is here, and a full table for species groups (at the level of domesticated vertebrates, invertebrates, etc) is here (reproduced below).

Short answer: amongst animals, invertebrates are where the mass is.

Don't invertebrates make up multiple phyla and not a single class though?

@MarchHo Good point. I read the question as 'group' in the informal sense, but that was based on the comments mentioning Kingdom-level groups, rather than the question itself.

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Why do teeth ache after fillings?
I had a filling which involved drilling the tooth, but the drilling did not touch the nerve. According to the x-ray taken at the same time, the nerve is in fact some distance from where the filling was taking place (lower right molar).
Now the local anesthetic has worn off, my tooth is aching. The gums do not hurt (so it is not caused by the dentist applying pressure to the area) and as far as I am aware there are no other nerves within the enamel of the tooth.
So, why does my tooth ache? Is it something to do with the nerve 'waking up' after being anesthetized?
Just to be clear it is not a severe ache or of any concern, only in the background, and I am curious as to the cause. The dentist did say it would ache, so it's obviously a normal thing, but I didn't think to ask why!

There can still be a pressure exerted on the nerve, the filling exerts a pressure on the tooth which then propagates through the entire tooth.

I didn't think of that - he did really seem to 'pack in' the filling and that could cause pressure inside the tooth.

See, since it was a simple drilling followed by restoration or filling, that means the infection was superficial, not involving the pulp where the nerves and blood vessels are situated.
Ok, so now to remove the superficial infection the dentist might have used an airotor. It's an instrument which rotates at high speed, has a hole for water spray to cool the fictional heat generated while it removes the caries or the infection from the tooth.High speed handpieces
Now as you may be knowing the crown portion of tooth has three layers- enamel, dentin and pulp. Only the pulp portion is innervated.
Now when the instrument is drilled into the tooth the infected enamel and superficial infected dentin must have been removed.
The dentin has numerous tubules known as dentinal tubules. These contain a fluid called dentinal fluid. Whenever there is any stimulus which has not yet reached the pulp, but may have reached the dentin, eg of stimulus in the form of pressure, temperature change, sweet food, sour food etc, cause the fluid to move or get displaced. The displacement of dentinal fluid stimulates nerve endings in the pulp and hence generates a pain/ sensitivity response to your brain.Hydrodynamic theory
Now the drilling causes heat generation, even though little, due to the coolant, plus pressure and hence causes the fluid to displace and hence pain. This pain usually ends after the treatment.
However the restoration placed, you should have specified which restoration- silver coloured (amalgam) or the tooth coloured. These again have chemicals. These chemicals can penetrate through the tubules to the pulp to elicit a painful response even after the treatment. To prevent this, a liquid known as varnish is applied which acts as an insulator. Also if the infection is deeper, a base or other material depending on the type of restoration is also applied to prevent other stimuli. Varnish and bases
So either there may be a failure in these insulating materials or your pulp may require some time to heal from the procedure. It may have got healed by third or fourth day, if it was due to procedural trauma. In either case you should contact your dentist.
Hope I have solved your question :)
References have been given in the parentheses


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how to solve gap reactions in genome scale metabolic reconstruction
I'm making a project about modeling of nannochloropsis metabolism. My model is in the refinement stage. However, it is not running in the FBA test. Then i found there are 87 reactions that did not run. But the reactant/metabolites for those reactions to run are there in the model.
Is there any one know what is the possible reason for this, and how to solve this problem?
Really looking forward to see your answer.
Thanks,

I'm not exactly sure what you're asking I'm afraid. Could you provide some more information?

Hi Good Gravy, it is about the result of FBA optimizeCbModel when i apply for my metabolic model. it gives f=0, no flux through my model. I think the problem is what @ Roland said.

It is common that reactions in stoichiometric models cannot carry flux because there is a "dead end" metabolite somewhere. The problem may not be in the immediate reactants / products, but can be several steps away, and is not always easy to find.
If you have a network visualization tool, one option is to highlight all reactions that cannot carry flux; often this reveals an entire blocked pathway ending in the isolated metabolites.
A more systematic method is to examine the dual solution of the linear program for maximizing flux through a blocked reaction; this shows the active constraints, which are precisely the metabolites that are lacking for the blocked reaction to be able to run.

Hi Roland, Thanks for your answer. Do you know which visualization tool that i can use in this case? I'm trying to make with cytoscape but it is quite a bit messy for me.

Cytoscape should work well, provided you have a graph layout you can just export the graph with node labels reflecting blocked reactions.  If you don't have a graph layout it's much more work --- this is not trivial to do automatically, I have always done manual layout. The LP dual method might be easier.


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Determining the osmolarity and tonicity of a cell
Consider a cell with urea concentration inside being 2mmol/L and outside being 2.5mmol/L. The cell itself is permeable to both urea and water. Ignoring the effect of other osmolytes,
A) Urea flows in, water flows out
B) Urea flows in, water flows in
C) Urea flows out, water flows out
D) Urea flows out, water flows in
I'm confused because I thought water would simply flow out of the cell to equate the concentrations inside and outside such that there is no net flow in urea.

If you consider the cell to float in a bucket of water you can quickly envision that the efflux of water from the cell will never equalize the concentrations.

The efflux of water isn't instantaneous. Since urea is free to move across the membrane, it will (and with a net movement from higher to lower concentration).


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Is it possible to grow E. coli K12 with algal amino acids as the sole carbon source?
Instead of glucose or glycerol, is it possible for E coli to grow on an amino acid mixture as the sole carbon source and, if so, what should the concentration be?

Why specifically algal amino acids though?

E.coli can do that and in fact does this a lot in a commonly used bacterial medium: The popular LB Medium. This is composed of three components:

Tryptone, a peptide mix made by digesting milk casein with the peptidase Trypsin (10g/l)
Yeast extract, made by autolysis of the cells (5g/l)
Sodium chloride (10g/l)

The original formulation of Bertani from 1951 (see reference 1) also contains 1g/l Glucose, which was later discarded, since the handling is easier without it (glucose cannot be autoclaved as it degrades).
Since the medium does not contain any other utilizable sugars as a carbon source, the bacteria use free amino acids (and small peptides up to 650 Da in size) for their growth. The reason for this limit is the exclusion size of the bacterial porin channels which allows the uptake of the peptides and free amino acids (see reference 2 for details).
Once these are exhausted, the growth stops, which is the reason why LB Medium is actually not very good suited to get really high densities (that's why SOC media are used for some applications). Read the excellent paper in reference 3 and the also excellent article in reference 4 if you want to know more about the topic.
I don't think it matters from which source your amino acids are coming. Regarding the concentration I haven't found any data, but in reference 4 it is estimated that only about 25% can be used by the bacteria. Since the mixture contains about 15 grams of protein lysate, this would roughly mean about 4 grams of free amino acids or more.
References:

Studies on Lysogenesis I.
Size Restriction on Peptide Utilization in Escherichia coli
Escherichia coli Physiology in Luria-Bertani Broth
The Limitations of LB Medium


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How to prevent blobs under the microscope?
My task is to take photographs of fungus spores under a microscope at x100 using oil immersion.
My problem is that I get all these little blobs. How do I prevent the blobs?
So, I have been instructed to first put the spores on the glass slide, then add a teensy drop of water to it (I use a syringe so I have exact control over the droplet) and then put the coverslip on top of that.  Then I tap the coverslip down with the eraser-end of a pencil to force the excess water out from under the coverslip.  The immersion oil goes on top of that and then I can view the spores and take the photos.
This is what I mean:

All those little blobs aren't supposed to be there.  I can't tell what are spores and what aren't, or if these spores have ornaments or not.  However, I happen know this spore does have ornaments (rhodotus palmatus).

Have you tried stirring the spores into the droplet of water (e.g. with the end of a clean toothpick) before adding the cover slip? I have no idea if it would help, but if the spores float on the droplet, it might give you a cleaner picture.

No, I haven't actually.  Thanks for the idea.

At least some of the blobs that you have appear to be air. Seating the coverslip carefully will help to prevent air-bubbles from forming under the coverslip. Lay one edge against the fluid and slowly ease it down.

You mention using an oil immersion lens. It is possible that water has come into contact with your lens. Oil finding its way beneath the coverslip could also introduce refractory blobs as well.

Hmmm.. I think you probably nailed it with the application of the coverslip - I'll have to try this out.  I don't think the problem is with oil underneath the coverslip because I'm pretty careful.  I'll try slowly easing the coverslip down, as you say.  After I try it, I'll come back here and tell you how it went.


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Is a wet-mount needed to use Immersion Oil?
When I prepare my slide to use immersion oil, do I really need to wet-mount the specimen?  Can I do it with just the coverslip?
I am preparing fungus spores.
Using water for the wet-mount gives you a sort-of time limit.  You have to do your work before the water evaporates else you get little rivers at x100.

The answer is that you cannot use the Immersion Oil without water-mounting the coverslip.
I tried it.
The water-mount "glues" the coverslip to the slide, effectively anchoring it in place.  Without doing this, when you add the Immersion Oil, the coverslip will slide around because the oil "grabs" the coverslip.  When you pan the stage, the coverslip is stuck to the lens and the slide on the stage is moved around but the coverslip doesn't move because it's adhered to the lens.
When you water-mount the coverslip, it is anchored so solidly that it is actually even difficult to push it with your fingernail.
Conclusion:  No Immersion Oil without a water-mount!

I’ve done plenty of bacterial smears without a cover slip; the oil is applied directly to the specimen. I don’t know if that would be applicable in your application.

Really? Without a coverslip, that means the oil-immersed bacteria would be right on the lens.

The bacteria are fixed to the slide.

Ah, okay.  I can't do that with mushroom spores.

When I prepare my slide to use immersion oil, do I really need to wet-mount the specimen? Can I do it with just the coverslip?

Ideally you shouldn't use either with immersion oil. You should match the mounting media index as closely as possible to the immersion oil index, otherwise you'll reduce the resolution and contrast of your image. See:
http://www.microbehunter.com/the-importance-of-mounting-medium-refractive-index/

Using water for the wet-mount gives you a sort-of time limit. You have to do your work before the water evaporates else you get little rivers at x100.

There are lots of options for higher index mounting media that will also preserve your specimen at least as well as air.

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Why isn't pure animal fat appetizing to humans?
When eating beef or lamb, humans almost invariably trim away the gristle. Tastes are a bit more varied with poultry and pork but, there too, most people don't like to eat pure animal fat. (Although bacon is very popular, and some people like to eat pure schmaltz or lard.)
But isn't this strange from an evolutionary sense? The fat is the most calorically dense part of the animal, so shouldn't we have evolved to find it appetizing?

Have you asked most people why they trim away fat? If they didn't like fat, producers of beef would not feed cattle in a way that produced optimal marbling. People would not eat potato chips. French fries would be disgusting. The snack food industry wouldn't be buying millions of tons of palm oi every year. Etc., etc. Your statement isn't founded in science.

Culture plays a strong part in food and taste preferences - it's not all genetic / evolutionary.

This question is based on the false premise that what is prevalent in the tastes of where the OP lives universally true. Go to a country where traditionally people don't have enough to eat like Vietnam and they're all about the lumps of fat. I guess you could compare it to a spoonful of crystal sugar. You probably don't find that very appetizing either because it's quite abundant now and it's better when accompanied by other things which you have been accustomed to. But when it is lacking, the pure stuff is going to seem really attractive.

I've just been reading a novel about the Inuit — “De pierre et d’os” by Bérengère Cournut. The Inuit are (or were) very partial to animal fat — raw of course — and much else besides that 21st century urban man would consider unappetizing. If they weren’t, they wouldn’t have been able to survive.
So before talking about human evolution it is advisable to think on a somewhat longer timescale than that of contemporary US urban civilization, and to recognize temporary cultural fads for what they are.

Not really, in my mind. I see your point, humans love sugary sweets, but why not fatty lumps of lard? Well, humans do love fatty lumps of lard! The American diet consists of disproportionately higher amounts of saturated fatty acids. So, people tend to go for and prefer calorically denser foods anyhow. As you mention, people still use lard for cooking incredibly often, so even pure fat is at least appealing.
However, the gristle we refuse to eat isn't really fatty and is mostly inedible depending on the cut of the meat. There is an incredible amount of sugar when you look at a tree, but do you get hungry? I imagine not, because the tree is mostly inedible. So even if the resources are there, they still have to be edible for anyone to want to eat them in the first place.

Humans love fatty lumps of lard, especially when sugar is added. It's called a cookie.

I have eaten roasted bone marrow, which is basically a lump of fat. then you have fatback, lardo, ect. we don't like almost anything a pure refined state, but as it exists in the wild eating fat is pretty common.


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Good model for comparative genomics in relation to temperature adaptation
Can anyone suggest any highly related bacterial or parasitic species which live at very distinct temperatures, which might be a good model for comparison of genomes in regard to temperature adaptation. For example, related pathogens of which one species infects warm blooded animals, and the other infected cold blooded animals? So far I have come up with one possible example: Salmonella enterica is a pathogen which infects warm blooded animals, whilst Salmonella bongori infects mainly reptiles.
Examples for which there are publicly available genomes, and which have been used in previous studies would be preferable.

As a starting point I would suggest you look at genomes of thermophiles and hyperthermophiles (organisms that thrive at upwards of 40 °C and 60 °C respectively), which are often found near underwater volcanos or hot springs.
For instance, one could do a genomic analysis of the archaean Methanocaldococcus jannaschii, comparing it to mesophilic species of Methanocaldococcus or Methanococcus. This organism is well studied, and genomic information for this organism is readily accessible.
Some studies have been done comparing the genomes of mesophiles and thermophiles. For example, Zheng and Wu (2010) found a correlation between GC content in coding/noncoding regions and temperature conditions.
At the other end of the spectrum you could examine psychrophiles (organisms that grow at low temperatures, −20 °C to +10 °C). However, few of these organisms are obligate psychrophiles, meaning many can thrive at higher temperatures as well and thus may not be suitable for your purpose.


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Exhaled air and lung capacity
I wonder if there is any connection between exhaled air and lung capacity. I need to implement some algorithm in my game to calculate points of how much time you blow and compare it maybe with some sportsman.

First of all nice idea! Secondly, wikipedia has very nice graph to answer your question (Image courtesy: wikimedia commons)

Look at the caption below figure in wikipedia for specific details. You will get all values you want plus how to calculations.
[Note: Sorry, I am not able to interpret why X axis is sinusoidal]

[It's sinusoidal because the x-axis is time and it's a graph of a person breathing]

Thanks! I thought so, but what's up with sudden bump ?

They're taking a really deep breath.

There is.
At a first approximation the total lung capacity is the anatomical dead space(the volume of your trachea, more or less) + the tidal volume(the volume of each breath). It's slightly more complicated than that based on the differences in how deep you breathe and how often you can breathe, but at a first approximation exhaled air + half a liter(plusminus) = lung capacity.

The way this is worded is confusing. The exhaled air you are referring to is from a maximal inspiration to a maximal expiration, also known as FVC or forced vital capacity.  FVC + another 1/2 liter is a good good approximation of total lung volume.

Is is, but I figured I'd gloss over most of it given the precision implicit in the question. If the speed of expiration isn't being measured "how much time you blow" won't give you an accurate representation of FVC at all. And the total lung volume is only first-order related to the VO2max, which you could meaningfully compare to athletes.


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Why mosquitoes sit on wall vertically (head upper side)?
I was curious to know why mosquito sit on walls or trees vertically like head towards sky, unlike other insects like fly, ants, termites sit with any direction.
Also, what they do sitting doing nothing (rest/digestion may be)?


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Front versus back in animal anatomy
Throughout various species, there seems to be a clear distinction between the front and the back. The musculature of the front, when engaged, closes or curls up the body, protecting it, while the musculature of the front straightens and stiffens. This feels intuitively to me like a pretty fundamental pattern.
Is this a "real" pattern at an embryological level, or just a common pattern of adaptation?
Is the innervation of the front and back musculature neurologically distinct in any way?
Which biological systems show a front to back separation?
How early in evolution does a front to back distinction occur?

I'm quite confused because the terms front and back are not very specific - it depends whether you're talking about front or back of humans vs quadripeds. For example, by front do you mean cranial (the head end) or dorsal (belly side)? https://en.wikipedia.org/wiki/Anatomical_terms_of_location

oops, that should read ventral (belly side)

@vervet I think the first paragraph ("musculature of the front closes or curls up the belly") makes it clear the question is about a ventral/dorsal distinction. I am not so sure about the clarity of the actual questions. What is a real pattern at an embryological level, what is a pattern of adaptation, and how do they differ? What is a "biological system", and how does one recognize a front to back separation in a "system" which is something else than one organism's body? The second and fourth points seem clear.


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Is there any evidence that any other species are "pre-intelligence"?
Is there any evidence regarding whether other species might, given time, evolve intelligence as humans have?
I realize "intelligence" is a vague word here, but I'm interested in throwing a wide net, since I imagine the small sample size of positive cases makes finding any evidence at all extremely difficult.
The only information I've been able to find so far seems vague and unscientific, but I'm expecting that is the best I'm going to be able to find.

Welcome to Biology.SE. Unfortunately, the use of the term intelligence really needs better definition. Many species are already much more intelligent than humans in several respects (such as memory for example).

Wiki > Animal Cognition is a long article but it may help you to focus your question and your interest.

@Remi.b Totally fair, and thanks for the link!

I found another article on here after I posted this question that is at least tangentially related to this subject, in case any one is interested: http://biology.stackexchange.com/questions/339/is-there-evidence-that-some-non-human-species-perform-sexual-selection-based-pri

I don't exactly know, what the intelligence is, but i've got an idea what it can be.
I've read about smth similar before. I suppose, we can measure intelligence with working memory (don't mix with shott-term-mempory)  term (like registers of processor).
There were many experiments that was provided to check how big a working memory of humans and apes.
According to information people got from these experimence, average WM of humans equal to 7, apes - equal to 4 (count of terms subject can manipulate without any significant mistakes). So, apes can be considered as pre-intelligence this way. But anyway it is still controversial question.
You can also google articles like this:  http://www.pnas.org/content/110/Supplement_2/10371.full.pdf

This doesn't answer the question at all well

Right, but i've just tried to make "intelligence" term more suitable for measuring and tried to think of what we can get from it. Actually, if we think of all apes, several of these (like gorrilas) are considered like in a "deadlock of brain evolution". Sometimes we can find some of chimpanzee for ex. or even gorrilas that shows outstanding brainworks and ability to learn something complex (bonobo Kanzi for example). But we should keep in mind, that such individuals are not general and we can't say it has intelligence as species.


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percentage of animal diseases caused by bacteria?
I know this is a long shot, but what is the approximate percentage out of all the animal diseases that are caused by bacteria? One of the Q&A websites answer it as 90, but is there any conclusive scientific evidence?


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Homeopathy is placebo, but isn't placebo good?
I never considered homeopathy as a serious and scientific medicine, and now we have plenty of evidence supporting this (http://www.theguardian.com/commentisfree/2015/mar/12/no-scientific-case-homeopathy-remedies-pharmacists-placebos).
But placebo effect is also a thing that works, strange as it may be. The placebo effect deals with the importance of the brain's role and perception in physical health. So, in my understanding, placebo is better than nothing.
But now I can't treat myself with homeopathy, because I don't believe on it. Other people believe, and are happy with it (benefiting from the placebo effect).
So, my question is, wouldn't be benefitial to illude someone (or yourself) in order to achieve the placebo effect?

I would consider making somebody else believe in something that does not work morally wrong. If there is another treatment option that works, it might keep them from using it (or if they try both at the same time, might interfere in the worst case). If there is no other option, you give them a false hope of healing. For yourself, feel free to try. I have trained my mind on homeopathic tablets to believe they make me more focused. I know it is just sugar, my subconscious is tricked into focusing.  It might be a Pavlov's response to the taste of those tablets. As it works, I don't care.

Welcome to Biology.SE. This question appears off-topic. It is not about biology but about sociology and ethics. I suppose it might be on-topic on philosophy.SE

It's maybe off topic (it's medicine / medical ethics I guess) but I do think it's a good question. There is actually a serious debate among healthcare professionals about whether placebo treatments should be used when no other options are available, because it does bring about a positive response. You can make an argument that it would be unethical to withhold any option that improves the life of the patient, even if we know the effect is merely psychosomatic. The answer is not obvious.

This is not about ethics or sociology but the mechanism behind the placebo effect. Great question.

@GoodGravy that ethical component comes from you, not the question.

@AliceD I think given the history of homeopathy, it is difficult to answer this question without ethical consideration. However, a similar question could be asked: "Is a placebo better than no treatment" is more objective. There is no need to mention homeopathy here, and doing so is distracting.

The point of a double-blind trial is that treatments are compared to placebo effect. Therefore, conventional treatments that "pass" double-blind trials are better than placebo.  If homeopathy is equal to placebo, that means that homeopathy is worse than conventional treatment.  Therefore, people who treat with homeopathy are giving worse than standard care.

But still better than nothing, right?

That's only relevant if the only option is "nothing", and in the developed world that is not true.  It's worse than the realistic options, so comparing it to "nothing" is deceptive.

Of course a proven uneffective treatment is unethical if there is a proven effective one. But there are many disorders in healthcare for which there is no effective treatment, even in the developed world. What then?

You are moving the goalposts, continually concocting new, less and less plausible, scenarios in an attempt to force the answer you want to hear.  If your only interest is squeezing out a positive answer for a wildly unlikely situation, and then claiming victory, you're in the wrong place.

@Roland there are many things that can't be cured, but there aren't all that many where no treatment at all, like pain relief or lessening of the worst symptoms, is possible

Placebos are good to use in case-control studies. Suppose you have a cohort with depression and a cohort without depression. If you gave the cohort with depression a homeopathic cure and their mood changes for the better, you can't take that as positive results yet. You first have to use a placebo on the cohort without depression to see if their mood remains stable.

But placebo effect is also a thing that works, strange as it may be.
  The placebo effect deals with the importance of the brain's role and
  perception in physical health. So, in my understanding, placebo is
  better than nothing.

If you think, say, that your lung function is improving, but it's actually not, that's not a good thing.  It would be better for you accurately know that you are not healthy, then to wrongly believe you are better.

you think, say, that your lung function is improving, but it's actually not - If you think this is the placebo effect, you have misunderstood it.


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Human Endogenous Retroviruses
I am reading this paper, which shows that a Human Endogenous Retrovirus (HERV) K provirus is present at the orthologous position of gorilla and chimpanzee genomes but absent in the human genome.
If it's not present in the human genome, why is it still called a HERV? Should it not just be an endogenous retrovirus?
(I am not a biology student, so I might not have understood the idea of a provirus/retrovirus entirely.)

First of all, the HERV-K virus is present in the human genome, in fact it is one of the most common endogenous retroviruses there (see references 1 and 2).
In a viral infection, these proviruses get integrated into the human genome and can be found later there. This is a useful tool when you want to find out details about the split of closely related species like the great apes and humans. If you find such a provirus in all analyzed species, the integration must have happened latest at the last common ancestor. If it is only found in a part of them, it happened after the species divided. The figure (from reference 3) shows this shematically:

The authors of "your" article did this and found the integration of the retrovirus in a specific locus in the genome of gorilla, chimpanzee and human and found it only in the first two. From this they conclude that the apes are closer related to each other than to the human.
So in summary it means that the HERV-K is not present at one specific site of the human genome, not in general.
References:

HERV-K: the biologically most active human endogenous retrovirus
family.
HERV-K(HML-2), the Best Preserved Family of HERVs: Endogenization,
Expression, and Implications in Health and Disease
Differences in HERV-K LTR insertions in orthologous loci of humans
and great apes.


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Single-cell ATAC seq arrays
As part of a data analysis project, I encountered two kinds of single-cell assays
for transposase-accessible chromatin using sequencing (single-cell ATAC seq) methods. The first uses combinatorial indexing (also called sci-ATAC seq  [link]), whereas the other counts the number of Tn5 cuts in peaks (called sc-ATAC seq  [link]). I'm not a trained cell biologist or biotechnologist so I am possibly overlooking subtle similarities between the two methods here.
To my knowledge, sci-ATAC seq generates a binarised array, whereas sc-ATAC seq generates a counts matrix. (I'm also aware that there are post-processing tricks to convert binarised arrays to other array types, eg, normalised counts arrays.)
My question is, what about combinatorial indexing results in the array being binary rather than integer-valued? I'm looking for an explanation that relates the data collection method and combinatorial indexing with the resulting array type.
Thanks in advance!


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Purpose of Fc Region
Could someone explain to me the role played by the Fc region of an antibody as well as the purpose of isotype switching? According to Wikipedia, it's to allow the antibody to be usable by different Fc receptors, but I don't get what Fc receptors are for.
For context,

I'm reading about affinity maturation and learning about how ecological and evolutionary processes --- division, selection, and mutation --- drive the maturation of B cells leading to high-affinity plasmocytes that can better target a foreign antigen. Because all this happens on the Fab fragment, it makes sense to me why the Fab region is important in the antibody.
I'm not trained in cell biology.
My goal is to understand the general purpose of the Fc region and how isotype switching may be a major determinant for specific immunological or physiological outcomes, although I'd love to hear anything interesting!

Thanks in advance!

Preamble
From the point of view of understanding I think it is better to talk about the constant and variable regions of antibodies, rather than Fab and Fc, as these are historical designations for fragments of the molecules that were useful in research, but do not exist as separate entities.
Cartoon representation
It is possible to represent the immunoglobulin molecule diagrammatically as shown below. In the left-hand diagram V = variable and C = constant, and the suffixes H and L refer to the heavy and light chains. The right-hand diagram, which purports to be more three-dimensional, shows how the variable regions are responsible for binding the antigen — different manifestations of the variable region have different antigen-specificity.

The different iotypes for an immunoglobulin with a particular antigen-specificity are shown next, with a pre-colour scheme that focuses on the difference between the constant regions of each isotype.

Functions of the constant region of different isotypes
The variable region of an immunoglobulin does the exciting stuff — it binds an antigen, but that is not sufficient for its action. As well as the specific discriminatory action of the variable region, there are roles in presentation and disposal that are the same for all antibodies of a class, but may differ between classes. That is what the constant regions do.
I am not an immunologist (although had to teach the biochemistry at one time in my life — hence the diagrams) so the examples I present are simplistic and incomplete. However here are a few:

IgM is made early in the immune response and hence is not very abundant. In order to enhance its response it forms pentamers in which the constant region of the heavy chain interacts with an additional J chain.
IgA is involved in immune protection in mucous regions of the body exposed to the exterior. It is directed there by interaction with a receptor on the appropriate epithelial cells, which binds the constant regions of an IgA dimer attached to a J chain.
IgE stimulates mast cells to produce histamine. These mast cells have receptors for the constant region of the heavy chains of IgE.

There are many sources on line dealing with this topic, including a section in Berg et al. that has a similar structural approach to that presented here.

Many different cells express Fc receptors that bind to the antibody constant region and act on that signal. Wikipedia has a fair page on Fc Receptors.

The Fc region is composed of the two heavy chain constant regions, and its amino acid composition differs between the different classes of immunoglobulin (antibody). The Fc region of the five immunoglobulin (Ig) classes (IgA, D, E, G, and M)confers upon each class of Ig certain capabilities or properties. For example, IgG can cross the placenta, has a long half-life in serum, and it is opsonic (i.e., binds to Fc-gamma receptors on macrophages, facilitating phagocytosis of microbes), IgE binds to mast cells stimulating hayfever-type allergies, IgA is secreted onto mucosal surfaces, and IgM (and IgG) can activate the complement system, etc.

1.The Fc region is used as binding site for different immune system cells after the opsonisation of a pathogen.
2.Complement protein C1 binds to Fc region of antibody bound to an antigen to trigger classical complement pathway which leads to destruction of that antigen-antibody complex or opsonised pathogen


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Gel Electrophoresis
we add Etbr within the agarose gel but we do not add Etbr directly in native PAGE ?when we make agarose gel, we add Etbr before its solidification but we do not add Etbr when the native PAGE gel is in liquid form, why ?

The fact that EtBr is a potent mutagen is why it is not commonly used in liuquid solutions as it is hazardous. So this way it's in liuquid form for the least amount of time resulting in less human exposure.

Perhaps EtBr inhibits the polymerization reaction (by absorbing, or quenching, the free radicals required to initiate the reaction)? That is just a guess. While some people prefer to stain, and then destain the gel afterwards, since the EtBr is positively charged you can just add some to the running buffer in the anode chamber and the dye will enter the gel.

In the long PAGE runs, EtBr will run out of the gel.

Actually, my friend added EtBr to acrylamide solution and polymerized it. It was polymerized. In addition DNA was detectable. One of potential problems could be migration of EtBr opposite DNA. You could not detect DNA the bottom of gel unless you supply EtBr. And I guess a slight difference between gel and running buffer may cause shift of migration speed at the boundary. Because resolution in PAGE is higher than agarose, shift of migration speed might be problematic.


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At which end does polymerization of microtubules occur?
My book says that polymerization and depolumerization of microtubules occurs on the + end however, I've found a note that says that depolymerization occurs on the - end. I need help please :) thank you

From my Campbell's Biology textbook (Ninth Edition):

Because of the orientation of tubulin dimers, the two ends of a microtubule are slightly different. One end can accumulate or release tubulin dimers at a much higher rate than the other, thus growing and shrinking significantly during cellular activities. (This is called the "plus end", not because it can only add tubulin proteins but because it's the end where both "on" and "off" rates are much higher.)

So in summary: polymerization and depolymerization occur on both the + and - ends. The "+" and "-" merely designate the speed/efficiency of polymerization and depolymerization.

I think this is also a good reference that explains how proteins assist in MT nucleation and constrain the direction of MT polymerization.

Both polymerization and shrinkage of microtubules take place at plus end and minus end is anchored within MTOC's..hence is the dynamic end

Practically speaking, microtubule nucleation occurs at the plus end. This is well established in vivo and in vitro. Notably, the minus ends within most cells are "capped", so dynamics do not occur (think of the centrosome).
However, recently there is a report of MT polymerization at the minus end in a cell; this is far from the consensus among professionals at the moment, and requires much more study. Nonetheless, the rate of any growth and shrinkage at the minus end is significantly slower than the plus end, as stated above.
So for a test question, plus end is the site of polymerization.


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How the chaotropic agents help in purification of DNA molecule?
Those plants which are rich in secondary metabolites and polysaccharides DNA isolation can be done using certain chaotropic agents? can any one explain how it works?

Chaotropes would disrupt protein structure. Maybe they help by removing the DNA binding proteins?

Chaotropic agents are cosolutes that can disrupt the hydrogen bonding network between water molecules and reduce the stability of the native state of proteins by weakening the hydrophobic effect. a chaotropic agent reduces the amount of order in the structure of a protein formed by water molecules, both in the bulk and the hydration shells around hydrophobic amino acids, and may cause its denaturation (biochemistry).
A chaotropic agent is often used in DNA isolation. It's purpose is
a. To degrade membrane lipids
b. To destroy the endoplasmic reticulum
c. To degrade mitochondria
d. To limit the amount of magnesium salts in the lysate
e. To destroy the three dimensional structure of proteins
To make it simple, a chaotropic agent destroys the 3D structure of a protein, thereby leading to subsequent protein degradation. It serves as a proteinase enzyme, cleaning the cellular proteins in your DNA isolation and purification process.
http://www.hindawi.com/journals/bmri/2009/574398/
http://www.ncbi.nlm.nih.gov/pubmed/16152629

Thanks a lot for valuable answer..... but does it also any effect on removing secondary product or lipid or polysachharides

Nucleic acids share many structural similarities with polysaccharides, and they will therefore co-purify through most fractionation steps.


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Are there any predators without camouflage?
Are there any predators that don't use camouflage?

If your question is related to "natural" camouflage, i.e. camouflage that is the result of genetic programming, then Humans would be a good example of predators that do not posses natural camouflage.

Raptors are also good examples. Eagles and hawks, are not really camouflaged, although their ability to be able to stalk their prey at altitude may make them unseen to their prey, unless they are hunting other birds such as pigeons.

Birds of prey, chimpanzees, bats... there's a lot of things that don't appear to use camouflage - but it's difficult to really say definitely, e.g. I imagine a neon pink chimp would be less successful at hunting than the dark furred chimps we see in nature, so one could argue that chimps are camouflaged... Most predators will benefit from avoiding detection for as long as possible, this could constitute colouration camouflage, but also behaviours to reduce detection (e.g. stalking slowly through bushes). Wikipedia say camouflage is "the use of any combination of materials, colouration..." ...

Could you therefore clarify/refine your question, perhaps ask for examples where colouration appears to make no effect on hunting success. E.g. that could be evidenced by studies showing no relationship between the colour variation in a population and the success of hunting.

As the answers show, the answer is definitely 'yes', but without a definition of 'camouflage' I think this should be closed as opition-based. What effectively counts as 'camouflage' depends on the the perception of the interacting species (prey) - so a species can be camouflaged against one species but not another one - and it can include multiple types of colouration or behaviours.

Poison dart frogs have aposematic colouration, making them the exact opposite of camoflaged.
They are also predators, since they feed on ants, termites and beetles.

What is a predator?
As discussed in the comments by @MarchHo and @AMR, there is discrepancy between the definition of predation in the biology literature and in the every day use.
Population definition
From the Oxford dictionary

predation- The preying of one animal on others; the behaviour of a predator (predator n. 2); (also occas.) an instance of this

Under this common definition, the answer is "Yes".
Scientific definition
From wikipedia (who uses the scientific definition)

In ecosystem predation is a biological interaction where a predator (an organism that is hunting) feeds on its prey (the organism that is attacked)

Under this scientific definition, predators describe whichever organism that feed on other organism. There exist no animals that do not predate (Elysia chlorotica is a quasi exception). So, the question boils down to "Are there any animals that are not well camouflaged?" and the answer is always "Yes".
Examples
The Lilac-breasted roller (just to name a nice colorful species) is very poorly camouflaged and feeds on various insects

Zebras do not camouflage (for predation purpose) when they predate grass (grazing).

Anteater do not camouflage (for predation purpose) when they predate ants

The Mandarinfish is also poorly camouflaged and predates on harpacticoid copepods, polychaete worms, small gastropods, gammaridean amphipods, fish eggs and ostracods.

As @AMR suggested in the comments, humans are poorly camouflaged too.

Not sure if this answer is intended in jest, but zebras are disruptively camoflaged

They do not camouflage for predation purpose at least. One could draw millions of other examples of this kind of course.

I like your answer +1, especially for defining predation (which also applied for microscopic organisms).

@MarchHo Zebras are camouflaged against their predators but not as themselves being predators. That is a different issue that plants don't have vision.

And you added birds and humans after I had commented on it. It is generally customary to attribute that.

@AMR I also thought at first that predators implied carnivores, but it is also used in the context of herbivores by scientists. I agree on the issue of attribution, though.

As @MarchHo said, predation have different meaning in the scientific literature than it its everyday use. I will add a word about that.

@AMR I added the bird and human example mostly in reaction to MarchHo 's answer. I also wanted a colourful species and I wanted to state the obvious. Took me a while to see where you commented on it. I am not sure who said it first though, we both said it 15 hours ago. I don't cite hawk an eagles so I'll have a hard time to give you credit for that but I will be happy to give you credit for thinking about humans first and I will edit my post.


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Middle European Spider Identification
Yesterday I've encountered the pictured spider in my home in Austria, Europe. The colors are pretty accurate in the picture, the head was striped brown/beige and black, the legs were multicolored with a subtle pattern and the back relatively black.

The body had a length of around 2.5 cm, with legs extended the spider occupied an area roughly the same as a circle with a diameter of 5 cm.
After catching it with a glass it repeatedly lifted its front legs and whole body, but after some time calmed down, pulled the legs towards the body and lowered the body to the ground, kind of like as it was lying down.
My inital research led me to the conclusion that it might be a Tegenaria atrica. Is this correct?

I wouldn't think Tegenaria; this looks like a Wolf Spider.  Unfortunately, I'm not a European Wolf Spider guy, so here are a couple of sites that might help you get an ID:  https://ednieuw.home.xs4all.nl/Spiders/spidhome.htm  http://www.jorgenlissner.dk/default.aspx

@JohnRobinson: Thanks for the excellent links, I am also inclined to think it might be some genera of wolf spider after consulting the pages.

This is a wolf spider.
It is not Tegenaria because you would see long spinnerets at the back end of the abdomen, and the legs would not have splotchy black marks, but instead have bands of dark annulations throughout the length of the legs.
Zooming in, you can see the lycosidae eyes that are diagnostic of wolf spiders. These are the two eyes that are on top of the head.
The two dark bands down the carapace are common in a number of genera of wolf spiders, but the faint radial lines that can be seen within the dark bands and the dark eye-shaped mark in the centre of the abdomen is reminiscent of the Hogna genus (although it can be found in other Wolf spider genera as well).
Here is a gallery of Hogna for you to compare:
https://bugguide.net/node/view/3381/bgimage?from=72
Unfortunately, distributions of the Lycosidae genera are hard to describe in Europe because the jurisdictional countries are relatively small geographic areas. But we can use iNaturalist to look at the user-submitted photos (and community-decided Identifications) of Wolf spiders in Austria here: https://inaturalist.ca/observations?place_id=8057&subview=map&taxon_id=47416&view=species
and it shows that the most common wolf spiders seen and identified there is Hogna radiata.
And here is a gallery of user-submitted photos of Hogna radiata observed in Austria:
https://inaturalist.ca/observations?place_id=8057&taxon_id=326871

Wow, thanks for the extensive information and the links!


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Are Sharks able to detect electromagnetic waves using their Electroreception ability?
I will include some publications and links that may help. I could not concluded an answer with my limited knowledge on the subject.
Shark Passive electroreception sensitive to low frequency (below 50 Hz).
Peer-reviewed Publications (Elasmobranch Research Laboratory).

Short answer yes sharks have an organ called the Ampullae of Lorenzini that allows them to sense electric fields given off by other animals. If you want to learn more check out this link http://www.sharksinfo.com/electroreception.html


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Is this bacteria or fungi?
I've been growing bacteria on an agar plate and after putting the dishes in the incubator, this is what I saw. I'm new to bacteria identification, and is this just contamination by fungi or is this actually bacteria colonies? I suppose it is fungi, but what about the white, round white circles on top of the fungi(the top, left picture), is that bacteria colonies?

Well what did you put on the plate? Currently it's extremely hard to answer because we know very little about your experimental protocol.

@rg255 I put my thumb on the plate, to see the amount of bacteria on it to then compare the amount with after washing the hand using different methods. I suppose the plate may have been contaminated from the air because of insufficient sterile technique.

How about a side view? Do you see spores in the stalks?

It's probably mostly fungal contamination if you did not sterilize and left the container open. This video on how to isolate bacteria better may help: https://www.jove.com/video/3064/aseptic-laboratory-techniques-plating-methods
Good luck!


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Problem with phosphorylated and total forms of antibodies
Antibodies are available that can detect both phosphorylated and total endogeneous levels of the given protein. I have a question here, why is it necessary to have equal amounts of total protein? This is a common assumption that variations come in phosphorylation status but since total detects levels of both phosphorylated and non-phosphorylated forms, it is supposed to be equal. Not necessarily! Depending on the requirement of cells, phosphorylation status may change. And so does the expression of the total protein itself specially if the non-phosphorylated form is acting as a transcription factor.This is what I find in my studies as well. But the literature suggests the opposite. Why?


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Why does ESR have to be waited for one hour?
It is said that the length of the column of clear plasma in a narrow tube left by erythrocytes which gradually sediments after one hour is the measure of ESR(erythrocyte sedimentation rate). Its normal values are found to be 3-5 mm after 1st hour for male and 4-7mm after 1st hour for female. What I want to know is why "1 hour" has been chosen. Why not 30min, 2hr, 3hr etc?

Does it really make a difference how long they settle, or why they chose that amount of time? At one extreme, you haven't really given them adequate time, at the other, there's no more useful information to gather.
The tubes in which Sed Rates (or ESR) are measured are 200 mm in height. Why wait three hours for the result (which is still expressed as a rate, i.e. mm/hr)? In three hours, they may (depending on how quickly they settle) have all settled an hour and a half ago. (If an ESR is 100mm/hr, it will hit the settled cells at the bottom before it finishes settling if two hours is the length of the test.
The test is simple, cheap, easy, with good sensitivity and specificity. And the results come back in a little over an hour. The sooner the diagnostician gets the results back, the sooner the answer helps in the decision tree needed for the treatment of the patient. Longer wait times aren't helpful and may not be accurate with very elevated ESRs.
Acute Phase Proteins Molecular Biology, Biochemistry, and Clinical Applications By Andrzej Mackiewicz, Irving Kushner, Heinz Baumann, 1993


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Can DNA be denatured at acidic pH?
Some say that DNA is denatured only at basic pH. And some say at both acidic and basic pH. So I want to know clearly why and how if DNA is also denatured by basic pH.

Alkaline denaturation neutralize the charge of acids but also cause hydrolysis of bases upon prolonged treatment. Strong bases will raise pH until the H+ shared between the N-base electronegative centers (N-H and O=) is stripped from the H-bond, effectively breaking them.
Organic solvents such as dimethyl sulfoxide and formamide, or high pH, could break the hydrogen bonding between DNA strands too. Low salt concentration could also denature DNA double-strands by removing ions that stabilize the negative charges on the two strands from each other.
Low pH (less than pH 1): both RNA and DNA hydrolyze (phosphodiester bonds break and the bases break off).
High pH (greater than pH 11): RNA hydrolyzes, DNA will denature but the phosphodieser backbone remains intact.
[salt]
Tm is sensitive to Na+ concentration.
Na+ acts to shield the negative charges of the sugar-phosophate backbone from interacting with one another. The repulsion between the negatively charged phosphate backbones is the major force destabilizing the double helix, therefore increasing Na+ concentration increases helix stability and decreasing Na+ concentration decreases helix stability.
References:
http://faculty.tru.ca/dnelson/courses/biol335/335notes/3recdna/4-hybrization/recDNA3a.html
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1367631/pdf/biophysj00681-0002.pdf

So could u please explain how denaturation differs from hydrolysis?

@AungT  As far as i know with the term denaturation is related to the change from a double strand DNA (dsDNA) to a single strand DNA (ssDNA) due to breakage of hydrogen bonds (it could be caused by heat), while in hydrolysis there is a degradation of the strands backbone eg phosphodiesterases enzymes hydrolyse the phosphodiester bond between different nucleotides.

Denaturation is a process in which proteins or nucleic acids lose the quaternary structure, tertiary structure and secondary structure which is present in their native state, by application of some external stress or compound such as a strong acid or base, a concentrated inorganic salt, an organic solvent (e.g., alcohol or chloroform), radiation or heat
The denaturation of nucleic acids such as DNA due to high temperatures is the separation of a double strand into two single strands, which occurs when the hydrogen bonds between the strands are broken.
DNA Hydrolysis is a chemical method of DNA denaturation.DNA hydrolysis is the breaking of DNA through the addition of water. It can be done in several fashions; enzymatic (exonucleases)or chemicals (acid).
In general, hydrolysis is defined as the cleavage of chemical bonds by the addition of water
References:
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2806061/
file:///C:/Users/user/Downloads/9783540201120-c1.pdf

So hydrolysis is also a kind of denaturation? The difference is just the method used?


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What protein(s) serve as the control antigen in Covid lateral flow tests?
Having recently been obliged to take a lateral flow test for Covid in order to fly from the UK, I idly wondered:

What is the control antigen for Covid lateral flow tests?

as (fortunately) that was the only band I saw.
Easy — just Google? You jest! “Other people asked”, “All you need to know” and even the scientific papers linked just talk about the target antigen.
This sort of thing really gets up my nose!
Could someone please tell me what it is up my nose?

You mean the red stripe at the upper control position of the test? See this question where it has been answered: https://biology.stackexchange.com/questions/101767/whats-happening-in-the-c-and-t-stripes-of-a-covid-test-kit

@Chris. I see. It is the test antibody itself. So this would seem to control only for addition of the test solution, and not whether I’ve swabbed my nose adequately. Is this correct? If so, it doesn’t seem correct.

@David, you are correct. Even if you don't swab the nose and put "clean" extraction buffer on the test card, you will get the "C" band. On my tests, even tap water gives the "C" band (although a bit lighter, but still clearly visible).

Absolutely correct. There is no control if you took the specimen correctly. Luckily most "corona skeptics" do not understand how this test works. As @Domen says, you get the control band with water only. Oh, btw. you can also fake a positive best by using a few drops of apple juice or coke.

@Domen Thanks. Well I’m waiting for a plane to take me to the ski slopes now. No point in going if I didn’t really test negative. First time in an airport for two years — never seen it so empty. Trust I can negotiate Swiss and French controls.


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Could You Boil Water from Blood?
According to Wikipedia...

About 55% of blood is blood plasma, a fluid that is the blood's liquid
  medium, which by itself is straw-yellow in color. The blood plasma
  volume totals of 2.7–3.0 liters (2.8–3.2 quarts) in an average human.
  It is essentially an aqueous solution containing 92% water, 8% blood
  plasma proteins, and trace amounts of other materials.

Does this mean it would be possible to boil water from blood for consumption? For example, in The Walking Dead, Rick and the gang are dehydrated and without water. When a pack of wild dogs confronts them, they kill them and cook them for consumption. Could they have collected the blood, boiled it, and used some sort of contraption to catch the clean, vaporized water?

It seems possible, vaporization can work for this.

This question doesn't make sense. Any substance that contains water can be vaporised and the water later distilled.

@MarchHo I agree with you, but I am still impressed by how Zulfe could think about this disgusting but interesting topic ;)

I'm voting to close this question as off-topic

Seems ok to me. It's framed properly in a biological context

This question is rather about chemistry and methods to seperate water from other liquid. Distillation is probably the solution indeed.


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How to construct tumor phylogenetic tree?
I would like to know if anyone has tried any software that constructs tumor evolution trees where the trunks represent the common mutations and the private alterations are noted on each branch. I can do it manually but the sample size is too big (nearly 100 patients). Here's a good example of what I'm after here on Figure4 http://www.nature.com/nm/journal/v21/n7/full/nm.3886.html
Any additional computational model suggestions are welcome.

I do not know if this is exactly what you are looking for. The ETE toolkit for python is possibly worth a look.


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What is the best test for SNV clustering?
I am looking for a method to cluster single nucleotide polymorphisms based on clinicopathologic data (mainly receptor immunoistochemistry). So far, I've came up with only two that handle dummy variables as long as I want to examine minor allele presence or absence;

Principal Component Analysis
A priori (association rules)

Do you know of any papers supporting the abovementioned methods, or maybe suggest an alternative one?


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Measuring tumor heterogeneity
I would like to ask if there's any method (established or not) in order to quantify heterogeneity found in mutations occuring in primary neoplasms and metastatic lesions (either common or private) and potentially correlate this number to standard clinicopathologic traits.

What kind of heterogeneity: genetic, morphological, biochemical?

The methods that come immediately to mind are mostly related to next-generation sequencing. You can do deep sequencing on your sample, which is just increasing the coverage as much as possible to find rare events. You can do RNA-seq to look at the transcriptome, ChIP-seq to look at chromatin modifications, and single-cell sequencing (a form of deep sequencing operating on individual cells) to get truly cell-by-cell data, either from the genome (DNA) or transcriptome (RNA).
If you are purely looking at phenotypes, flow cytometry is quite useful for analyzing relative expression levels of proteins, using both extracellular and intracellular markers and stains. FACS is an extension of flow cytometry that allows for the sorting of various cell populations into separate containers. These "purified" samples can then be used in any of the methods listed above.


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How to compare diversity between different ecosystems?
I've used the Shannon Wiener Diversity Index for a single ecosystem (species as categorical variables). Do you know any alternative indices, especially ones that compare diversity between different samples/ecosystems ?

You should have a look at Magurran. 2003. Measuring Biological Diversity

Have a look at the Wikipedia page on Diversity Index
Here are the indices that the wikipedia page describes

"True Diversity" Index
Species Richness
Shannon Index
Rényi entropy
Simpson index
Inverse Simpson index
Gini–Simpson index
Berger–Parker index

The article also links to related concepts such as

$\alpha$ Diversity
$\beta$ Diversity
$\gamma$ Diversity
Isolation Diversity
Relative Species Abundance

The literature is important on the question of measuring species diversity, ecosystemic function diversity and genetic diversity. What you want to use very much depends on your interest. Just to cite one other example: In the conservation literature, total sum of branch length over a phylogeny is sometimes used as measure of diversity and is sometimes used for prioritize populations (see for example Curnick et al. 2015). This method implicitely assume that more distantely related branches have different ecosystemic functions and keeping many of these functions is good for conservation purpose.


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What's the difference between CREs and DHSs?
I would like to know what's the difference between cis-regulating elements and DNase I–hypersensitive sites, in order to produce a meaningful segregation of non coding elements affecting gene expression.

Have you read https://en.wikipedia.org/wiki/Cis-Regulatory_element and https://en.wikipedia.org/wiki/DNase_I_hypersensitive_site ?

Cis-regulatory elements are simply DNA regions upstream or downstream of a gene that can affect its expression (basically they have to be in the same chromosome).
DNAse-I hypersensitive sites (DHS) are regions of chromatin that get digested during the DNAse treatment because they are exposed i.e. not protected by a protein (complex). The protein complex can either be a nucleosome or a transcription factor. It should be noted that a DNA region can be DNAse insensitive also because of its conformation.
Usually the cis-regulatory elements exert their effects by serving as a binding site for a transcription factors (or chromatin remodellers). If the proteins bind at these sites then these regions would be protected from DNAse digestion thereby making them not-DHS. However, it is known that DNA elements can act in trans as well (see papers on 3C- chromosome conformation capture, and its variants). Moreover, whether a site is protected from DNAse or not does not tell anything about its function.


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Why do dogs come in all shapes, but cats are generally all the same?
Minus hair and fur, cats (the domestic kind) seem to be just scaled versions of the same thing.  Dogs on the other hand can have long necks, short necks, long bodies, short legs, long ears, short ears.....

To my knowledge, there are quite a number of cat breeds (domestic) which have the same distinct features as listed by you above, such as longer tails, long ears (Devon Rex), short tail (Japanese Bobtail), different eye colours (Khao Manee), short legs (Munchkin)... what knowledge/source did you base your statement on?

They don't actually come in all shapes. They were bred like that as explained in the answer.

it's artificial selection

Until recently, cats were not extensively selectively bred, but were allowed to roam freely and therefore interbred randomly.  Darwin pointed this out, contrasting cats to species that were routinely "enclosed":

On the other hand, cats, from their nocturnal rambling habits, can not be easily matched, and, although so much valued by women and children, we rarely see a distinct breed long kept up; such breeds as we do sometimes see are almost always imported from some other country.

In contrast, dogs and some other species were selectively bred for certain characteristics "each good for man in different ways":

The key is man's power of accumulative selection: nature gives successive variations; man adds them up in certain directions useful to him. In this sense he may be said to have made for himself useful breeds.

Why were cats not selectively bred, while dogs were? This gets to be somewhat speculative, but it's clear from looking at dog breeds that many of the different breed functions need to have a larger animal than a cat, as well as one with different personality: Herding sheep, hunting foxes or badgers, fighting bulls, etc.  Cats' function for humans has traditionally been to hunt mice and rats, a role for which they're already beautifully adapted.
(There are a number of small dog breeds, of course, but these parallel cat breeds in that many are ornamental, or else originated as rat-hunters.)

Also, if a cat is to be out hunting mice & other vermin, it has many opportunities for random mating.

Indeed, we'd have guard cats, hunting cats, retriever cats, rabbit warren cats, racing cats... let's go to the cat races!

Cats are small size for hunting closer on the ground for small rodents
dog were born with longer legs for travel linger distance because of great stamina
cats dont have stamina like dogs but they are great sprinters to run 30mph for short burst


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Need to solve a "pseudo-metabolic" network for rates
following problem:
I have data on a certain complex association network (from monomers 1 ... 8 to complexes of all combinations, such as, 12 ... 13 ... 18 and so on until 12345678, so that I know

the structure of the network (255 vertices)
the edges of the network
the concentrations of the vertices

From this data I now wish to infer the preferred route(s) of assembly for those complexes - which should be the rate constants for the edges, such as 1 --> 12 or 145 --> 1458. Does that make sense?
I have now tried various standalone applications for network creation/analysis as well as R packages. Metabolic flux analysis seemed promising for me, but it turned out that it only works with set external concentrations and assumes steady-state for all metabolites within the network. Which is not the case for me. Do you know of any alternative method?
Thanks and best wishes,
Simon

Hi. May be this question would be more suitable for cross validated, for example. But anyway, if i got you right, you are trying to put some marks for edges that is associated with the way they need to be assembled? I'm not biologist at all, just try to get your full task.

Thanks for your recommendation, I will look into posting it over there.
Yes, exactly, I want to find out the relevant routes of assembly (=paths), which should be the ones with the highest "flux" there...

yes, but the best resource for this question, i guess, this https://www.biostars.org/

Flux balance analysis always assumes steady-state, and in this case concentration data is irrelevant.  It sounds like you're after some type of dynamic method that can handle time-varying concentrations. In this case the problem is much more complex, and you really need to describe the problem in more detail. What kinetic assumptions are you willing to make? (Michalis-Menten, or ... ?) Are you going to fit time series data? What are boundary conditions? What type of data do you have, a pulse experiment (unit step input), or ...  ?


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What are these Insects?
I live in my hostel in NIT Tiruchchirapalli, in India. My hostel is infested with these beetle-like insects.

These insects posses a hard shell, if you flick them off the wall, they make a "tap" sound when they hit the ground. They're capable of flying but mostly stay on walls, sometimes even motionless. They also seem to be rather stupid, even for an insect. They don't attempt to escape even in life-or-death situations
tl;dr
What are these insects?

they are definitely beetles. size is important to know, and a better picture would be helpful too.

@picapica They're approximately 0.8cm from head to abdomen. I can't get a better picture as my phone camera can't focus that close up.

I'm trying to answer my own question. I did a bit of searching, and I found out that my insect resembles the Mupli beetle the most. From Wikipedia:

The Mupli beetle, Luprops tristis (ഓട്ടുറുമ in Malayalam), is a plant detritus eating Darkling beetle found in parts of India. The adult beetle is black and around 8 millimeters (0.31 in) long.

I hope someone can verify if my findings are correct or not.

Tenebrionidae is correct. Your ID may be correct.


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Insects are attracted to light, what if the light is too bright?
Insects are known to approach light sources. I know that they use it as navigation tools, by maintaining a constant angle between their path and the light beam. However, if a light source is exceedingly bright, I mean like "blinding" bright, would an insect still use that as navigation tool?
What I have been thinking is, the insect wouldn't use it, and try to escape from the light source. I believe this because the extreme blindness may cause the insect to damage it's eyes, although I am neither knowledgeable nor capable of confirming this.
Such a thing usually doesn't happen in nature, so I'm unsure if such a test has been made before. Nontheless any help would be great. I also understand that my definition of "bright" isn't well defined, since I don't know the maximum intensity an insect can handle. I also haven't mentioned the insect, so for consistency sake, assume it to be a Black Witch moth (Ascalapha odorata)
tl;dr
Would an insect use a light source that's exceedingly bright to navigate?

First, your assumption that insects use light as navigation might be wrong, the flight-to-light behaviour is still far from understood. Link. Secondly, I doubt a light can be too bright. The incandescent lights that are often used for trapping them are so bright that human are blinded by them.


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Are all cone cells connected directly to the brain?
Coming from a computing science background, I noticed that cameras have orders of magnitude fewer wires than pixels. For example, the Raspberry Pi Camera v2 has 8 megapixels, but only 10 wires connecting it to the board. In human-made systems, it is preferred to time-multiplex pixels over few wires or, even better, already compress or encode image information on the camera.
I was wondering if the human optical system features something similar. Does the eye compress, encode or time-multiplex the image "pixels" it captures before sending the information to the brain? Or is each cone cell ("pixel") connected directly to the brain?
(In case the latter: Wow! The optical nerve must have a huge bandwidth.)

This isn’t my field so hopefully someone can give you a better answer, I just wanted to say that there is some processing in the retina. The signals from many photoreceptors are integrated by and/or into retinal ganglion cells, whose axons make up the optic nerve and number much less than the total number of photoreceptors.

Are all cone cells connected directly to the brain?
No.  Cones connect to ganglial cells.
Let's explore the numbers.  Our eyes contain about 6 million cone cells, 90 million rods, and comparative handfuls of additional photosensitive cells (ipRGC's) that don't play a role in vision.
The optic nerve is a bundle of roughly 1 million fibers (perhaps up to about 1.7 million).  So by just running the numbers, it doesn't fit.
I was wondering if the human optical system features something similar.   Does the eye compress, encode or time-multiplex the image "pixels" it captures before sending the information to the brain?
Let's focus on photopic vision (color vision, which happens when lighting conditions are sufficient).
Our perception of color starts not with the cones, but with ganglial cells in the retina.  This is different than how an RGB camera works; our brains don't process color in terms of "pure cone signals".  Instead, color is processed in three channels; a "red-green" channel that measures the difference between L cones and M cones;  a "yellow-blue" channel that adds input of L and M cones and subtracts out contributions from S, and a "brightness" channel that computes the sum of all cones.  This is referred to as opponent processes.  Maybe we can call this encoding.
In addition to this, there are ganglial cells in our retina that contribute to edge detection.  These cells work similarly to ganglial cells that perform difference measurements for opponent processes, only they connect to the same cone types.  Since ganglial cells connect locally, if there's a large difference between stimulation of two cones next to each other, it's an indication that there's an image of an edge of something projected onto that spot.  If we can't distinguish individual cones, but these things can distinguish edges which to us are the more interesting property, maybe we can call this lossy compression.
Outside of this, a huge amount of our brain is devoted to visual perception.  There are some really strange quirks about our eyes; most popular is the existence of the blind spot.  Additionally, our 90 million rods are squeezed more into peripheral vision, leading to fuzzier imaging in photopic conditions the farther away we are from the fovea.  Furthermore, chromatic aberration can be quite a pain, but L and M cone sensitivities are very close to each other.  So where absolute sharpness matters, we have less S cones around; in fact, in our foveola, there's nothing but L and M cones.  Our brain makes up for this, by stimulating us to move our eyes constantly and rapidly (saccades).  As we do so, the visual cortex goes into overdrive, filling in that blind spot, crisping up that periphery a bit, painting in an illusory blue in our center vision, etc.  Though this involves "moving the camera around", we could maybe call this a sophisticated, high level form of time multiplexing.
Much of this information is available from wikipedia articles, though you might need to know what to look for; so here's a starting guide:

Cone_cell for cone cell counts
Fovea_centralis for cone density in center in vision, with picture
Optic_nerve for count of optic nerve bundle fibers
Opponent_process for opponent process theory
Receptive_field contains discussion of edge detection

Fascinating to read your answer! We basically have a Sobel operator in our retina.


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'Obviously True' Statements that turned out to be false?
As someone who studies mathematics, there are plenty of examples by which some theorem that was considered as "obviously" true later turned out to be completely false. I was discussing this with my friend when she asked me to cite examples outside of math. The first thought that popped in my mind was the notion of spontaneous generation, but I'm not sure if it was so completely agreed on to be true that it was "obvious". As she is currently a biology undergraduate, I wish to tailor my examples to her interests.
In short, I'm wondering if there are any examples in the history of biology where some "fact" was so seemingly simple and obvious that researchers took it for granted, but it ended up being found to be completely false.


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How many proteoforms are theoretically possible?
Initially, I was going to ask how many proteins were possible. But, while researching the question, I learned the word proteoform and have been reading a lot of stuff I don't really understand, but from I do think I get,  the word "proteoform" was created because sometimes the "typical" or "canonical" forms of a "protein" can take different forms, or "proteoforms" based on environmental and possibly other factors, despite being coded for with the same DNA. So, a "protein" will often (always?) have several different "proteoforms". As I understand it, it is part of the protein-folding problem, and the complexity is huge. I was trying to see if anyone has calculated or figured out what would be needed to calculate how many proteoforms were possible, but I don't find anything. I imagine the number is tremendous, I just wanted to know how tremendous. So, how many proteoforms are possible? If that's not known,  what would be needed to know this? Thanks.

Possible duplicate?: https://biology.stackexchange.com/questions/108908/is-there-are-theoretical-limit-to-the-number-of-proteins-possible-and-their-resp I know this is about proteins rather than "proteoforms", but the distinction does not seem particularly important at scales like this.

@BryanKrause I think the question is a duplicate, at least in the sense that the question+answer note the existence of isoforms/alternate structures making the upper bound of the answer huge.

Does this answer your question? Is there are theoretical limit to the number of proteins possible and their respective structure?


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Is there a specific word for fertile hybrids?
The way "species" has always been described to me is that a species is different if the two animals cannot have fertile offspring, with the caveat that language is imprecise and sometimes different species can produce fertile hybrids. For example, "pizzly/grolar" bears, which are grizzly/polar bear hybrids produce fertile offspring. Another example is coywolves, which are wolf coyote hybrids. So, I was wondering if there is a specific name for fertile hybrids. The Wikipedia page on Hybrids doesn't specifically talk about fertile hybrids as a group. To be clear, to me, "fertile hybrids" is a sufficient descriptor. I just wanted to know if there was a more scientific term that is used in place of "fertile hybrids." My guess is that there is not, because I think I would have come across it by now, but I just wanted to be sure. Thanks.

"Admixed individual"? there are a variety of archaic and rather nasty words that mean more or less this, but as a society we have thankfully moved away from terms like "bastard"; "mongrel" is equally nasty when referring to people, but seems to still be standard for e.g. dogs.

The definition you're using for species there is called the "Biological Species Concept". It has a lot of problems.

In animals it is simpler, but in plants fertile hybrids are extremely common in certain families (e.g., Rosaceae) and even hybridogenous apomyctic lineages are often sexually fertile to a certain degree and give birth to new hybridogenous types that cause extremely complicated taxonomy in brambles, dandelions and similar.

Not that an exhaustive list is possible, but the hybridisation of neanderthals & homo sapiens is of particular interest, & undergone recent dynamic change in understanding. & the ape chromosome fusion that seems to have initiated the speciation of hominids, is an interesting example of a highly unlikely set of chance circumstances, leading to a significant biological change - a punctuation in equilibrium, rather than steady mutation.

I'm not aware of a single word term in use, "fertile hybrid" seems like a reasonable descriptor. Something like 4000 hits on Google Scholar so it appears it's definitely used, hybrid fertility matches about 3000. In cases where the hybridization is quite well known to be fertile, I'd expect people to drop "fertile" and just speak of hybrids, especially among plants (which may or may not be designated the same species; species are just labels and can be messy).
Another relevant term is introgression, which occurs when hybrids breed with one of the parent species and therefore has the ultimate effect of transferring genes from one species to another. Describing introgression as occurring also may clarify a bit what sort of hybrid fertility you're talking about, because it may be that hybrids are only fertile with one of the parent species, or either parent species but not another hybrid.

Another term related to introgression are hybrid swarms. Without introgression we can get hybrid speciation.

Genetically viable?

Genetic viability is the ability of the genes present to allow a cell, organism or population to survive and reproduce. The term is generally used to mean the chance or ability of a population to avoid the problems of inbreeding. Less commonly genetic viability can also be used in respect to a single cell or on an individual level.

authors: Vladimir F Героям слава


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How difficult is it to determine species by a single tooth?
I saw a U-Haul truck with a sign about the Gray Fossil site in Tennessee. The U-Haul specifically mentioned a red panda being found at the site, so I googled "gray fossil site red panda". The first page that came up said, "One of the most exciting finds was the tooth of a red panda, found in 2002." This kind of amazed me, because it makes it seem like they found the tooth and, without other remains, knew it belonged to a red panda, which they named "Bristol's Panda". To be fair, the next paragraph says, "Over the years, the paleontologists found more teeth and more bones of the red panda", so maybe they only identified the tooth as belonging to a red panda after they had more evidence, and the article just words it to sound differently.
Either way, my question is, how difficult is to determine the origin species of a single tooth; i.e., how reliable is an identification of species that is based on a single tooth? Is this even possible? I'm reminded of a famous case where a scientist (maybe more than one) misidentified the tooth of a pig as an extinct human species, but I don't remember much of the details other than that the error was quickly caught and rectified. It just seems astonishing to me that teeth would be so unique between all species so as to correctly identify the owner of a tooth, with nothing other than the tooth.
When I try to research this answer on my own, all of the articles that come up regarding dental identification deal with either identifying specific humans by their teeth, or how human teeth are different from animal teeth, but where they fail is that none of these talk about the reliability of species identification based on a SINGLE tooth. So, how reliable are species identifications based on a single tooth?

Disclaimer: I'm no anatomist or work on these things at all.
I believe that identification of the family and possibly genus and species of a specimen based on a tooth is fairly easy. Richard Owen, the famous biologist who founded the Natural History Museum in London UK and coined the word "Dinosaur" wrote a treatise on this in the late 1800's titled Odontography: Or, A Treatise on the Comparative Anatomy of the Teeth; Their Physiological Relations, Mode of Development, and Microscopic Structure, in the Vertebrate Animals which was a seminal work on the anatomy of teeth and included many of the recently discovered dinosaur and other fossil teeth. You can read the whole book on Google Books.