text:
Special bacteria in infants
This question is similar to a previous question, but is not the same.
I was told, you are born with a bacteria in your digestive track that are made by the body. Can a body in development create it's own bacteria from nothing? Also said by the teacher the first time you take an antibiotic it is gone forever?  Can a body in development create it own bacteria from stem cells? Is there such a bacteria, can it be cultured and re-introduced into the body?

No, no human (or any other eukaryote lineage) are able to "create bacteria". The story you were told is wrong.
However and interestingly, female parasitoid wasps seem to "create viruses" (Herniou et al. 2013). The viruses are part of the wasp genome (lysogenic phase) and detach (lytic phase) in the ovaries only. The viruses, then infect the caterpillar in which the mother lay its eggs. The viruses ensure to reduce the immune system of the caterpillar in order to protect the wasp egg (and later larvae) and ensure its development to adulthood.

Whoever told you this story is wrong. Bacteria are prokaryotic single celled organisms, humans are eukaroytic multicellular organisms. These are so different, that it is impossible to convert one into the other.
When babies are born, their digestive tract is sterile (see reference 1 for details and a huge amount of additional references). However, it is colonized by different species of bacteria in a matter of hours, depending on the delivery and also the feeding methods.
References:

Newborn baby digestive tract
Postnatal Development of Intestinal Microflora as Influenced by
Infant Nutrition
Why is initial bacterial colonization of the intestine important to
the infant’s and child’s health?

Pasteur and Redi disproved spontaneous generation a century ago.  So no, babies are not magically making bacteria in their guts.


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

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

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

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

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

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

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

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

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High pressure cryonics
In this link, it is suggested to use high-pressure cryonics to freeze living cells, tissues or small organism as opposed to various and potentially toxic anti-freeze agent. The core idea is that over a certain pressure, ice is anamorphic and will not form ice crystals. Thus, organic manner will not be destroyed by said crystals.
Detailed information about the proposal can be found at this link:
https://www.benbest.com/cryonics/pressure.html
I have considering self-financing the experiment. Could anyone chip in with some advice? Do you see any red flags, design tips, etc.?

I’m voting to close this question because it is: 1) unclear, 2) appears to not be about biology as defined in the [help], 3) requires following an external link to understand, and 4) solicits opinions and advice instead of requesting a fact-based answer. Each of these alone is sufficient reason for closure. Please take the [tour] and then go through the [help] pages starting with [Ask] questions effectively on this site and delete or [edit] your question accordingly.

The linked material seems quite old. High-pressure freezing of cellular and tissue samples for electron microscopy is now routine, automated machinery is commercially available: Leica EM ICE
I have used this machine's precursor, EM PACT2, it was able to vitrify samples up to 200 microns in diameter. The new machine is likely to have the same size limitations. Rather than pressure, what prevents the formation of ice crystals is rapid cooling; nanometer-thin samples can be vitrified at ambient pressure. Increasing the pressure slows crystal nucleation down, so heat has time to exit larger samples. The sample size cannot be increased arbitrarily, though; high pressures need a strong vessel, and thick walls will insulate the sample, preventing rapid cooling. In the EM PACT2, the copper tubes used to contain the sample would occasionally rupture from the applied pressure. Use of exotic materials might allow higher pressures with similar thermal conductivities, but it's unlikely you'd be able to reach the millimeter scale, even.

One premise of the full proposal is that the freezing process should avoid the formation water crystals which prevent structural damage of membranes and proteins and keep the integrity of the life organism being frozen under high-pressure cryonics.
I have not seen a discussion on the thawing process which I always thought was a problem for example when thawing cells for in vitro cell culture.
For the design I would try small with for example mammalian cells like HeLa. Maybe full organisms like worms or flies for "tissues" and "full organisms".

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3cm Worm Found in a Glass of Tap Water - please help identify

3cm Stripy Worm Found in a Glass of Tap Water - please help identify. The worm was found in the beginning of July in a glass of tap water, in Ireland. It was about 3cm long, had a round shape and was moving quickly. It had no legs.

Welcome. Don't you by any chance have a better quality picture?

I don't have a better picture unfortunately...

You need stereo microscopes to take a better picture with more resolution.


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I am trying to identify this little "bug"
I am trying to identify a bug. I find this little guy in Paris, at the rooftop near plants, in the streets without plants. I let one on my t-shirt, and it was trying to unpick it. I took a picture :

I think remembering having seen such bugs in old closets, on clothes, when I was kid, but I am not sure.

The focus isn't the best, but it looks to me like a lace bug (order Hemiptera, family Tingidae); not knowing the French fauna forbids further depth from me.


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Can bacterial DNA solutions, which include other cellular components, be stored without compromising DNA stability?"
Question
Can bacterial DNA solutions, which include other cellular components, be stored without compromising DNA stability?"
Details
I'm using the boiling extraction method to extract acinetobacter bacteria's DNA, as following:

The bacterial deoxynucleic acid (DNA) was extracted by the Boiling
method of Chen et al., (2020). About 3-5 colonies of each
Acinetobacter isolate were emulsified in 100 µl of sterile dist.
water, incubated at 95 °C on a heat block (Thermo Fisher Scientific,
UK) for 15 min., and centrifuged at 10.000 rpm for 10 min. The
extracted DNA was stored at -20°C for amplification of the target
genes using PCR.
https://nrmj.journals.ekb.eg/article_276319.html

It works as the reading of the spectrophotometer are:

dsDNA conc (microgram/millilitre): 113.26
Ratio A260/A280: 1.77

Today the centrifuge stopped working. To keep to a timeline and to not waste the opportunity of having over night cultures (that were cultured for another purpose) at hand , can I store the suspension after the boiling step, then when the centrifuge device gets fixed, I can go on as usual?

It would depend on which variant of the method you are using. What's in your lysis buffer?

No lysis buffer, just 95 Celsius water bath. Tbh i haven't tested the long term stability of the product i get because i haven't done this method for a long time. I have a dummy sample that i'm have been keeping intentionally at room temperature to for 10 days compensate for the time factor, i'm going to measure it.

Normally this process is done in the presence of a buffer of some sort - it helps keep the DNA stable; i.e. pellet bacteria,  resuspend in lysis buffer, boil... Measuring the concentration is no indication of stability. You need to measure degradation using a gel or similar method. Also what sort of DNA are you after - plasmids are different to chromosomal.

Chromosomal, sorry I'm a beginner. I got this method from a published article. My downstream purpose is conventional pcr-amplification of partial gene (350 bp)

The article didn't mention any buffer, but it didn't mention how they stored their DNA,maybe they just extracted it in distilled water then added the buffer after that?

A link to the protocol would be useful as an edit in the question - unanswerable in this state. Most likely it will depend on the bacterial species too, so would be helpful to add this to the question too.

Done this part .


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How is the zone of inhibition formed in disk diffusion?
Question
How is the zone of inhibition formed in disk diffusion?
What I mean by the formation of the zone of inhibition is not the ultimate visibility of such zone but the circumstances that result in the matter becoming settled and further incubation being merely done to reveal the endpoint of the experiment:

In general, the entire process is completed and the position of the
zone of inhibition determined within the first few hours of
incubation.
Barry AL. Procedure for testing antibiotics in agar
media: theoretical considerations. In: Lorian V, ed.
Antibiotics in laboratory medicine. Baltimore: Williams &
Wilkins, 1980:1–23.

Prior research

The zone of inhibition is formed when a critical concentration of drug
(that amount that is just capable of inhibiting microbial growth under
the test conditions) reaches, for the first time, a density of cells
too large for it to inhibit. The size of the zone of inhibited growth
is determined by the distance that the critical inhibitory
concentration can diffuse into the agar medium before a particular
density of cells is reached. Thus, the diffusion test is actually a
race between the drug diffusing from the reservoir and the
microorganisms initiating growth.
Barry AL. Procedure for testing antibiotics in agar
media: theoretical considerations. In: Lorian V, ed.
Antibiotics in laboratory medicine. Baltimore: Williams &
Wilkins, 1980:1–23.

I can't get to understand what's a/the critical concentration.
How I understand the matter:

The zone of inhibition is formed when a concentration of drug reaches,
for the first time, a density of cells too large for it to inhibit,
and any additional drug concentration reinforcement arriving from the
reservoir won't make a difference.

if my understanding is right, how does it go with the prior explanation?

Something important that I don't see mentioned in the answer below is that you generally cannot determine the minimum inhibitory concentration of a drug by measuring the inhibition zone of a disk diffusion assay.

Read the last part of my answer (at-least).

I have improved this part, could you please check it?

Despite its simplicity, the disk diffusion test is based on
sophisticated physicochemical principles governing the dynamics of
diffusion of antibiotics simultaneous to bacterial growth in an agar
system.

Wanger, A., Disk diffusion test and gradient methodologies. Antimicrobial Susceptibility Testing Protocols, 2007
Inhibition
The process of keeping the cell mass in a given area constant.
Critical concentration
A critical concentration is the antimicrobial concentration required to inhibit a certain cell mass in a given area decisively so that it's irrespective of any future decrease in this concentration due to diffusion of the drug further from this area.
It seems to me that's why rapid AST (results being read immediately after the appearance of visible growth) can't be performed in some cases: the inhibition zone becomes smaller with further incubation as the drug concentration becomes less than the critical concentration for the current cell mass at the edge of the inhibition zone:

Occasionally there is another faint inner ring of delayed growth that
represents viable cells initially inhibited by the concentration of
drug at that point. As incubation continues, inhibited cells will
eventually grow when the concentration of drug is reduced either by
continued diffusion outward or by deterioration of the drug at
incubator temperatures. An inner ring of delayed growth is most
commonly seen with drugs which are primarily bacteriostatic. As
incubation continues the inner ring of delayed or partial growth
becomes increasingly visible and thus it would appear that the zone of
inhibition becomes smaller as the incubation time continues. It is for
this reason that the period of incubation must be standardized and
held constant.
Barry AL. Procedure for testing antibiotics in agar media: theoretical considerations. In: Lorian V, ed. Antibiotics in laboratory medicine. Baltimore: Williams & Wilkins, 1980:1–23.

Critical mass
A critical mass is the cell mass required to counter a certain antimicrobial concentration in a given area decisively so that it's irrespective of any future increase in this concentration due to the diffusion of more drug concentration to this area.
The Critical concentration
It's a critical concentration for the cell mass found at the outermost point inside of what's going to be the zone of inhibition at a certain time called the critical time.
The Critical mass
It's a critical mass for the antibiotic concentration in the point just outside what's going to be the zone of inhibition at a certain time called the critical time.
Formation of the zone of inhibition at the critical time

A zone of inhibition is formed when a critical concentration of drug [the critical concentration]
(that amount that is just capable of inhibiting microbial growth under
the test conditions) reaches, for the first time, a density of cells
[the critical mass] too large for it to inhibit.
Barry AL. Procedure for testing antibiotics in agar media: theoretical considerations. In: Lorian V, ed. Antibiotics in laboratory medicine. Baltimore: Williams & Wilkins, 1980:1–23.
The position of the zone of inhibition is determined at a point of
time [the critical time] when the critical concentration of drug reaches, for the first
time, a density of growing cells too large for it to inhibit. When the
antimicrobic is added at the time incubation is started, the position
of the zone of inhibition is determined after a critical time.
Barry AL. Procedure for testing antibiotics in agar media: theoretical considerations. In: Lorian V, ed. Antibiotics in laboratory medicine. Baltimore: Williams & Wilkins, 1980:1–23.

MIC vs Critical concentration
In broth microdilution, the MIC has access to all the cell mass equally and immediately, unlike in disk diffusion, where critical concentration reaches its coressponding mass gradually as time passes. This causes the fact that any cell mass will be subject to a subinhibitory concentration of the antibiotic before the inhibitory critical concentration. I think this needs to be considered when trying to relate the two factors.
To add, critical concentration is a concentration gradient not a concentration per se like MIC: as for the aforementioned reinforcements and outward diffusion.

I removed the part that included naive conclusion about MIC being equal to the critical theoretical being the most adjacent to the disk.

Generally antibiotics don't actually kill the bacteria, all they do is inhibit growth so that you don't get any new cells formed.
Thus, if you have a drug diffusing away from the disk, at some point the drug will reach a concentration that allows growth of standard concentration (often 0.5 McFarland) of the bacteria applied to the plate. Even if the zone of high concentration extends out further from the disk due to diffusion, these bacteria will still be there (remember inhibited, not killed), so you will see these bacteria and have determined the zone of inhibition.
Now, you might be thinking this should result in a halo where you don't get much growth but still get some before the drug reaches inhibitory concentration. In practice, you do see this, but it tends to be minimal for the reasons below:
The concentration at any given point is dependent on the square of the radius of the zone (area = pi*r2. To reach a higher concentration you need a lot more drug to shift the point. For a made up example - if you have a zone of inhibition with a diameter of 2 cm (i.e radius of 1 cm). To get this same point out a further centimetre, you would have a radius of 2 = 22 = 4x as much drug at each point around the circle. (I'm aware there's some problem with this math, it's just an illustration of the problem).
Diffusion rates in agar are also slow; in the order of 1-10 micrometres per second IIRC. This works out to be somewhere in the range of 100-1000 seconds (1.67 min to 16.67 min) per millimetre, which, in combination with the need for much more drug per increase in radius, results in the sharp zone of inhibition seen.

There are bactericidal antibiotics, like the beta-lactam antibiotics (and several other). They affect the formation of the cell wall leading the bursting of the cells.

@Chris For sure, though I didn't have the B-lactams in that group in my head; I knew they inhibited cell wall synthesis, just thought that inhibited division; time to go back and review my textbooks methinks.

Why would you think it would matter for this experiment that the antibiotic kills or inhibit the bacteria? Maybe it's not that the antimicrobial inhibits bacteria instead of killing them that results in lawn growth in areas outside the inhibition zone even if post inhibitory conc reaches these areas. If my reading is right، there is a critical cell mass for every dynamic antimicrobial conc that if reached, this conc and the highest it could reach as a result of reinforcements arriving from the disc, won't be able to counter the growth rate in this area.

I think it goes like this: For every cell mass of a certain organism, there is a critical conc of antibiotic, if this conc reaches this mass, it would result in inhibition of growth. Then each spot in the plate could be thought of a gradient itself for different antibiotic concentrations, not just the disc. Then and in the same way, for each conc gradient, there is a critical cell mass, that if the mass in the vicinity of this gradient reaches, growth won't be inhibited.

These multiple gradients are themselves being changed by the fact of reinforcements arriving. I think that what a dynamic gradient means.

@FreezingSoul Then each spot in the plate could be thought of a gradient itself for different antibiotic concentrations, not just the disc. No, the gradient is dependent on the disk. The antibiotic kills/inhibits growth so you don't get growth in those areas. The cell mass at each area is defined by your McFarland standard spread on the plate, so it should be consistent across the plate.

Read my answer, please. I will try to refine it over the time.


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Can placing a culture plate upright introduce contaminants from the lid?
Discussion
I have developed a habit of keeping culture plates always inverted, especially those of non-selective media. This precaution is followed after the poured plate is placed inverted in the incubator for 24hr to dry and test for contaminants. The reason is that I'm afraid when the plate is opened for streaking or subculturing, some contaminants might fall on the lid which is not given as much care as the dish itself when used for inoculation or subculturing: as the lid is kept on the bench underneath the bunsen flame. I fear that such possible contaminants might fall from the lid when the plate is kept upright on a surface, as I need when taking pictures of the cultures.
My fear might be right in theory, but i hope I'm missing something that would make such a scenario practically impossible.
Question
Can placing a culture plate upright, as for taking pictures, introduce contaminants from the lid?

Are you careful not to have your arms/hands over the lid when you inoculate your plate ?
If yes, then I would not worry. But the best way to know if you worked clean enough is to have a control handled in the same conditions (and non inoculated of course).
You said "the lid is kept on the bench under the Bunsen flame" right ?
The habit of keeping media plates upside-down is mainly to prevent condensation from flooding your inoculum.

If condensation can fall, so do spores/cells. I meant to say the lid is placed on the bench with the side that normally faces the base being upward.

I would say that if your lid is not clean, whether the plate is upside-down or not will not matter.

-Upside-down: contaminants would have to go against gravity to reach the culture
-Upright: ......... with gravity

Why don't you just try ?

What if its a borderline theoretical concern: has 10% of practical occurrence?


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Reverse protein biosynthesis in nature
This is more of a funny question to think about, but I am wondering, theoretically if it is possible in cells to synthesize nucleic acids(DNA, RNA) from proteins.
What might this be useful for and how could it be working?
Good luck and thanks for your time.

In biological systems, the central dogma states that genetic information flows from DNA to RNA to proteins, and the reverse process, synthesizing DNA or RNA from proteins directly within cells, does not occur. It has not been observed, and I doubt some hidden reactions exist, as a lot of enzymes would be necessary for this process. Since we do whole genome sequencing today and also have extensive knowledge about genomes, I think we would have discovered these enzymes. If you think of reverse transcriptase, this has even been discovered before all these methods and data where available.
However, in the realm of theoretical and synthetic biology, scientists have been exploring the possibility of creating artificial biological systems where unconventional processes could take place.
In terms of how it might work, it would require the development of enzymes or chemical processes that would reverse work somehow like the processes necessary for the synthesis of proteins. You would need some enzymes (or reactions) that "read" the protein sequence and have a way of converting it into a DNA or RNA sequence. This has a lot of challenges connected to it, including the specificity (choosing the right sequence for a given amino acid), steric problems (amino acids vary quite a lot in size and charge), the degenerated code (choosing the right codons) as well as the stability of the resulting nucleic acids.


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How migration creates Linkage Disquilibrium
I want to know how admixture and migration creates linkage disequilibrium? I am reading about it but I really don't quite get it.

Imagine one population is fixed for A1 at locus A and for B1 at locus B. Here is a representation
--- A1 --- B1 ---

Another population is fixed for A2 at locus A and for B2 at locus B. Here is a representation
--- A2 --- B2 ---

Further imagine that the recombination rate between loci A and B is 0 $(r=0)$. Any migration rate will cause some individuals --- A1 --- B1 --- to be present in a --- A2 --- B2 --- population (and/or vice-versa). So linkage disequilibrium is complete.
If the recombination rate is in between 0 and 0.5, then there will be some level of linkage disequilibrium at equilibrium that can be calculated for a specific demography (incl. migration rate).

Thank you :) I just have one more question. When you say that A1 is fixed at locus A and B1 at locus B, does that mean that A1 and B1 are in linkage disequilibrium too?

Linkage disequilibrium is defined for a pair of loci, not for a pair of alleles. It is defined as $D=p_{ab} - p_ap_b$ (see wiki). I think the misunderstanding you may have has more to do with the definition of linkage disequilibrium than about the effect of migration and recombination on linkage disequilibrium.  Without migration, each population in the above example is at linkage equilibrium (because there is no variance), while the overall metapopulation is at complete linkage disequilibrium.

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What is this? Found crawling across ground under oak tree. Six arms waving, I broke off 1 trying to pick it up. Less than 1 inch long
Crawled like snail.  No slime trail.  Less than one inch.  Six arms, I broke one off.

Where in the world is that species located? And at which season?

Hi D.J., welcome to Bio.SE! Please add a location, approximate size, and preferably additional (clearer) photos of your specimen. Thanks

That is a Hag moth caterpillar

Don't touch.


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Phenol Red Broth question; what is point of broth without carbohydrate?
Without carbohydrate in the broth (some) bacteria would then degrade the peptone, which from its end products would increase pH and then turn zhe phenol red pink. So I think this is some type of control just to make sure the test parameters can produce a pink broth. Is there something more here that I'm missing though? The question is asking what function phenol red broth without carbs serves, and that's only thing I can think of. Is this correct or is there something else that is more relevant?

Indicators in media are usually used to monitor the degradation of the media due to growth. If the pH falls too much, living conditions are much worse to the point that the cells will die. So this is more a quick check.

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text:
Can a non-pure culture be used for reliable rapid phenotypic diagnostic tests?
Can a non-pure culture be used for reliable rapid phenotypic diagnostic tests (e.g. catalase, oxidase & gram stain)?

"Slide Test Method
Obtain a pure culture of the organism to be tested. Using an inoculating needle or applicator stick, pick a well-isolated colony
and transfer to a glass slide. add 1 or 2 drops of the Catalase
Reagent to the smear." Manual of Liofilchem® - Catalase Reagent

"Test isolates should be in pure culture and 18-24  hours old" Manual
of Oxichrome Reagent, Thermo Fisher Scientific

"A pure culture is required for identification tests. However, the
tests can be applied directly to colonies removed from isolation
plates if there are many suspect colonies that have been correctly
isolated. In the latter case, the test must be repeated after
reinoculation of the colonies tested, to obtain a pure culture.
Identification tests are as follows: appearance and motility, if
living: Gram staining, oxidase test and catalase test." Manual of Standards for Diagnostic Tests and Vaccines: Lists A and B Diseases of Mammals, Birds and Bees, Chapter 2.3.2 Bovine genital campylobacteriosis [Campylobacter fetus]

Is it a concidence that the author stated the usability of these tests with non pure cultures when the concerned organism, Campylobacter fetus, has a positive result in all of  them?
What i mean, the author could be indirectly implying that these tests in such condition are useful only for pre-screening purposes (i.e an experimental positive result with an expected positive result should be interpreted that at least one organism from the tested growth is positive, where an experimental positive result with an expected negative result doesn't necessarily mean that our subject organism is not there)?
I want to understand correctly why a non-pure culture with discrete subject colonies can be bad for atleast some diagnostic procedures. Is it because "Where there is one rat, there are more"? In other words, a fast-growing thus apparent type of contaminant means that there could be more slow-growing thus inapparent types of contaminants, which can be within discrete colonies of the subject organism.
If this is the correct reason, then it sounds to be a problem for highly sensitive molecular methods (e.g. PCR) and culture-based tests (e.g. OF-glucose test & simmon's citrate test) where the number of contaminating cells will be magnified, but not for rapid phenotypic tests as those mentioned, which are relatively insensitive and on-spot.
If this wasn't just a theoretical concern that was commonly exaggerated, then this leaves Gram-negative selective media as MacConkey, not usable for such tests even in pure culture, as:

In obtaining a pure culture, it is important to realize that the
selection of a single colony from a plate does not necessarily assure
purity. This is especially true if selective media are used; live but
non-growing contaminants may often be present in or near a colony and
can be subcultured along with the chosen organism. Krieg, N.R. (2005). Identification of Procaryotes. In: Brenner, D.J., Krieg, N.R., Staley, J.T., Garrity, G.M. (eds) Bergey’s Manual® of Systematic Bacteriology. Springer, Boston, MA. https://doi.org/10.1007/0-387-28021-9_5

A quick comment - the tests in the title are not definitive tests. Definitive tests are the ones that make your presumptive test(s) certain.

I'm not speaking about presumptive or definitive identification, anyway it's still not the best way to reflect what I mean, it's going to be "reliable".

Isn't the answer in the quote you provided from Manual of Standards for Diagnostic Tests and Vaccines? The results won't be reliable.
Having pure cultures by re-streaking the ones you suspect and only using single, isolated colonies for subsequent tests is the very foundation of diagnostic microbiology.
The same quote is specifically talking about campylobateriosis, so mentions those tests because those are the ones to perform on that organism. It is also talking about abundance - if you see lots of colonies of one organism, then that could well be the problem, and should be treated as a presumptive diagnosis. 1 rat = more rats in your analogy.
Of course you can perform (as in, you can physically do them) the tests on non-pure cultures, but they should be repeated on a pure culture to be certain of any result obtained. The risk you run is that an impure culture might give you a result that is not the correct one for the organism you expect, or is misleading. This is especially so if there is more than one organism or strain in the colony being tested. An example of this might be if you have Streptococcus agalactiae and Streptococcus pyogenes in the same culture (both B-hemolytic) - these two will be indistinguishable by Gram stain, but not by further biochemical testing, where a mixed colony would give you both group A and group B Lancefield typing.
Your quote from Bergey's Manual is talking about selection from impure colonies on an early plate or on a selective plate. Of course you can sub-culture contaminants along with your target organism, but the selection of isolated, single colonies lowers this chance, and dilution applies; the more times you streak out, the more likely you are to have a pure culture. The risk of carrying over contaminants by culturing from selective media is that you can't see the contaminant when you select your colony because the contaminant hasn't grown, but is there in a non-replicative state, whereas you are more likely to visually see this contaminant on a non-selective plate as it will grow happily alongside your target organism.
PCR, depending on the primer target(s), is highly specific and usually very sensitive for identification, so shouldn't give an ambiguous or incorrect result, even on a contaminated culture. However, this is dependent on exactly which PCR test used and how the results are presented. For example you might have a multiplex test that detects Pathogen A and Non-pathogen B. Both are common on the body, grow on your medium, and are similar in appearance. You select a colony, which just so happens has more B than A, so the PCR might show up as B present and background A, when A is actually the one causing the problem. Pure culture would give you the correct result.
For any test used in the medical field (including veterinary) will be required to adhere to some form of standardization (ISO etc.) and accreditation for its purpose, and, as a result, should perform reliably when used correctly according to the standard and with appropriate controls. If you start doing things outside the standard, then you are treading in dangerous waters. Follow the procedures correctly, if this means using a test on pure culture, then that is what you should do!

"The results won't be reliable."  why is that? why do you think the results might not be consistent? The first two quotes from the reagents' manuals don't strike me as the quote from the book, because it should be more concerned with the practical matter. Theoretically, there could be an organism with a very strong catalase/oxidase activity that would give a positive result even with an inapparent growth/microcolony hidden under a discrete subject colony. But if such organisms are found in the present, then these manuals should add that this pure culture should be in a non selective media.

"It is also talking about abundance" I think they mean an abundance of discrete subject colonies because, unlike confluent growth, these discrete colonies can't hide something. That makes sense until they tell you to go back and reperform the tests once in pure culture.

@FreezingSoul not reliable because you can't tell if the cultures are pure or not; thus you need to repeat them on pure culture. Yes, you can get the right result with a contaminated culture, but how can you be sure that your result isn't because of a contaminant. Pure culture is always done on non-selective media, so the assumption is that this is how you are doing it, not the converse. though some tests don't apply to certain media types. e.g. catalase can't be done off blood agar because of catalases in blood.

@FreezingSoul ... Remember that lives/health might be at risk here - which is better: do it right and get a result you can be certain of, or do a quick job and get an uncertain result that you then have to repeat and takes longer because you have to go back to the plate, re-sub and do it correctly? If you are doing med lab science, you MUST follow the standard procedures or your regulatory body will be very very unhappy with you when a mistake catches up with you.

@FreezingSoul Yes, discrete colonies was implied in the text. Just because you have a discrete colony from a sample, doesn't mean you have a pure colony; you can get contaminated single colonies, and re-streaking for pure culture will show these to you as the contaminant(s) should show up as abnormal colonies on your sub-plate.  You are overthinking it (again)...

"A. baumannii isolates were obtained from clinical specimens by standard methods, followed by isolation in pure culture on MacConkey agar plates" https://journals.asm.org/doi/10.1128/jcm.02263-09
What I want to say is that if we are going to consider theoretical concerns one time, why don't we do it all the way? If non-pure cultures could mean that our subject discrete colonies might not be as pure as they seem, then it renders selective media not usable for obtaining pure cultures, as Bergey mentions.

@FreezingSoul the risk of impure cultures is orders of magnitude reduced each time you sub it. Remember that a sample might have dozens of species of bacteria in it, but when you pick from a colony you take a very small amount (still millions of cfu) from a colony that might have 1-2 species, streak that out and you should see any contaminating organisms, and then pick a single colony from that. Discrete colonies from a sample might (made up numbers) have a 1:100 chance of contamination, but a colony on a sub-plate might have 1:10,000 or more...

@FreezingSoul ...The I read your quote as meaning they maintained pure culture on MAC. Also note that it is for a study looking specifically at that species, not clinical/diagnostic microbiology, so what they do there is up to them. Likely they got plates of already identified A baumanii and sub-cultured them - that's how I would do it, rather than taking random samples  and having to do all the culturing again.

Does that mean that colonies can have invisible growth that passes their margins and maybe theoretically extend to every side of the plate like radiation?

@FreezingSoul sometimes, motile bacteria can do this. You might not see it easily on a plate depending on the transparency of the medium and effects of the bacterium on the medium.

Let us continue this discussion in chat.


text:
Basic question about symbiosis( or about kinds of symbiosis)
Is there a type of symbiosis where an organism is harmed and the other is neither harmed nor helped?
If not, do you think there's a term for this sort of relation between two organisms?

Related: http://biology.stackexchange.com/questions/53975/is-apparent-competition-a-suitable-term-in-situations-where-one-species-is-not-n

Related: answer to "how to determine the relationship of competition or cooperation"

I see that there exists some confusion over the meaning of Symbiosis itself [in reference to the comments and answer(s)].
Your question/ query seeking information about "some type of Symbiosis" that harms one organism without affecting the other in any form is very much legitimate.
Amensalism (as responded by Sanjukta) is indeed the answer, but saying that "No. There seems to be no intimate association (symbiosis) that does not benefit any partner" is suggesting that Amensalism is not Symbiosis (which is not true).
Amensalism is one of the types of symbiotic associations only (Symbiosis is nothing but 'Living Together' of two / more organisms - which may or may not benefit/ harm either or both or none of the parties involved in the association).
Point to be taken is that, Symbiotic relation refers to the members of two different species (i.e., two populations) engaging in interaction and the interaction can be of any type (Amensalism is just another Symbiotic association).
Edit:
If one looks into the Etymology of the word, Symbiosis, he/she should be able to decipher the meaning of Symbiosis:

One may support the argument using latest updation of Encyclopedia of Evolutionary Biology (Amensalism=Symbiosis) and the classical example of Walnut tree (which tends to kill or inhibit the growth of shrubs that grow around its roots) may be cited. Their growth is inhibited,  but their niche still remains the same. More importantly, the Honeybee - wasp relationship (a long term one) is best fit for Symbiotic Ammensalism.
So, Mutualism, Commensalism, Amensalism, are all Symbiotic Relations.
References:
Miami College of Arts and Sciences, Department of Biotechnology Lecture Notes
Wiki Link about Biological Interactions

The books I've been referring to do not include Amensalism as a symbiosis. Symbiosis is not a synonym of biological interaction. It is an association,often phrased 'intimate association' between two species(something that doesn't exist between amensals). Book.

Hi Sanjukta,
I just added the Etymology of Symbiosis, hope that helps in clearing the doubt...

Yes it is so. But amensals do not live together.

This reference is from the latest updation of Encyclopedia of Evolutionary Biology (http://www.sciencedirect.com/science/article/pii/B978012800049600189X) and the classical example of Walnut tree (which tends to kill or inhibit the growth of shrubs that grow around its roots) may be cited. Their growth is inhibited,  but their niche still remains the same. More importantly, the Honeybee - wasp relationship (a long term one) is best fit for Symbiotic Ammensalism.
But I very well acknowledge the point you are trying to put forth. I guess, it's a clash of two different schools of thoughts..

Is there a type of symbiosis where an organism is harmed and the other is neither harmed nor helped?

No. There seems to be no intimate association (symbiosis) that does not benefit any partner.

If not, do you think there's a term for this sort of relation between two organisms?

Yes, Amensalism is the  biological interaction you are talking about in which one organism inflicts harm to another organism without any loss or benefit to itself.

A clear case of amensalism is where sheep or cattle trample grass. The presence of the grass causes negligible detrimental effects to the animal's hoof but the grass suffers from being crushed.

For more read wikiedia.

And good to add that strictly speaking, it's not exactly a symbiosis

@BioGeo Yeah. It'll add it to the answer.

@AlwaysConfused Yes, indeed. But when I was taught ecology, things were simpler... :)

@AlwaysConfused To be honest, symbiosis etymology means living together. Depending on the perspective, we could take it as mutualism or as all kinds of interactions... But maybe if one dies in that interaction, there is not really "living" together... hehe


text:
Cell type that expresses 90% of the genome
Cells that are differentiated express the genes that are necessary for their own usage. I've heard that some cell type expresses about 90% of 30,000 proteins that are encoded in the genome. Can anybody tell me what this cell type is?

Can you point us to a source that says that?

I'm thinking of thymic medullary cells, but I don't know how many genes they express.

I've rolled your edit back because it completely changes the meaning of the question and renders the answer irrelevant. If you have a different question, ask it in a new post.

I'm voting to close this question because the asker stubbornly insists on edits that change the question to something meaningless.

Please stop editing the question so that the answer gets meaningless and open a new question instead. I will roll back it to the last version where answer makes sense and then lock it.

Well, I found this paper:
Danan-Gotthold M, Guyon C, Giraud M, Levanin EY, Abramson J. 2016. Extensive RNA editing and splicing increase immune self-representation diversity in medullary thymic epithelial cells. Genome Biol 17:219.

Medullary thymic epithelial cells [mTECs] express ~85 % of the entire coding genome
...to better determine the fraction of genes expressed in mTECs and other mouse tissues, we took advantage of RNA-seq technology... The analysis... revealed that most of the tissues [see below for those tested] express 12,000–14,000 genes (i.e. 60–65 % of the coding genome). The lung and two immunologically privileged sites, brain and testis, were the only tissues that expressed a larger fraction of the genome, in the range of 70–75 %... In line with other recently published studies, the mTEChi population expressed nearly 18,000 genes, which represents ~85 % of the coding genome, while Aire-deficient mTECs (AireKO) expressed approximately 15,000 genes, suggesting that Aire is responsible for the induction of ~3000 genes in mTECs. Interestingly, even in the absence of Aire, the mTECs expressed a relatively large fraction of the genome (~75 %), considerably exceeding the overall genome expression in other peripheral tissues. Interestingly, neither [cortical thymic epithelial cells] nor [skin epithelial cells] demonstrated higher overall genome expression than other tissues, suggesting that promiscuous gene expression is indeed unique to the mTECs population.

These cells express such a wide complement of proteins because they are involved in T-cell maturation, specifically negative selection.

List of tissues tested in the study:

brain, testes, liver, kidney, lung, colon, skeletal muscle, spleen, cortical thymic epithelial cells, skin epithelial cells


text:
What is the reproductive success of a biting mosquito?
Female mosquito can lay ~50-100 eggs in each batch. It takes some time between the hatch and until the time the female mosquito bits. During this time many of them will die.
What is the average percentage of the eggs that mature (in other words, if a female mosquito lays one hundred eggs, how many of them will become grown females that bite)?

The amount (percentage) of eggs to mature varies greatly and depends on many factors and off course varies by season.
The correct (but not really satisfying) answer is that from every 100 eggs, between 0 and 100 eggs will mature. On average, this number is greater than 1 (otherwise the species would go extinct), and much smaller than 100 (otherwise the world would drown in mosquitoes). Because the question doesn't include the complete lifecycle, it is not exactly 1, but greater than 1.
Some explanation
Mosquitoes lay eggs in water, and the larvae are easy prey for predatory invertebrates (larvae of dragonflies, beetles etc.) and fish. Many mosquito species choose small, isolated waters (like small pools and plant-pots) where there is likely to be little predation. This however carries a risk: these waters often dry out (reproductive succes 0%), offer little resources (reproductive succes low) and offer no shelter against an unforseen predator (reproductive succes low). If they choose wisely however, reproductive succes can be very high. Because of this large variation, an average number is really not so informative.

I think the number has to be almost exactly 1 (not more than 1) for the population to remain stable. And that's 1 maturing egg for the entire life of the female, not 1 per batch nor 1 per 100 eggs. See my answer for more details.

@Stephen_Thomas The question is not about the complete lifecycle, so it must be greater than one.

So suppose the answer is 2. Then, for every batch, 2 females would reach maturity (and, we're assuming, breed). And for a complete lifecycle of, say, 5 egg-laying batches, 10 females would reach maturity. In that case the mosquito population would grow 10-fold at each generation. Clearly that can't be correct.

Ah, I get it now. My answer is indeed incorrect.


text:
How "unique" human vagina is?
Regading penis Dixson showed that it is not really unique and complex. This argument (and there were some others) was used against the idea of human polygynandry.
But what about vaginal shape? I know it is wider as deeper it goes and cervix is convex shaped, which could  give an advantage for storing semen. However, I am actually wondering if other primates have similar vaginal shapes (because it can shed light on the question of mating system). Are there any studies on the topic?

Check the wiki page for clitoris and some mammalian orgasm research... ostriches have a clitoris and other species such as spider monkeys and spotted hyenas have clitorises as long as their male counterparts, so we are different form spider monkeys.

@com.prehensible Well, I know, say, that bonobos have 3x larger clitores (given they are smaller). But I am asking about unique features of human vaginas, not primates'. I am pretty sure there are primates with clitores comparable in relative size with human ones.

This page talks about labia http://aquatic-human-ancestor.org/anatomy/sexual-features.html


text:
Does sunlight interfere with the efficiency of compound light microscope?
I have access to an olympus bx41 microscope. The table on which sits the microscope is in front of a large window and unfortunately no curtains are available. I'm starting to relate that whenever the sunlight is strong, the microscope picture appears dim.
Does sunlight interfere with compound light microscope?

I'm not sure that this is exactly biology, more physics, however the answer is sometimes, though this depends on the type of microscope and how the light is impinging on it.
This answer assumes a common upright compound microscope.
The reason I say this is that microscopes used to (and some still do, such as this one. I have no affiliation with the linked site nor is this an endorsement of the site) have mirrors for reflecting the sun so that you could see your sample.
However, what you are seeing is that your samples appear dim when there is bright light in the room. What is actually happening here is that your eyes are compensating for that level of brightness in your peripheral vision, constricting your pupil so that less light enters the eye. This is called the pupillary light reflex and happens every time your eye is subjected to light. Because of the constriction of your pupil, the central (microscope) image appears dimmer.
Having said that, bright light entering the condenser, not from the (diffused) point-source of the bulb can cause loss of image definition because the light source is not linearized and condensed fully by the condenser arrangement. This results in some images being a bit less sharp. Nikon's MicroscopyU has some detail on how this works.

I actually forgot to say that my eyes + phone pictures both appear dim. If it's the last case then its the condenser that i need to protect for intruding light.

Any idea of how could this be possible?

@FreezingSoul It would depend on the exactly how the phone is taking the images, but light leakage might pay a role in that. You would need to set the shutter speed and aperture for it to take a consistent photo of set brightness, not rely on automatic mode. It's as simple as creating a shade for the microscope - a piece of card taped to the window would work...

i forgot to mark this is as the accepted answer for which it is an accepted answer. i hope i get an illness for this mistake.

@FreezingSoul no need to feel bad - as you might have noticed, most questions with answers don't receive an accepted answer mark.


text:
Why do nerve gas victims have chronic neurological issues?
The article on Wikipedia says the following:

The effects of nerve agents are long lasting and increase with continued exposure. Survivors of nerve agent poisoning almost invariably suffer chronic neurological damage and related psychiatric effects.

Unfortunately, the original paper seems to be paywalled. Why does this happen? Is it because it takes a long time to replenish the acetylcholinesterase inhibited by the nerve agent?
Here is the link to the original paper.

I will have a look at it in the next days.

I would like to add a bit to Chris' answer. While it is true that the underlying mechanism of the long lasting effects of nerve gas has not been established, several hypotheses exist (reworded from Jokanovic et al, 2010):

Long lasting effects could be derived from withdrawal of nerve gas after repeated low-level exposure or acute exposure. This means that the synapses are degraded or even the neurons die because of the constant excitation caused by the nerve gas.
Nerve gas may affect neuropeptide metabolism through the release of endogenous opiates and/or through interactions with yet unidentified receptors
London et al. (2005) reported that exposure to nerve gas may cause serotonin disturbances in the central nervous system, which are implicated in depression and suicide in humans.

Most of the nerve agents (and quite a number of commercially used pesticides) fall into the class of organophosphates (OP). Their mechanism of action is the inhibition of the acetylcholin esterase which leads to the build-up of acetylcholine in the body and thus a permanent activation of mucarinic and nicotinic acetylcholine receptors.
Irreversible inhibitors of AChE may lead to muscular paralysis, convulsions, bronchial constriction, and death by asphyxiation - and organophosphates can act as these. See here for some more information.
According to reference 1, four different toxic effects can be differentiated:  The cholinergic syndrome, the intermediate syndrome, organophosphate-induced delayed polyneuropathy (OPIDP) and chronic organophosphate-induced neuropsychiatric disorder (COPIND).
The cholinergic syndrome is happening in the acute phase of the OP poisoning and can be explained by the inhibition of the acetylcholin esterase.
All quotes are from reference 1:

In cases of human poisoning, general acute symptoms of peripheral
  nicotinic and muscarinic intoxication are clearly apparent.
  These symptoms include miosis
  (unreactive to light); sweating, rhinorrhea, lacrimation, and
  salivation; abdominal cramps and other gastrointestinal symptoms;
  respiratory difficulties and cough; dyspnea, constriction sensation in
  the chest, wheezing; twitching of facial muscles and tongue, tremors,
  and fasciculations; bradycardia and ECG changes, pallor, and cyanosis;
  anorexia, nausea, vomiting, diarrhea, and involuntary urination and
  defecation. These signs and symptoms are accompanied by central
  effects such as dizziness, tremulousness, and confusion; ataxia;
  headache, fatigability, and paresthesia. Finally, seizures,
  convulsions, twitching, coma, and respiratory failure may also occur.
  If the subject survives the first day of poisoning, personality
  changes, mood swings, aggressive events and psychotic episodes
  including schizoid reactions, paranoid delusions, and exacerbations of
  preexisting psychiatric problems may also ensue.

The intermediate syndrome happens after the acute phase, around 7,7% of the patients develop it.

The term Intermediate Syndrome (IMS) was first described by Senanayake
  and Karalliedde (1987) because it appeared in the interval between the
  end of the cholinergic crisis and the onset of OPIDP. Following
  exposure to various OP pesticides, clinical manifestations of IMS
  typically occur within 24–96 h, and affect patients without
  fasciculation or other cholinergic signs. The reported incidence of
  IMS ranges from 7.7% to as high as 84% (Shailesh et al., 1994).
  Although IMS is well recognized as a disorder of neuromuscular
  junctions, its exact etiology, incidence, and risk factors are not
  clearly understood. IMS generally occurs among patients with prolonged
  and severe inhibition of AChE, although not every patient with severe
  AChE inhibition develops IMS. Other risk factors of IMS include
  delayed metabolism of OP pesticides due to toxicokinetic factors or
  impaired organ function, severity of poisoning, elevated muscle
  enzymes, plus adequate or late oxime therapy. IMS has been linked with
  exposure to specific OP pesticides displaying the dimethyl phosphate
  moiety (e.g. fenthion, dimethoate, monocrotophos, dichlorvos,
  methylparathion) but has also developed after exposure to parathion
  (ethyl phosphate) and methamidophos (phosphoramidate; De Bleecker et
  al., 1993; Yang and Deng, 2007).

The organophosphate-induced delayed polyneuropathy (OPIDP) cones later and has been connected to the phosphorylation and subsequent ageing of the neuropathy target esterase by the OP (see reference 1 and 3).

OPIDP is relatively rare neurodegenerative disorder in humans that is
  characterized by loss of function and ataxia of distal parts of
  sensory and motor axons in peripheral nerves and ascending and
  descending tracts of spinal cord. The early neurological symptoms
  usually are sharp, cramp-like pains in the calves, tingling in the
  feet and hands followed by distal numbness and paresthesia. Pain and
  weakness in muscles spread rapidly and patients become unsteady and
  unable to keep their balance. Progressive leg weakness occurs,
  together with depression of tendon reflexes. Symptoms may also appear
  in the arms and forearms. Sensory loss may be mild. Muscle tonus of
  the limbs gradually increase and spasticity appears in the lower
  limbs. Physical examination reveals distal symmetrical and mainly
  motor polyneuropathy, with wasting and flaccid weakness of distal limb
  muscles, especially in the lower limbs. In severe OPIDP quadriplegia
  with foot and wrist drop were observed as well as mild pyramidal signs
  (Lotti, 1992). There may be some functional recovery in less severe
  cases with more distal involvement and sparing of spinal cord axons,
  but pyramidal and other signs of central neurological involvement may
  become more evident with time. The recovery affects only sensory
  nerves, while motor neurons may permanently lose function as indicated
  by Morgan (1982) who described the lack of improvement over 47 years
  in 11 patients poisoned with TOCP.

The chronic organophosphate-induced neuropsychiatric disorder (COPIND) happens to persons with a chronic exposure to OP and is most likely caused by permanent damages to the central nervous system (CNS), but the real cause is not known yet.

The most common symptoms of COPIND include cognitive deficit
  (impairment in memory, concentration and learning, problems with
  attention, information processing, eye-hand coordination and reaction
  time), mood change (anxiety, depression, psychotic symptoms, emotional
  lability), chronic fatigue, autonomic dysfunction, peripheral
  neuropathy and extrapyramidal symptoms such as dystonia, resting
  tremor, bradikynesia, postural instability and rigidity of face
  muscles

References

Neurotoxic effects in patients poisoned with organophosphorus
pesticides
Long-term health effects of nerve agents and mustard
Neuropathy target esterase (NTE) and organophosphorus-induced
delayed polyneuropathy (OPIDP): recent advances

While I feel that Thawn's addition provides a better answer for my original question, I really appreciate your answer too. That was an interesting read, thank you!


text:
How do Kangaroo mothers deliver the correct kind of milk to the correct joey?
Mother kangaroos are able to rear multiple joeys (young kangaroos) at different stages of development at the same time. According to Wikipedia, "the mother is able to produce two different kinds of milk simultaneously for the newborn and the older joey still in the pouch." What biological mechanisms are able to ensure that the correct joey gets the correct kind of milk? Do different teats produce different types of milk and somehow the joeys know which teat to suck from; or is each teat able to deliver both types of milk and the teat is able to tell from the mouth conformation (or something else) which type of milk to deliver?

i shouldnt wonder if the joeys prefer the taste of the milk that is best for them..

The younger Joey remains attached to the teat from which it receives its milk for the period of nine months until it leaves the pouch. So that would be teat from which milk suitable for the newborn is available (reference 1 and reference 2). The older Joeys also have an incredible sense of smell by which it can detect the teat from which it gets the milk it requires but it stands to reason that they cant get milk from the teat to which the younger joey is attached. (reference)


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Can single-Use Gloves carry bacteria on their outer surface?
In bacteriology, can I touch items (e.g. oxidase discs) with my gloves not fearing to contaminate these items?
Are these gloves (e.g. Disposable nitrile gloves) made so that bacteria can't adhere to them?

Because maybe that's only true for viruses not bacteria? Maybe because they are not durable enough to be used many times with confidence?

i saw a microbiologist in a video touching an oxidase disc while performing oxidase test with his gloves, maybe he was treating his hands aseptically so overall it won't matter
edit: actually he was touching other non sterile things with his gloves.

As @bob1 stated, and I want to emphasize, gloves in a box, regardless of what they're made of, are not sterile. Someone (or something) put them there, and you don't know what's on them. To my knowledge, there are no antibacterial gloves. Sterile gloves come in a special wrapper and are very much more expensive, and require a special technique to put them on to keep them sterile..

I wasn't differentiating between contaminating Stocks, to be incubated test medium (e.g. citrate agar) and sensitive on-spot testing platforms (e.g. PCR), and insensitive on-spot tests( e.g. catalase, oxidase, etc). The oxidase disc is a relatively insensitive on-spot test, the small number of microorganisms on the gloves will not affect the result. The stock of oxidase discs is however the main concern and should be dealt with aspectically.

Short answer - No!
These gloves are neither produced nor stored aseptically unless you get ones specifically for surgery. You should always use good aseptic technique when working with viable organisms in the lab.
General advice for oxidase discs is to pick them up with flamed forceps.

I meant to "contaminate the items" not "the gloves", maybe gloves adhere too strong to bacteria as to trap them so they can't be transferred elsewhere or not let them adhere at all.

@FreezingSoul No, bacteria etc do not especially adhere to the gloves. The gloves are there to protect you from your sample, and to protect your sample from you! They do not prevent transference of biologicals from one surface to another. If you contaminate your gloves (as you do when you put them on) and then touch another surface, you will contaminate that surface, whether it be you or a sample, test, phone, tube or anything else. Hence the advice to use aseptic technique. Gloves are not sterile in the box!


text:
How do microbiologists decide whether two morphotypes on the same plate belong to the same strain?
Background
Colony: A colony, in microbiology, is a visible cluster or mass of microorganisms (such as bacteria or fungi) that has grown and multiplied on a solid agar medium. Each colony represents a population of genetically identical microbial cells that originated from a single cell or a small group of cells. Colony formation is an essential step in the isolation and identification of microorganisms.
Colony morphology refers to the visible characteristics of a bacterial or fungal colony when grown on a solid agar medium. It includes features such as size, shape, color, texture, and edge appearance. Each type of microorganism may exhibit distinct colony morphologies, aiding in their identification and classification.
"It should be noted that when a microbiologist examines an agar plate and determines that mixed bacterial
types are present, it is actually mixed bacterial colonial types (morphotypes) that are being observed. These
visually distinctive colonies often represent different species (or even genera), but they may also represent
phenotypic variants of a single genotypic organism."

Koneman's Color Atlas and Textbook of Diagnostic Microbiology. 7th.
Wolters Kluwer; 2017

Question
In diagnostic microbiology and in order to save time, how do microbiologists decide whether two morphotypes on the same plate belong to the same strain?
I'm not talking about great differences in morphologies as Lactose fermenters vs Non-Lactose fermenters on MacConkey agar, but ones like these: The center in Type A is purple while the center in Type B is pink.

Pure culture of Acinetobacter on MacConkey agar plate

They don't look any different to me from your photo. Perhaps a closer photo might help. All I see is some difference in thickness (depth?) of the colony perhaps, so one appears lighter colour than the other.

I will try to find a more clear example and I will add more essential quoted text to the background section about "Phenotypic Variants of Bacterial Colonies"

You have to remember that when a microbiologist looks at a plate, they are looking to observe a particular something, which depends on exactly what they are doing, and they will have some idea of the range of morphotypes expected for those species and/or strains.
They also aren't doing this in isolation - they will use tests to further confirm what they see, often starting with simple tests like Gram staining and going on to other biochemical tests, genetic tests (sequencing possibly or PCR), or even MALDI-ToF.
Experience also plays a part - if this is something being done routinely, say in a clinical lab, then the investigator know what species to expect, and which ones are things to further investigate for that particular sample type. This means they will have some idea (it may not be formal knowledge, as in taught, just experience) of the range of potential morphotypes for a particular species and be able to use that information to assess a plate quickly and accurately. Exact identification of a strain and/or species is often impossible without further testing  (e.g. you can't normally tell the difference between antibiotic resistant and non-antibiotic resistant strains without susceptibility testing, or even the difference between various Streptococcus species without testing), though pathogenic factors such as bacterial capsules in some strains of a species (e.g. capsules in *E. coli*), might be obvious from colony morphology immediately.
In the case of a pure strain streaked on a plate, as in your photo, changes in colony morphology might or might not indicate genetic changes reflected by phenotypic changes. An example might be loss of flagellae, means the bacteria are no longer motile, so the colony is less spread-out than ones with flagellae. Pigementation changes might also indicate a phenotypic and/or genetic change - perhaps processing a metabolite by a different pathway or able to do it only under certain conditions - no genetic change, just a phenotypic.

"There may also be variation in morphologies of colonies of the same
strain. Hence categorization if isolates based on specific colony
characteristics should be broad and based on several aspects of
morphology rather than on only one or two characteristics. "
What could be the variable characteristics that one should not always rely on? From my example color seems to be one.

@FreezingSoul Categorization based on colony characteristics is necessarily broad. It is usually the very first step in ID, followed by more specific tests to discriminate between species or groups of types.  If you were using a dichotomous key, it would be one of the first steps in ID it's that fundamental.

@FreezingSoul There's no one variable because it changes with each organism. An equivalent (at the risk of sounding racist; no racist intention here) might be comparing races of people - Asiatic peoples tend to have straight dark hair, so it's not a good characteristic to separate them internally into regions, but is useful to separate them from Caucasians and Africans (=genus from colony in bacteria), but in Caucasians hair might be useful for separating out groups internally (Germanic = blonde; Hispanic = dark, curly; Hibernian = red, equivalent to species within a genus for the bacteria)

Are you saying that one should learn about the possible colony variation for the potential species that could be obtained in a given case?

@FreezingSoul Yes. There's no "one answer fits all" here.

But in diagnostic microbiology, especially when the number of possible pathogens in a situation is high, there must be some terms that can be generally applied. I'm starting to become convinced that color and size are two characteristics that one should be skeptical of when interpreting. Do you have any personal experience or text that could go with this?

@FreezingSoul not really, if you know the sample type, then there are well known pathogens that are the prime candidates. E.g. for a throat sample, think streptococci, not E. coli, so looking for small creamy entire colonies +/- hemolytic on blood, then narrow down using specific tests. Try Mim's diagnostic microbiology.

Yeah, maybe i need to use this approach.

@FreezingSoul 100+ years (since the late 1800's) of diagnostic microbiology could have given you a hint that the processes and easiest ways have already been worked out. As I said in the answer, none of this is done in isolation, you have other information about the sample that can help to solve the puzzle.

Maybe, I might be wrong at some obvious cases as the throat sample. But what about the number of candidates that different types of nosocomial infections feature? Each type of infection (UTI, pneumonia....) can be caused by a good number and to make matters worse, causative bacterial species can overlap between different infection types.

@FreezingSoul You are overthinking it. In the medical training axiom: "If you hear hooves, think those are horses not those are zebras". Yes, some pathogens might be missed for rare cases, but that's where further investigation (repeat samples etc.) comes in. Overlap can be a problem, but the problem species is usually the most abundant species in the sample. Experience and training will tell you when this isn't the case!

Yeah, that's me honestly. I'm putting my hand in the jar and trying to get everything out, then end up getting nothing. Thanks for your time and help.


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Difference between NCBI's /genomes and /1000genomes
Wondering what the difference is in the data hosted here:

ftp://ftp-trace.ncbi.nih.gov/1000genomes
ftp://ftp.ncbi.nih.gov/genomes/

Also (sidenote), would be interested to note what the difference between ftp-trace and just ftp is. But there is probably over 1TB of data in /genomes, and I assume something of "a thousand genomes" is in /1000genomes, but I'm not sure what data exactly. Would like to know what is i thse two folders, and where the 1000genomes data is exactly. It looks like /1000genomes/ftp/data/ has "sequence data", but I'm not sure how that compares to the /genomes list of species names (and I'm also not sure what "sequence data" entails exactly).

The simplest difference is the scale and range. The aim of 1000 genome project was to provide comprehensive library of human genetic variation. DNA of individuals coming from different ethnic groups, geographic locations were sequenced and the results of the study were published here.
Genomes from NCBI come from different organisms and the number of sequenced individuals differ between species (including human). This database is constantly growing. Detailed description can be found here.

In fact these two things are very different and I would say quite opposite.
NCBI genomes are collection of information on genomes of various species including sequences, maps, chromosomes, assemblies, and annotations. Basically it's a catalog of reference genomes.
1KG is a catalog of human genetic variations from a genome-wide association study.


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Is blood pressure in the aorta and brachial artery the same or different?
Does the blood pressure at the root of aorta equal the blood pressure in the brachial artery?
I've heard it does, but it doesn't quite seem to make sense as I'd think the blood pressure would be lowered the further it travels?

Blood pressure is mostly dependent on the height from the heart. Therefore, if it is below the heart it will have higher blood pressure and if it is above the heart it will have lower blood pressure.
Here you are asking from two parts of body that have same height as the heart,

so they will have approximately the same blood pressure.
For more see:
Netter's Anatomy Page 136 and Campbell Biology

You can quote Pascal's law too :)

Hmm. Right , Thank u for every thing , for editing my posts , for helping me to improve my knowledge  and for many other things, Thank U...      :)

But I'm confusing , Why no one vote up my posts?????

It is up to the community.. If someone finds your post useful then they'll vote, don't worry.. If you can add some references or calculations in your post then I'll be happy to upvote..

I think I did. :)

U know since I joined this community I just want to be active as u are but that was a little bit hard, But I'm always trying to be . :)

Well done @M.Y.Ard.Ir - much better!

Thank u my friend , U taught me and u helped me ...   :)


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How do muscle cells synthesize glycogen?
Hexokinase enzyme is present in all cells (including muscle cells) and can be suppressed by excessive G-6-P product. So that's why in the liver, glucokinase can act on glucose without inhibition of it despite excessive G-6-P product; that's why it can generate glycogen and not let excessive glucose flow back in bloodstream. My question is then: why muscle cells can generate glycogen despite having HK instead of GK? Because as i said above, HK activity is dependent on intracellular glucose level, and cannot phosphorylate glucose to hold it inside the cell. So glucose enters back to bloodstream and prevents the synthesis of glycogen?

@user4147 I reworded your question. If you don't like it, you can change it back.

@user4147 - can you please clarify your question above? You mentioned that hexokinase kinase activity is dependent on intracellular glucose level and cannot phosphorylate glucose glucose to hold it inside the cell – but that's exactly what happens (?) – Can you clarify your above text because it doesn't make any sense – thanks!

the HK enzyme activity is suppressed by excessive product (G-6-P) that is why when the cell is well fed (having enough ATP) it wil not consume unwanted glucose therefore not phosphorylating it and thus it can go back to bloodstream to maintain glucose level.my question was on muscle cells that then why they make glycogen when they have only HK enzyme

"...back to bloodstream to maintain glucose level" this is done by liver. "when the cell is well fed (having enough ATP) it will not consume unwanted glucose therefore not phosphorylating it..." and thus it will convert glucose to glycogen for storage. I think you should have a look at cori's cycle (https://en.wikipedia.org/wiki/Cori_cycle) and @sunboyharry's answer.

The answer to the question is that under conditions favouring glycogen synthesis (e.g. the fed state) G6P only accumulates in skeletal muscle cells when the capacity of those cells for storing glycogen has been reached. Until then the G6P is immediately converted to G1P and on to glycogen, in the reactions in sunboyharry's answer.
The question suggests a misunderstanding of the role of glucokinase in liver, which can be better considered if we first make clear the role of liver and skeletal muscle in glucose metabolism. The role of the liver is to deal with excess glucose after a meal by trapping it in the cell as G6P. Although initially the G6P may be converted to G1P and hence to glycogen, this is not the only fate of G6P. Subsequently it may be directed to glycolysis and to the pentose phosphate shunt to provide the acetyl units and reducing power (NADPH) needed for fatty acid synthesis. (The fatty acids are converted to triglycerides and exported to the adipose tissue.) When the blood glucose falls the role of the liver is to release glucose into the blood to supply those tissues that depend on it (brain and erythrocytes in starvation, skeletal muscle if the fall is due to muscle exercise). The skeletal muscle, in contrast, is only concerned with storing glucose as glycogen when it is available, and converting it to G6P for glycolysis when it needs ATP to power muscle contraction.
Glucokinase has a key role in the regulation of blood glucose concentration by the liver. To paraphrase (and edit slightly) Cornish-Bowden and Cardenas: "Mammals have two types of enzymes to catalyse the formation of G6P from glucose. Glucokinase [hexokinase D in their nomenclature] differs significantly from the other type [generally just referred to as hexokinase]. Its abundance varies markedly with hormonal status; it requires much higher glucose concentrations (about 10 mM) for half saturation, and is insensitive to physiological concentrations of G6P. It is thus well adapted to respond to variations in blood-glucose concentrations."
To clarify, 10mM is in the region of the blood glucose concentration (ca. 5mM) so the glucokinase reaction will be affected by the relative concentrations of blood glucose and intracellular G6P in a standard mass action manner, which will determine whether the liver takes up glucose or releases it into the blood. If glucokinase were inhibited allosterically by G6P like hexokinase, this couldn't work.
Now let's turn to G6P and hexokinase in skeletal muscle. Hexokinase has a much higher affinity for glucose than hexokinase and will convert it efficiently to G6P. As long as G6P is then converted to G1P for glycogen synthesis, G6P will not build up. However when glycogen synthesis stops because the capacity of the muscle to store glycogen is reached, the concentration of G6P will increase and turn hexokinase off. This, in turn, will cause a build up of intracellular glucose and prevent glucose transport into the muscle. This makes sense, because with full glycogen stores, and in the absence of need for contraction, glucose will not be metabolized by the muscle; it will be left in the blood for the liver to handle.
Thus, the key point about G6P inhibition of hexokinase, and the apparent source of confusion in the question, is that it only occurs at concentrations that are reached when the G6P is not being metabolized within the cell.
Reference and Footnote
Ref for citation: Cornish-Bowden, A and Cardenas, M.. (1991) Trends in Biochemical Sciences 16, pp281-2. (This article also makes the point that the kinetics of glucokinase are sigmoidal and not hyperbolic as stated in most texts, and that the enzyme is not specific for glucose. Neither of these points affect the argument here. The former does indicate that my reference to glucose control of glucokinase operating in "a standard mass action manner" is a simplification. It does respond to changes in glucose concentration in the blood range, but in a more sophisticated manner than an enzyme with simple Michaelis-Menten kinetics.)

Hexokinase catalyze glucose to form G-6-P is only the first step of the glycogen synthesis, and then the G-6-P will continue to processing a series reaction and finally become glycogen. So once the G-6-P forms, it will keep reacting, which will not inhibit the activity of hexokinase.

You should add a reference to the source where you obtained the reaction pathway scan.


text:
How does the pancreatic beta-cell know how much insulin to secrete in response to glucose?
How do $\ce\beta$-cells know how much glucose is in the blood?
I know that when glucose enters a beta cell it triggers the cell to produce insulin. $\ce\beta$-cells trap glucose by converting it into glucose-6-phosphate, this means $\ce\beta$-cells actually consumes glucose.
So my question is: how do $\ce\beta$-cells decide when to stop producing insulin? (To do that the cells must know the level of glucose in blood, right?)

Yes, pancreatic beta cells can indeed sense the level of blood glucose. They respond to high glucose concentrations by secreting insulin, and stop (or reduce) secreting insulin when glucose concentration falls. This is a classic example of feedback regulation (homeostasis) in physiology.
Exactly how the glucose sensing in beta cells has been the subject of much research for decades; a freely available review is here. You are correct that phosphorylation and further metabolism of glucose by the beta cells is required for sensing. The current theory is that mitochondrial oxidation of glucose leads to increased ATP levels, which is detected by ATP-sensitive potassium channels at the plasma membrane, which in turn leads to secretion of insulin.
When glucose levels fall, beta cells reduce their glucose metabolism because they use the glucokinase enzyme to phosphorylate glucose, and glucokinase is a low-affinity enzyme that becomes inactive at lower glucose levels. Therefore, uptake and oxidation of glucose is reduced, ATP levels fall, and insulin secretion stops.
This is the current consensus I believe. But these metabolic processes are difficult to study, and the precise nature of the connection between glucose metabolism and the ATP-sensitive channels is still somewhat controversial.


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When glucose production is low, the brain begins using ketoacids as energy... how does that work?
Can someone very generally describe how the brain consumes ketoacids/ketone bodies when blood glucose has been completely depleted?

Human body is a glucose driven machine which intake carbohydrates and converts to glucose. Energy is yielded from the glucose and glucose is stored as glycogen. When the carbohydrate intake is somehow reduced then body will shift its mechanism and uses the fatty acids to produce energy. Liver synthesis ketones from fatty acids in our diet or from body fat. Ketones(acetoacetate and acetone) are released into the blood, which is absorbed by the brain and synthesis energy from it through their mitochondria.

The brain gets a portion of its energy from ketone bodies when glucose
  is less available (e.g., during fasting, strenuous exercise, low
  carbohydrate, ketogenic diet and in neonates). In the event of low
  blood glucose, most other tissues have additional energy sources
  besides ketone bodies (such as fatty acids), but the brain has an
  obligatory requirement for some glucose. After the diet has been
  changed to lower blood glucose for 3 days, the brain gets 25% of its
  energy from ketone bodies.After about 4 days, this goes up to 70%
  (during the initial stages the brain does not burn ketones, since they
  are an important substrate for lipid synthesis in the brain).
  Furthermore, ketones produced from omega-3 fatty acids may reduce
  cognitive deterioration in old age.
  Reference

When the body starts using the fatty acids for energy production, one problem arises in the brain and that is the blood-brain barrier( barrier that separates the circulating blood from the brain extracellular fluid in the central nervous system )Brain cannot use long chain fatty acids because they cannot cross the blood-brain barrier due to their bondage with albumin. As ketones are medium chain fatty acids which can effectively cross the barrier. So brain uses the ketones for energy production by a process called as ketosis. The ketone bodies are then incorporated into acetyl-CoA and used in the citric acid cycle.

The citric acid cycle – also known as the tricarboxylic acid (TCA)
  cycle or the Krebs cycle – is a series of chemical reactions used by
  all aerobic organisms to generate energy through the oxidation of
  acetate derived from carbohydrates, fats and proteins into carbon
  dioxide and chemical energy in the form of adenosine triphosphate
  (ATP).
  Reference

Metabolic pathways to produce energy

I've linked to your answer in this question.

Actually there is fatty acid transport through the BBB. Maybe the rate of this transport is not enough, I don't know, I think it does not really matter.
What really happens here, that the liver prepares the fatty acids, so the brain can use them more easily in the form of ketoacids to produce energy.

fatty acid catabolism shared between the liver and the brain - ref

What you tell is astonishing: you learn about fatty acids being prohibited from being turned into glucose. With this that doesn't seem to be true: fatty acids to Acetyl-CoA and then clockwise through the TCA cycle, left hand,  to Oxaloacetate, then pyruvate, then: glucose. It looks as if it is a matter of plentitude of carbon to burn, as by being shuffled through the TCA cycle CO2 two times is being set free.  -  Should be written in all the textbooks!

@PeterBernhard Yes, in the human body there is no fatty acid -> carbohydrate biochemical pathway or it is very slow (note that this is not true for all animals). Same is true for fructose and ethanol, that's why they cause oxidative stress, fatty liver and diabetes. I think many times you can prevent diabetes by avoiding fructose (pratically most of the sweet foods and drinks) and alcohol. I think this information about carbs and fatty acids is already in textbooks, at least I learned it in the university 10+ years ago. The fructose part is a lot more recent.

Pun on "prohibition"? I mean alcohol and fructose sound icy to me, take my excuses for my strange English, by the way; the graphic has a link but the ref does not tell about which book that the graphic is from. As it occurs to me...even in wording that question could have been me. Maybe my comment truly tells - not the whole "stuory fur" sure, as you mention fructose - so how does prohibition of fructose from being turned to sweet work? Can you e-"leber"ate?

@PeterBernhard Last time I read about fructose, it was something new and very logical. Now according to new reviews it is not as certain as it was. https://www.mdpi.com/2072-6643/9/2/96/htm https://www.mdpi.com/2072-6643/9/9/981 https://www.sciencedirect.com/science/article/abs/pii/S0168827818300667 https://academic.oup.com/ajcn/article/100/3/833/4576481?login=false https://scholar.google.hu/scholar?hl=en&as_sdt=0%2C5&q=fructose+fatty+liver+review&btnG=&oq=fructose+fatty+liver

Again, thank you for clarifying what maybe is some common non having understood: e.g. medscape.com: "High levels of acetoacetate in blood may result from the following: Diabetic ketoacidosis and alcoholic ketoacidosis". As for me, I needed advice on that being the other dark side of the medal (no German) of ketose being needed. So, your shed new light on some, literally, half-knowledge. Diabetes, alcohol seem to imitate the need that must be: of calories, to starve is exhilarating.
To sum up: with your answer "ketoacidose" becomes understood, it's good, not bad, it's regular.

"Last time I read about fructose..." - Fructose, interesting to know about that..., does not seem to share any "prohibition", thus beyond topic: fructose can easily be converted to glucose by the body, ain't right? Is there any preference the link you added (not very accessible for the common people?)  is about? Fructose might be preferentially turned to ribose of DNA?

"Last time I read about fructose..." -  Fructose, interesting to know about that..., does not seem to share any "prohibition". It can easily be converted to glucose by the body.  Is there any preference the link you added (not very accessible)  is about? Fructose might be preferentially turned to ribose of DNA? Some other item is  that insuline production does not react to   fructose input, fructose heightening blood sugar in diabetic and non-diabetic in the same way.

@PeterBernhard Just use the google scholar link and you can find many similar articles. Some of them are not paywall protected. These are scientific articles published in scientific journals. You can read them in libararies or in universities. Sci-hub is another way, but it is more or less illegal, it depends on country though. https://en.wikipedia.org/wiki/Sci-Hub

Yeah, it is "fruct"(verrückt in German, dialect I use) - to chat it all up: fructose does seem convertible into glucose. 10 years ago it's use in chocolate was considered anti-diabetic. In my thinking, there is a way to store away some fructose-elevation of blood sugar if not to glycogen, then in a very regular, i.e. non-insuline way as fatty acid in adipose tissure, and in my thinking your mentioning "fatty liver" is very valuable: glucose - like "starch" seems to correlate to glykogen and maybe white fat, and fructose, just extrapolative, to "brown fat". Guess you're not German too.

@PeterBernhard Looks like normally it is converted into glucose in the small intestine, but in big quantities it reaches the liver where it is converted into fatty acids afaik. from other studies. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6032988/ So consuming fructose as sweetener in big quantities (as we do nowadays with corn syrup) can cause health problems.

@PeterBernhard Another interesting thing here that it might affect cholesterol levels too. https://www.sciencedirect.com/science/article/abs/pii/0006294469900453

Mentioning cholesterol in that context seems irritating, I find it highly educating. Lately, I found myself "occuring" to me that cholesterol is either built into cell or veins' walls, however, cannot be burned, and - please help, correct me - cannot be converted into blood sugar. So, in that respect, cholesterol looks like some fat, and rightly suits this question.

@PeterBernhard The category is called lipid. It is transported with triglycerides and it is apolar, so we can call it fat. High level of blood cholesterol is problematic from atherosclerosis perspective.

I will say "lipid" not fat any more... So, I guess its trivial to know that cholsterol "cannot heat"...


text:
Synthesis of Fatty Acids Longer than 16 Carbons
I understand that the human body when performing Fatty Acid Synthesis can synthesize only until C16 (palmitate). However the ER has desaturases and elongases. I know that desaturases are used to add double bonds, but do humans have elongases to add even more Carbons to a double bond? If so, then this would mean that the human body can synthesize fats longer than C16?
Lets take a hypothetical case and say that humans have both desaturases and elongases. Would it be feasible to add double bonds to palmitate via desaturases, then add more carbons to the chain via elongases and then add more double bonds via desaturases? This way, the resulting fatty acid will have an increased length and more unsaturated character (i.e. more double bonds than the prescribed 4 that humans can add at positions 4, 5, 6, and 9)?

Short Answer: Yes.
Long Answer: See this article:

The diagrams presented show how fatty acids are synthesized in microorganisms and list the enzymes found in Escherichia coli. These reactions are performed by fatty acid synthase II (FASII), which in general contain multiple enzymes that act as one complex. FASII is present in prokaryotes, plants, fungi, and parasites, as well as in mitochondria.
In animals, as well as some fungi such as yeast, these same reactions occur on fatty acid synthase I (FASI), a large dimeric protein that has all of the enzymatic activities required to create a fatty acid. FASI is less efficient than FASII; however, it allows for the formation of more molecules, including "medium-chain" fatty acids via early chain termination.
Once a 16:0 carbon fatty acid has been formed, it can undergo a number of modifications, resulting in desaturation and/or elongation. Elongation, starting with stearate (18:0), is performed mainly in the ER by several membrane-bound enzymes. The enzymatic steps involved in the elongation process are principally the same as those carried out by FAS, but the four principal successive steps of the elongation are performed by individual proteins, which may be physically associated.

Another article from NCBI states:

Primers for several mouse, rat, and human elongases have been reported elsewhere.

...and cites here for this:

Fatty acid elongases and desaturases play an important role in hepatic and whole body lipid composition. We examined the role that key transcription factors played in the control of hepatic elongase and desaturase expression...In conclusion, these studies establish a role for PPARalpha, LXR, SREBP-1, ChREBP, and MLX in the control of hepatic fatty acid elongase and desaturase expression and lipid composition.

Indeed, humans do synthesize stearic acid (C18) in their body; mainly liver and adipose tissue. See this article:

Fatty acid biosynthesis from acetyl-CoA takes place primarily in the liver, adipose tissue, and mammary glands of higher animals. Successive reduction and dehydration reactions yield saturated fatty acids up to a 16-carbon chain length. Stearic acid is synthesized by the condensation of palmitoyl-CoA and acetyl-CoA in the mitochondria, and oleic acid is formed via a mono-oxygenase system in the endoplasmic reticulum.

Now, would it be feasible or not to synthesize unsaturated fatty acids is a matter of debate. Maybe this could be helpful in this matter.


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Why are carbohydrates the most common short-to-medium-term energy storage form in biology?
According to this table, gasoline has a specific energy noticeably higher than fat and more than twice that of carbohydrates; even short-chain hydrocarbons like ethanol and even methanol offer an improvement in specific energy over carbohydrates. Given this, why are carbohydrates the most common short-to-medium-term energy storage form in biology?

Two quick reasons: (1) those compounds are toxic to cells, or may give toxic metabolites when metabolized; or (2) they might actually be great energy sources, but enzymes to process them have never evolved.

I would argue that the toxicity is as much a result of the "choice" of energy storage as a cause, since toxicity is basically metabolic/physiological incompatibility; also, numerous organisms have evolved toxin immunity quite quickly where advantageous. (Also, the metabolites of hydrocarbons are simply water and carbon dioxide, the same as carbohydrates)
Secondly, my question is essentially why those enzymes haven't evolved? Complexity seems an odd reason, since straight-chain hydrocarbons are simpler than carbohydrates, so what advantage selected for the latter rather than the former?

I agree with your comment about metabolic compatibility, but toxicity is not determined simply by elemental composition. The rest sounds similar to many questions on this forum of the form "why haven't cool function X evolved". Evolution is cannot plan ahead, so it gets stuck in local optima all the time. Photosynthesis somehow (randomly?) evolved to produce sugars from CO2, and thereafter sugars became a common currency. This may well be just a coincidence. But these are so early events in evolution that we really don't have any way of knowing.

I fully understand that evolution tends to an immediate optimum rather than a long-term one, in which case the answer I am looking for would be the local optimum which made carbohydrate metabolism more (immediately) advantageous. Given that hydrocarbon-based metabolisms have evolved and currently exist, the implication is that carbohydrates offer or offered some selective advantage over hydrocarbons.


text:
Is there a non-directed way to probe proteins in a given sample?
I'm familiar with various ways to probe for specific proteins in a given sample(antibody/antigen, aptamers, etc). But these techniques seem to require an understanding of what protein you're looking to probe.
Is there a way to probe for unknown proteins? Some sort of molecule that enables proteins to bind, and through many interrogation reactions would allow us to know what that protein is?

If you have no idea: Proteomics using Mass spectrometry
Mass spectrometry is a powerful
method that (in theory) identifies every proteins in a given solution. However, I don‘t know how robust this method is in terms of sensitivity in the presence of large background signals. Usually, people pre-process the sample, e.g. they separate the raw protein extract in a 2D PAGE (polyacrylamid gel electrophoresis), separating the proteins by size and isoelectric point in a gel. Then they cut the gel into pieces, extract specific proteins and then identify protein fractions using mass spectrometry.
Advanced mass spectrometry methods seem to be able to identify proteomes from imaged tissue samples Ryan et al. 2019
A pulldown assay is also powerful method to pre-isolate unknown components of a protein complex. But for that you need one component or an antibody that binds to a component of the protein complex.