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What cells in mosses behave analogously to mammalian embryonic stem cells?
The Washington Post article Ancient life awakens amid thawing ice caps and permafrost describes the work of Peter Convey, an ecologist with the British Antarctic Survey and his team, and includes a discussion of some mosses that have survived over 1000 years in permafrost, and sprung to life once "revived" in a laboratory setting.
This passage caught my eye:

It’s not easy to survive being frozen solid. Jagged ice crystals can shred cell membranes and other vital biological machinery. Many plants and animals simply succumb to the cold at winter’s onset, willing their seeds or eggs to spawn a new generation come spring.
Mosses have forged a tougher path. They desiccate when temperatures plummet, sidestepping the potential hazard of ice forming in their tissues. And if parts of the plant do sustain damage, certain cells can divide and differentiate into all the various tissue types that comprise a complete moss, similar to stem cells in human embryos.

What are these cells in moss called, and how similar are their functions to mammalian embryonic stem cells?

Convey and his team announced that they had awakened 1,500-year-old moss that had been buried more than three feet underground in the Antarctic permafrost. (P. Boelen/BAS)

The growing tips of roots and shoots contain regions of rapidly dividing cells in all plants that are called apical meristems. Apical meristems contain the plant's stem cells, which are not fundamentally different from the stem cells of animals.
You can begin learning more about this subject from this Nature scitable article.

This is just what I needed... reading now, thanks!

Great! Glad I could help.

Cambium also has totipotent stem cells as you might know that some plants can be propagated by planting stem cuttings.

@WYSIWYG — True and also from callus, but unless I'm misremembering only vascular plants have a cambium and so that didn't seem relevant to bring up in a post about mosses.


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Chorophyll and photosynthesis in plants with coloured leaves
Do plants that have only coloured leaves (e.g. ‘ornamental’ plants) contain chlorophyll and perform photosynthesis?
If they don’t, how do they obtain energy and metabolic intermediates?

Most of ornamental (often variegated ) plants do performs photosynthesis. They do have chlorophyll even if their color is not green. They have non-green color due to various different pigments. These extra color has their own functions like blocking harsh sunlight or protection from insects (Karageorgou and Manetas 2006).
In many non-green plants carotenoid content is way higher than chlorophyll. One of the main functions of these carotenoids is to expand the range of wavelength where photosynthesis can happen (Hashimoto et al 2016). This is especially important for such plants living in low light conditions or other stress factors are dominant.
Some comparison of content in different color leafs of Acer saccharum is enlisted in table below. Image is taken from (Junker and Ensminger 2016)

Photosynthetic activity of such plants can be measured by chlorophyll fluorescence techniques (Borek et al 2016). Photosynthesis performance of many of these plants (like Actinidia kolomikta) is actually properly maintained (Wang et al 2016) and does not have high Photosynthetic Cost.
Just to extend this answer for little general information, plants without any chlorophyll (like Cuscuta europaea) are often parasitic plants and they need host to survive and get nutrients.

Your answer should stick to the point in the question and answer that. The illustration of a plant you cite has green leaves. You do not say whether plants with e.g. red leaves contain chlorophyll. That was the question. You should do this and cite evidence for your statement.

@David , it was implied in my first sentence. However, now I have explicitly mentioned it.

Fine. But it needed spelling out.

source: Stack Exchange

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

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What is this little owl-like bird?
I was walking outside (location: Netherlands) and just saw this little bird:

Unfortunately I had to take a long range picture with my cell phone so the quality is quite bad, however I hope still someone can identify this species. Personally I think it escaped somewhere as we have never seen it before and also did not seem to be scared of us.

This looks a lot like a double-barred finch (Taeniopygia bichenovii). Your note about this being an "owl-like" bird is supported by it's less common name, the "owl finch", so named for the dark ring around the face.

 Source: Wikipedia; Credit: Glen Fergus
If this is in fact the bird you saw, you're right that it's not native to your country (or continent or even hemisphere!). The Taeniopygia genus is in the Estrildidae family, and it only contains two species native to Australia! According to Wikipedia, T. bichenovii is found:

in dry savannah, tropical (lowland) dry grassland and shrubland habitats in northern and eastern Australia

You can read more at eFinch and The Atlas iof Living Australia.

@KingBoomie If there are any zoos in your area, you may want to give them a call to ask if they are missing this little fellow.

@AndrewKozak good idea; also any local pet stores that sell exotic birds. Could be one of their customers has lost a pet!

Public aviaries (volière in Dutch) are also a possibility.  Most exotic birds are not on the list of allowed pets in the Netherlands and although uncommon, aviaries are more common than zoos.

@AndrewKozak  Probably from a public aviary, while it had a ring there was no number on it so we gave it to a relative having birds himself and he would figure our where to bring the little fellow ;)

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


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How does the stomach handle continuous eating?
In biology class, we learned this familiar story:  Food enters the stomach, the stomach churns it with acid and enzymes, and then, somehow, the stomach senses when the stew is ready and releases it into the small intestine.
But this simple narrative implicitly assumes that all the food of a meal comes into the stomach at about the same time, and only then does the digestion process begin.  This is often not the reality.  What happens when we eat continuously over many hours, such as at a Super Bowl party, or an all-day summer barbecue, or a long afternoon at an all-you-can-eat crab shack?
Does every new bite cause the stomach to reset its process to zero?  "Uh oh, detecting fresh, undigested food...  better start over..."  But if the stomach resets to zero with every new bite, wouldn't it eventually grow overfull?
Or does the stomach eventually get fed up with all the new introductions and just start releasing whatever it has into the small intestine, ready or not?  In that case, when and how did it decide to proceed with incomplete processing?

First of all, the stomach releases the digested food continuously. Simply put, during digestion the pylorus regularly opens a bit so that small food particles (< 1-2mm) are able to leave the stomach – it's not a batch process (see also this question).
However, because humans tend to ingest a lot of indigestible materials (e.g. bones), there is a need to pass the larger indigestible particles – and this process only happens after all digestible food has left the stomach and thus is "reset" every time you ingest new digestible food.
So if you would continuously ingest food that contains indigestible parts (e.g. mice or other small mammals), the larger bones of those mice would accumulate until you take a longer break and the stomach could complete it's digestion – but for normal food, this does not matter since it will be broken down enough to leave your stomach continuously.

Source: According to Estimation of gastric residence time of the Heidelberg capsule in humans: Effect of varying food composition, 1985 (PDF), the  interdigestive migrating myoelectric complex (IMMC) is responsible for the emptying of of large undigested particles:

Recently, Hinder and Kelly (1), using radiolabeled techniques, demonstrated differences in the gastric emptying patterns of a liquid, a digestible solid, and an indigestible solid in dogs. Based on such experiments, it has been suggested that the emptying of large (>1 mm) indigestible objects from the stomach
  is dependent on the interdigestive migrating myoelectric complex (IMMC)

Furthermore the study shows that the IMMC gets triggered only after all digestible matter has leaved the stomach:

The longer GRT of the Heidelberg capsule compared with the t1/2 of the 99mTC-DTPA is consistent with the finding that large nondigestible solids are emptied by the IMMC once all of the digestible materials have passed through the pylorus into the duodenum

and

the interdigestive migrating myoelectric complex can be markedly delayed by frequent feedings with solids, and the interdigestive migrating myoelectric complex is delayed by both liquid and solid meals

and

Feeding has been shown to interrupt the IMMC; resumption of myoelectric activity is necessary for the passage of large nondigestible particles such as the Heidelberg capsule

Does the stomach need to start over after every bite? No. When the stomach digests food and some new food comes in, it just continues to digest the old and new food. The stomach releases small particles first and continues to crush large particles.
In the stomach and small intestine, there are mechanoreceptors and receptors that detect gastric acid, amino acids, etc., which stimulate the release of gastrointestinal hormones and the vagus nerve, which all together act as brakes or accelerators of stomach emptying (Nutrients, 2016).
In both continuous and "few meals a day" pattern of eating, the stomach emptying can be greatly affected by various food factors:

Consistency. Liquid foods empty faster than solid foods.
Particle size. Small food particles empty faster than the bigger ones.
Volume. Greater volume of food will stimulate gastric emptying sooner than a small volume.
Energy value: 300 Cal meal will empty faster than 600 Cal meal; the stomach tends to release a certain amount of calories per time
Water and drinks up to ~7% of sugar empty faster than those with >8% sugar (regular fruit juices and sodas)
Macronutrients:
Fat and soluble fiber (such as glucan from barley or pectin from apples) can slow gastric emptying.

Human factors that can slow down gastric emptying:

Psychological factors, such as anxiety
Physical factors, such as exercise
Diseases, such as diabetic neuropathy
Medications, such as antacids and opioids

Other sources:

Gastric Emptying, Claudia Cheng (Department of Anesthesia and Intensive Care, Faculty of Medicine, The Chinese University of Hong Kong)
Advances in the physiology of gastric emptying (Neurogastroenterology & Motility, 2019)


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Confusion about result of monohybrid cross in Mendelian genetics
I was studying monohybrid crosses in genetics where the character considered is stem height. Whenever I came across punnett squares, I used to calculate the probability of the genotype of the offsprings which can be formed as a result of a cross between 2 heterozygous plants. In the F1 generation, these are obtained by crossing homozygous dominant(Tall) and homozygous recessive plant(Short). Now when these plants of the F1 generation are crossed, each plant produces 2 types of gametes where each gamete is having only 1 allele of the gene.
Now my question is that when we cross these plants, is it necessary to get 'one- fourth' dwarf plants and 'three-fourth' tall plants? Doesn't the punnett square only gives the probability of the possible genotypes of the offsprings formed, while the real cross could result in say 50-50 percent tall or dwarf plants? Is it necessary that the actual cross follows the probability of predicted by the punnett square ?
If no then why is this statement given in my book that 'One fourth of the plants obtained in the cross were dwarf while the rest were dwarf'? Couldn't this proportion be anything  other than this proportion ? If so then how could this proportion be obtained isn't that a chance factor?

while the real cross could result in say 50-50 percent tall or dwarf
  plants?

Sure it's possible, but if you have dozens of offspring, the odds of you being very far away from the 1:3 ratio are very small.   If you look hard enough, you can find Mendel's actual results, and a chi-square test is the usual way to show that his results do not deviate significantly from the expected ratios.

That is these results( punnett square) are the most probable results


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Oldest Triceratops fossil
In most books, Triceratops is listed to live between 68-66 MYA (million years ago), however some books list Triceratops as living between 70-66 MYA. The Campanian age ended about 72 MYA and then came the Maastrichtian. Many articles state that Triceratops is "late Maastrichtian" dinosaur. All these citations do not give a clear answer: when did Triceratops live? All sources agree that Triceratops lived up to the K-Pg extinction 66 MYA, but when did the earliest Triceratops live?
This may be vague question so put it more empirically: what is the oldest age that a Triceratops fossil is dated to? Not when the first fossil of Triceratops was found but what is the earliest age (in MYA) at which Triceratops are known to have existed? Are there Triceratops fossils from 68 MYA? And from 70 MYA?

late Maastrichtian,  Maastricht is the name of a restaurant.

Thanks. From where I am coming from, the term localized as "Maastricht" but thank you for your comment how it is used in general/international.

late Maastrichtian is probably it.
Part of the problem you are running into is the Triceratops genus is in flux, there is debate about whether certain species belong in the genus. Such as whether triceratops and torosaurus are the same species.
The other problem you are running in to is the accuracy of dating methods, many fossils are dated indirectly, by bracketing (distance in section) with ash beds but this means they have a decent margin of error, 69MYA +/- 2mya is completely possible. Many were collected before such dating was even done or suche detailed measurements were taken leading to an even wider error bar. Especially given the best dates for the Hell Creek Formation itself has an date range error of about +/- 0.7MY and begins with a unconformity. Many studies are just going not going to calculate a date that has a high degree of uncertainty. The date for the end is more solid because it is an ash bed, thus directly datatable.
The most recent analysis of triceratops I know of is here many of the specimens were collected in the 1800's so late Maastrichtian is about the best you are going to get for an uncontroversial date.


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DNA replication - 2 new strands or original (parent) and child?
this is my first time here, so go easy on me! I've been trying to find out more about the actual process of DNA replication. Specifically, I am wondering if, when the DNA replicates during cellular division, the result is the original DNA strand and a copy? Or is the original strand destroyed in the process and there are 2 child copies that are identical (aside from mutations) to the original?
I am pretty confident in the end-result, but maybe whoever answers can verify this for me too. My understanding is that the original cell itself is destroyed in the end, but the daughter cells are constructed from the substance of the parent's cell. The initial question will help clarify this process for me too, because I am curious if one of the two daughter cells has the literal DNA from the original, or if basically the entire original cell "dies" in the process and the two new cells are completely new.
Update (to demonstrate research effort):
I have learned how a helicase enzyme untwists the DNA and severs the hydrogen bonds between the nucleotide bases, then single-strand binding proteins bind DNA polymerase to the ends of the strand and begin molding, creating a complimentary strand for each side. It seems evident that half of the "original" is found in each daughter, and the DNA polymerase forms the other half. So, the original is still present, but not in its original form, which is why I'm not sure what the "official" diagnosis is. Is it a parent-child, or two children?

"It seems evident that half of the "original" is found in each daughter, and the DNA polymerase forms the other half." - Thanks for doing some self-research: looks like you found your answer! It's okay to write up an answer to your own question. However you still ask: "Is it a parent-child, or two children?" - as the answer you found shows, the answer as far as the DNA molecule itself is neither.

Thanks Bryan. I think the answer I'm looking for lies a little deeper, but maybe I don't know how to word it. Read my reply to Alex Reynolds' response and see if that helps you understand what I am asking. It may be that we don't actually know the answer yet, but maybe somebody that understands this deeper than I do can enlighten me.

Via: https://en.wikipedia.org/wiki/Semiconservative_replication

Semiconservative replication describes the mechanism of DNA replication in all known cells. It derives its name from the fact that it produces two copies of the original DNA molecule, each of which contains one of original strand, and one newly-synthesized strand. (emph. added)

Thanks for the feedback. I suppose my question can be tailored more. A cell's nucleus is considered to be its brain-center. In all living things, there is a controlling consciousness (like our own consciousness that controls our body as a whole). If the DNA is the code that determines cell function and operation, then is the DNA the consciousness? If so, when the DNA splits, what happens to that original consciousness? Does it take up residence in one of the two, newly-formed strands, or is the original destroyed and two "newborns" are produced?

"In all living things, there is a controlling consciousness" including at the level of a cell is not a statement that is supported by any scientific research that I am aware of. Besides some religious perspective (that seems to run into a problem here), there is nothing "controlling" a cell, rather a cell is made of molecules (some of them quite complicated) that respond and interact with their local chemistry. Clearly in DNA replication, as Alex's answer mentions, the DNA molecule in each of the two cells after division is half new and half from the parent.

I see. Thanks for clarifying all this. It has helped me tremendously!

I'm afraid I don't know what "consciousness" means in this context. Cells are just bags of chemicals where reactions take place. DNA is just a molecule. If the right parts of it are accessible to protein-making machinery and energy (ATP), then life happens. Unless there are errors in replication or cell division that change a copy, one copy of a DNA molecule has the same chemical properties and utility as another copy, all else the same.


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Optimal carbon dioxide concentration range for the human body
Previously I had thought the maximum concentration of  CO2 for human health to be given by the ‘Pettenkofer CO2 level’ with a maximum of 1000 ppm.
But according to this post

a growing body of research suggests CO2 levels as low as 1,000 ppm
  could cause health problems, even if exposure only lasts for a few
  hours.

Therefore it looks like a lower value than 1000 ppm would be healthier for the human body. Is that so?
What would be the target CO2 level inside a passive house? Since outside it is in the range 3-400 ppm. So with more ventillation we could get closer to 3-400ppm, which is Nature’s default (which shouldn’t be bad?)
Perhaps 750 ppm would be ideal — is there any research on that, either cognitive or related to blood vessels.

What suggests that any $\ce{CO_2}$ concentration is beneficial, let alone a concentration between $400\ \mathrm{ppm}$ and $1000\ \mathrm{ppm}$?

well, outside, in the nature, there is 3-400ppm.
AND:
that x>1000 is bad = Pettenkofer advise

Just cause something's in our natural habitat doesn't make it beneficial for us. We've evolved to tolerate starving and fighting too.

oh, hokay. Thanks :) good idea. but maybe this is not a well-researched topic, since I cannot find some exact facts, what would be the most healthy for the human-body.

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7575229/  Little researched is a good comment in this time of hysteria.  It is known that the flora starts to die at 180ppm but finding the level the human body can tolerate is difficult.  I would GUESS that 500ppm would be the highest we should generate in order to level out the temperature differentials between the solar minimums and maximums.  We could allow the level to rise at the beginning of minimums like we are currently entering and lower it as we approach maximums.  Again I would guess guess 300ppm would be a satisfactory cooling level of atmospheric CO2.  The plant life would love a higher level and we would love a lower level.  We cannot live without the flora remember.  Both flora and fauna must be accommodated as we control the climate.  Weather cannot be controlled but we can do something about climate.  https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7575229/


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What adaptations does the human body have to handle frequent and sustained changes in orientation?
Most animals are horizontal with the ground.  When they lie down, they get closer to the ground, but their orientation does not change.
Humans, on the other hand, stand up straight and tall, perpendicular with the ground.  And when we lie down, we make a complete 90° turn.  So we spent 2/3 of our day at one orientation, and 1/3 of our day at the exactly orthogonal orientation.
It's difficult to think of many other animals that change their orientation so completely on a regular basis, or spend much time in different orientations.  (Sure, prairie dogs, bears, lemurs, and apes stand upright now and then, and I've seen pictures of whales sleeping vertically, but it's never for long, sustained periods.  Giraffes seem so tall and vertical, but it's all neck and legs — the organs of their body are always horizontal with the ground, and this orientation is maintained when they lie down.  Birds, maybe?)
For humans, regular changes in orientation must surely cause biological stresses, and therefore there must be some biological adaptations to those stresses.
Even non-biologists are aware of plenty of orientation-related malfunctions:
— middle-aged people start to get acid reflux and indigestion when they lie horizontally
— elderly people with certain heart conditions and arrhythmias cannot lie horizontally
— some people are affected by changes in blood pressure when they lie down or stand up
— some people have dizziness or balance issues when lying down or standing up
— knees and feet start to have problems from a lifetime of bearing all the weight
What specific adaptations does the human body have to handle these daily changes in orientation?

I guess posture would be a more appropriate term instead of orientation.

For "— some people are affected by changes in blood pressure when they lie down or stand up" and "— some people have dizziness or balance issues when lying down or standing up
", see the discussions of mechanisms in the Wikipedia articles for Orthostatic Hypotension and Reflex Syncope.

For "— knees and feet start to have problems from a lifetime of bearing all the weight", the protective adaptations will largely be identical to those for any joint - even those that aren't supporting the entire body. This can include processes like the release of Synovial fluid.


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Can different cell lines of same type symbolise samples from different patients in ChIP-seq?
Can I simulate different patients by using different cell lines of the same cell type and from the same tissue? Can I also study apoptosis in an immortalised cell line?
I have a gene X (transcription factor) which from wet lab experiments induces apoptosis in  cell type A (endothelial cells) and proliferation in cell type B (smooth muscle cells).
I want to address this differential behaviour using ChIP-seq of antibodies against gene X.
I do not have enough patient samples and I wish to purchase immortalised cell lines to perform ChIP-seq with 4 biological replicates per condition: untreated control and over expression of X.
I plan each biological replicate to be a different cell line of the same cell type and preferably the same tissue. Is it possible to have such?
I will also be very grateful if anyone provides me a link or good article containing the best practices in planning for a ChIP-seq experiment.
Thanks in advance.

It is difficult to say anything conclusively unless we know what kind of cells you are talking about.

@ WYSIWYG Thank you for your response. I will use microvascular endothelial cells from the skin and or lungs.

Can you please [edit] your question to add this information? And do you plan to use cell lines like lung/skin cancer as a proxy?

@WYSIWYG  Please I am completely new to Chip-seq and I do not properly understand the meaning of "proxy" in this context. But I think I will only be using non-cancerous cell lines from the skin or the lungs.

I used "proxy" in a general sense. Using something in place of the other (a substitute that is expected to represent the original condition). In your case, the cell lines being proxy for the patient samples. There are commercially available human microvascular endothelial cells. Are you planning to use them?

Again, I would point out that it would be difficult to say anything conclusively unless we know what the patients really suffer from and whether the experimental model replicates these disease conditions accurately. A general answer would most probably be "no" as we can expect that most cell lines would not properly represent the actual condition. In some cases, however, the cell lines can be a good model. So, as I said before, it is difficult to comment without knowing more details.

@WYSIWYG  Thanks a lot for your response. Yes I plan to use commercially available human microvascular endothelial cells from the skin or the lung. Could you please recommend for me a link  or links where I could find such cells? I need 5 different human skin microvascular cellines  per treatment condition (untreated and overexpressed). I have been searching the internet but I cannot find the number I want.

Moreover, I think you are asking multiple questions here. First is whether cell lines represent the patient conditions reasonably well. Second is whether different cell lines derived from the same tissue are more or less similar (and if they are available commercially or otherwise). The last part about ChIP-seq guidelines is somewhat off-topic. There are plenty of articles available on this topic.

Regarding purchasing the cells: I have no experience on this topic but google gives me many hits to vendor websites: Lonza, Thermo and some other smaller companies.

@WYSIWYG  Thanks a lot for your elaborations. In addition to having a better understanding, You answered all my questions.


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Effects of Great Pacific Garbage Patch to Phytoplankton?
I was wondering if the decrease in light received by the area comprised by the Great Pacific Garbage Patch (GPGP) could affect Phytoplankton enough to reduce its potential in that area as a carbon sink.
I mean, it is an area that gets plenty of sunlight, but compared to the overall size of ocean coverage it is not that much and maybe the cover is not intense enough to reduce completely photosynthesis in that area, so maybe the effect is negligible.
I couldn't find any article reviewing this.  If someone can point me to some literature at least.
I found this: https://www.researchgate.net/publication/325022723_Impact_of_microplastics_on_phytoplankton
But I find these results hard to interpret and was hoping more for an ecological studies.
Rephrasing the question for clarity: how much does the GPGP effect C02 capture by effects of disrupting phytoplankton?

PS: Back of envelope calculations:
with a GPGP area of 15e6 Km^2 (source wikipedia)
and a total ocean area of 360e6 Km^2
we have lost 4% of CO2 capture from plankton. But if plankton captures 30-50% of all CO2 emissions, then we lost 2% of all of our carbon capture potential.
But more so, if we assumed that tropical phytoplankton captures more CO2 than from other regions (suppose all of it), then with about 40% of oceans in the tropics we have:
15/(360*0.4) ~ 10% CO2 capturing phytoplankton lost
which would yield 3-5% reduction on our total carbon capture capacity (I am taking this number as a maximum possible impact )
This, to me, seems like a pretty important number, so I must assume that either:
(1) tropical phytoplankton does not contribute majorly to CO2 capture, so its loss would not be impactful
(2) this is very difficult to study and model
(3) some other reason I haven't thought of
In any case, thank you for your attention!

Do you have a source to support your claim of losing 4% of carbon dioxide capture from plankton (phytoplankton)? Is this a hypothetical figure?

completely hypothetical, just trying to do basic estimations since I don't have any information.


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How long can Legionella survive at 60°C?
I'm coding some stuff for water heaters and one of the functions is anti-Legionella.
Anyway, I've read on wikipedia that 90% Legionella dies in first two minutes if the water temperature is 60°C, but I'm interested in how long should the temperature be 60°C for 99.99999% of Legionella to die? (I guess I can never get to 100%)
Follow-up question: On what intervals should this be done so that the water isn't contained? Should it be one week, two weeks, several days?
Final question: If the water in a water heater has 60°C for 30 minutes every 2 weeks, would the water be safe?

If the water can be repeatedly contaminated, you would probably need to continuously keep its temperature at the disinfection level to limit the risk of contamination to 0.00001%.

Usually cell death would follow first order kinetics.
$$X=X_0e^{-kt}$$
where $X$ is the number of cells at time $t$, $X_0$ is the initial number of cells and $k$ is the death rate constant. You can get the constant by solving for 90% reduction in 2 minutes. Then just substitute and get the time required for 99.99999% reduction — 10 minutes.
For your follow up questions, see the same wikipedia article.

Moist heat sterilization (superheating to 140 °F (60 °C) and flushing)
  is a nonchemical treatment that typically must be repeated every 3–5
  weeks.

It also depends on how much is the bacterial load in the input.
Other sources (Farhat et al. 2012; Whiley et al., 2017) suggest 70°C treatment for 30 minutes.
However, Legionella has been shown to survive heat treatment of 70°C/30min (reviewed by Whiley et al., 2017). Legionella can also be "protected" by other micro-organisms such as certain types of Amoeba, in the water.
So, probably multiple levels of disinfection is needed.

Ok, great, this is just what I needed


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Is the genetic term "polycistronic" still used in modern biology?
Is the term "cistronic", meaning an ORF on a mRNA, still commonly used in modern genetics? I´ve seen "polycistronic" being applied to prokaryotic mRNA in old textbooks, but I´ve rarely stumbled upon this in recent papers, except for research focusing on plasmid engineering.

The thing that I think biologically interesting about this question has perhaps not been emphasized sufficiently in the answers so far which document that the term is still in use. This is why the term is still in use. As the poster states:

I’ve seen “polycistronic” being applied to prokaryotic mRNA in old textbooks, but I’ve rarely stumbled upon this in recent papers

The reason to expect that it would have fallen out of use is:

The shift in research from prokaryotes to eukaryotes in the last 40 years or so
The initial impression that all eukaryotic mRNAs were monocistronic.

It is the discovery of, and the interest in, exceptions* to the latter that has, in my opinion, kept the term in use. There are dicistronic and polycistronic mRNAs in eukaryotes (not just their viruses).
This is illustrated by the first two references in the answer from @theforestecologist, which refer specifically to eukaryotes in their titles.
*Footnote
The exceptions vary with species, but, to take an example that puts things into perspective, of almost 14,000 protein-coding genes in Drosophila there are only about 70 for which polycistronic mRNAs (usually dicistronic) have been established. See the p. D811 of the paper on FlyAtlas 2 and supplementary Table S6. It’s not too surprising that authors of basic text books choose to focus on generalities in an attempt to explain the main ideas in a complex subject.

Yes, it's still used.
If you search Pubmed for "polycistronic", it offers you a chart showing the counts of the term by year (top right). Downloading the CSV and making a chart shows that it's never been a very common term, but it's still used. I suspect, but don't have time to check, that if you were to divide the use of the term by the number of published papers by year its use-per-paper would be pretty much a flat line.
Edit, re-reading the question, it may be about "cistronic" as opposed to "polycistronic". "Cistronic" is also still used, but not nearly as often as "polycistronic" -- 13 times in 2018 to "polycistronic's" 81.

@iayork's answer provides a great approach to examining this question. I just want to corroborate it by using a slightly different approach.
A Google Scholar search for "polycistronic" limited to results since 2015 provides >200 hits.
Some examples include:

Gordon, S.P., Tseng, E., Salamov, A., Zhang, J., Meng, X., Zhao, Z., Kang, D., Underwood, J., Grigoriev, I.V., Figueroa, M. and Schilling, J.S., 2015. Widespread polycistronic transcripts in fungi revealed by single-molecule mRNA sequencing. PloS one, 10(7), p.e0132628.
Karginov, T.A., Pastor, D.P.H., Semler, B.L. and Gomez, C.M., 2017. Mammalian polycistronic mRNAs and disease. Trends in Genetics, 33(2), pp.129-142.
Liu, Z., Chen, O., Wall, J.B.J., Zheng, M., Zhou, Y., Wang, L., Vaseghi, H.R., Qian, L. and Liu, J., 2017. Systematic comparison of 2A peptides for cloning multi-genes in a polycistronic vector. Scientific reports, 7(1), p.2193.


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Why doesn't the soil get depleted after repeated clearing of vegetation?
In my neighborhood, there is a hillside owned and maintained by the local municipality.  The hillside is generally overgrown with vegetation.  Work crews clear out the vegetation multiple times throughout the spring and summer, yet it always grows back quickly.
The workers don't leave the cuttings there.  They haul them away.  So that means the soil of the hillside is losing nutrients.  Yet why does the vegetation always grow back?
Hypotheses:

It all looks like weeds to me, but maybe there is a natural cycle of crop rotation going on that I can't appreciate.  I.e., in year 1 it was all Type A weeds, then in year 2 it was all Type B weeds, then in year 3 it was all Type C weeds, and then in year 4 it was back to Type A weeds again.
Maybe some other natural process is bringing nutrients back to the soil of the hillside.  Bird droppings?  Earthworms?  Insects?  Underground fungus and bacterial colonies?  Small mammal feces?  (I don't think rain runoff is bringing many nutrients because there is nothing but a highway above the hillside.)
Maybe the hillside is getting depleted and will eventually become barren, it just takes a while.  I guess you have to keep clearing, year after year, until it gets down to the very last and most hardy of the weeds before it becomes truly barren and lifeless.

Yes (kind of) to all your hypotheses. You'd benefit, for starters, by reading about succession, pioneer species, plant strategies, nitrogen fixation + plant symbioses (e.g., refer to legumes), and nitrogen content of animal waste

@theforestecologist — If you post your comment as an answer, I'll give you the checkmark.


text:
Species diversity in cheese and yoghurt?
There have been studies on the number of species on humans and in various other environments. I was wondering how many species including: viruses, bacteria, yeasts, and fungi inhabit ordinary farm yoghurt, supermarket yoghurt, and cheeses like parmesan, edam, and blue.
I can find some studies, but not an actual count of species diversity in living dairy products.

Does the work you found include that by Rachel Dutton (http://www.theduttonlab.com/publications-1/2017/6/14/publications)?  It would be helpful if you could summarize what you have already found.

Nice find, I didn't see that. http://www.asmscience.org/content/book/10.1128/9781555818593.chap12 sais that there are relatively few species in cheeses. And this study suggests that there are 5-7 main bacteria in the ecosystems, although I didnt find a specific reference on the total diversity. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4222527/figure/F3/

Great — I hope you'll post an answer your own question once you feel like you've digested the available literature!

We did some work on mozzarella cheese: https://www.ncbi.nlm.nih.gov/pubmed/30621867.
However, we only studied bacteria. The group of Danilo Ercolini is leading a lot of work in metagenomics of several kinds of cheese (I mostly took inspiration from their work). You can look there for some reference.


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Question about alternative polyadenylation
I know that alternative polyadenylation creates different transcript isoforms. My question is whether alternative polyadenylation ever results in differences in the terminal/last exon? The only case I can think where it might be is if the terminal exon is alternatively spliced?
EDIT:
I think what I was trying to ask was for a given gene, what factors could cause the transcripts to end in different locations. I drew a picture and it helped me figure it out a little
Here are 4 transcripts for a given gene, each of which end at a different location. Exon's C and D end in different locations because D is completely different exon than C that is being spliced to exon B. Exon on C and E start at the same location, but exon E is shorter, due to a UTR-Alternative polyA event. Exon B and F start at the same location, but F is shorter due to a Coding APA change. So alternative polyadenylation drives the formation of transcripts 1,3,4 while alternative splicing drives the formation of transcript 2. So I guess to rephrase my question, are there any other biological process that can affect where a transcript ends

I am finding it difficult to understand your question. Could you draw a diagram to explain what you mean please?

Are you asking if alternative polyadenylation is always associated with alternative splicing of the last exon?

@Vinay Swamy: I hope my suggested edit didn't change what you were trying to ask!

According to a 2011 review1 alterntive polyadenylation sites can be located upstream of the 3'UTR (i.e. within introns or exons).  When these sites are used it results in transcripts missing exons at the 3' end and can force alternative splicing.  This alters the final protein product.
This figure from that paper may help make this clearer.

Figure 1. Schematic Representation of CR-APA and UTR-APA
CR-APA produces mRNA isoforms with distinct C-terminal coding regions,
  resulting in distinct protein isoforms. UTR-APA produces distinct mRNA
  isoforms with different-length 3′ UTRs but encodes the same protein.
  Longer 3′ UTRs usually contain cis-regulatory elements, such as miRNA
  and/or protein binding sites, which often bring about mRNA instability
  or translational repression. CR-APA, coding region-alternative
  polyadenylation; UTR-APA, 3′ UTR-alternative polyadenylation. Light
  green boxes, untranslated regions; light blue boxes, shared coding
  regions; dark blue and yellow boxes, unshared coding regions; lines,
  introns.

Reference:
1: Di Giammartino, D. C., Nishida, K., & Manley, J. L. (2011). Mechanisms and consequences of alternative polyadenylation. Molecular cell, 43(6), 853-866.

Alternate splicing can result in the same protein. Perhaps you can add a note below the figure.

@WYSIWYG — I'm undoubtedly missing something, but I'm not sure how that relates to the OP 's question or to my answer ...

I mean that alternate splicing need not affect just the CDS, it can change the UTRs and can potentially expose cryptic polyadenylation sites, zipcodes etc. See this article, for an example.

@WYSIWYG — Sure, but my understanding is that the question is about whether alternative polyadenylation ever alters the protein produced.  You seem to be discussing how alternative splicing can affect the transcript.

Frankly I didn't understand what OP is asking. They didn't clarify.


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What is the identity of this flower found in Mavericks Beach in Half Moon Bay, California, USA?
Please help identify this flower I saw in Mavericks Beach in Half Moon Bay, California. It was smelling soooo good, you can feel from distance. I want to buy and plant in my garden.
Thank you,

Based on the habitat, color, and size that lupine looks like Coastal bush lupine (Lupinus arboreus).
Please note that Coastal bush lupine can be invasive, so be responsible about where you plant it!
You can also learn more about this plant and its growth requirements from the California Native Plant Society
Images for comparison:


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Does this article call into question the theory of evolution?
https://www.quantamagazine.org/neutral-theory-of-evolution-challenged-by-evidence-for-dna-selection-20181108/
The article above challenges how mutations work in evolution. Does this disprove the theory of evolution?

That article is discussing the fine points of how to interpret mutations and says nothing that seems even remotely related to the validity of evolutionary theory?  If there is something in that article that makes you think it might conflict with evolutionary theory please add it to your question and make sure it is clear that you have taken the time to understand this theory.  Otherwise your question is likely to be perceived as creationist trolling and will probably be removed.  A useful introduction to evolutionary theory: https://evolution.berkeley.edu/evolibrary/article/evo_01

Would you please quote the relevant parts instead of just posting a link? Posts should be self-contained, to make sure they are still valid in a future when the link isn't working anymore.

Questions on this site must be intelligible in their own right. The site is intended as a self-contained Q&A site, and in any case it is impolite to expect users to go to some other site to read something. It may also be dangerous as an external site may be booby-trapped. I need to understand your question by itself. That is why I have voted it off-topic as unclear. If you are able to present the argument yourself in a manner that conforms to allowable questions for SE Biology — for which you should take the Tour (you haven't) and read how to ask a good question — I shall reconsider.

First, please note that the article you link is not a peer reviewed article. It is a popular, easy-to-read article.

Does this article call into question the theory of evolution?

No, it does not. What makes you think it does?
The article talks about a very old (and somewhat still ongoing) debate about the relative importance of genetic drift vs selection in evolution. I suppose that you may have portrayed selection as being the only evolutionary process and I suppose that reading about genetic drift as being another evolutionary process may have make you feel like "we were wrong all along" while in truth we have always known a bout it. Note that even Darwin with his very limited understanding of evolutionary processes (compared to what we know today) knew that there are other evolutionary processes than selection.
You might want to read about genetic drift. As a start you could read the following:

Evo101 > Genetic drift
Biology.SE > Why is the strength of genetic drift inversely proportional to the population size?
Wikipedia > Genetic drift

Don’t feel the trolls.

@David — How do we know the OP is a troll as opposed to someone who is starting to explore the limits of their indoctrination?

You will know from experience that there is a body of people who are generally not biologists but do not believe in the theory of evolution on religious, rather than scientific grounds. Such people — possibly from motives they consider morally justified — seek to take every opportunity to publicize their views and frequently abuse this site. One post-hoc means of identifying them is that they never accept an answer. How many of yours have been accepted? (cont.)

…This is a question and answer site so I think one should attempt to discourage such trolls by rigorously applying the site's criteria for on-topic questions, especially when, as in the current case, one is dealing with a new user (no evidence of a previous interest in biology) who hasn't taken taken the trouble to take the tour even (evidence of no interest in the site). A biological question asks for a biological answer. A question of the type "doesn't this prove the theory of evolution" is an attempt to start a discussion (off-topic), at best, or to use the platform to make a statement…

…In this case the question is not self-contained so — as you should be aware — does not fit into our model. We do not exist to discuss articles published elsewhere, nor do we have a mission to convert the indoctrinated. If you feel you must respond, use the comment box to explain why the question is off topic but provide your links to point out where counter arguments can be found.

@David — Thank you for your detailed and thoughtful response!  I know you're correct about fundie trolls, but I also know of individuals who have managed to escape their programming.  Unless you can prove this individual is only here to troll I see no harm in pointing them at places they could begin educating themselves or in Remi.b giving a brief answer and additional links.  While it looks to me like my original comment was in line with your suggested response, I'm happy to hear how it could be improved!

@tyersome — whether or not the poster is a troll, the pertinent question is whether the question is on-topic. You may not realize that users with sufficient points ('reputation') who wish to vote to close a question are presented with several defined categories, as well as a free-form onet. Remi.b will be familiar with this. The question indsputably falls in the "unclear" category as it is not comprehensible by itself. This is a self-contained Q&A site not a missionary. I have no idea what the argument is. If the poster wishes an answer, he must first ask a question that conforms to the site.


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What species of wasp is this? And how to get rid of them?

Yesterday while moving a chair in my garden I got stung by a group of wasps. During the night I went hunting for their nests and managed to neutralize 3 of them: one was in the chair's legs, about the size of a child's fist and with a dozen on them inside. It was made of grey hexagonal cells, similar to paper in appearance.

(Sorry for the blurry image, I was a bit scared :-P)
Then I've found another one in a water hose tube that was slightly smaller, but quite active.
And finally a third one in a vase, it was very small, only had a couple of cells in it and wasps were working on it, almost as if they were building it from scratch.
Given the number and size of the nests I'm afraid that they could be spreading in the garden. I have already noticed that a couple of them survived the massacre of last night and I'm worried that unless I kill every of them they might keep nesting.
I don't know much about the hierachical society of wasps, but I was not able to identify the queen (although I haven't checked every single one I've killed). Reading online I've found that killing the queen might mean that the worker would eventually die.
So what kind of wasp is this? What can I do to make sure that they do not keep bothering me?
EDIT: by the way, I live in northern Italy

For species identification questions, you should also mention the geographic location of the object in the picture.

Long hind legs, two yellow spots on the otherwise striped bum... I would just ignore these, for two reasons: First, depending on where you live it may cost you a lot of money if you are caught killing them, and second, this particular type is quite harmless and non-aggressive, and most importantly, they feed on mosquitos. My enemy's enemy is my friend, so...

@Damon I wouldn't say harmless and non-aggressive. Just by moving that chair around I got stung and it was quite painful

Where is your chair and garden located?

These are European paper wasps.
(They look very similar to yellowjacket wasps but you can notice the antennae; they are brown here whereas they are black in case of yellowjackets. There are other subtle differences too.)
See this post on Gardening & Landscaping stackexchange about getting rid of wasps.
(This part is probably not really on-topic here and I don't want to copy-paste an existing answer in another stackexchange site.)

If you are upvoting this post then please also upvote the original one in G&L SE

Do European paper wasps count as "dangerous" for the purpose of the accepted answer on the question you linked to?

@T.E.D. I haven't faced them myself. In general wasps are more aggressive than bees. This one is less aggressive than yellowjackets.

Stay vigilant. As you've noticed, once wasps get established in an area, they'll reproduce and spread out. Continue to watch for and eradicate nests. Hardware stores will sell a variety of chemical sprays, but a mix of liquid soap (dish detergent) and water works just as well.
Use wasp traps to prevent wasps from establishing new nests in your area. You can buy them from most stores or make them yourself using directions similar to those provided here: https://www.bobvila.com/articles/homemade-wasp-trap/.

To keep these pests away from your house and other areas, on the underside facing up use a sky blue paint, along soffits, including the bottom of some patio furniture. When these see the sky blue they think its the sky and will go some place else to build a nest. It's a common practice down in the South such as NOLA or other Southern places.


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Why do leeches lose septae due to parasitism?
So I found this piece of information in my textbook without a proper explanation, and I can't seem to find the relation between the two.

Welcome to Bio.SE! What attempts to answer this question have you already taken? We ask that all question posters here attempt to search for an answer to their own question and explicitly indicate what research they've already done, what they learned, and what is still confusing or unknown to them. Our goal is not to simply be an answer site, but rather a site that promotes self-learning with some expert help along the way :). Please take a moment to edit your post with this additional detail, and it will likely be received more positively by our community. Thanks!

Please start by editing your post to include the source of your information (in other words, cite your textbook), and please provide a direct quote referencing your piece of information. After dong that, please indicate what other research you've attempted on your own and what you've found out. Thanks.


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Why does the colossal squid range over only the Southern Ocean?
Wikipedia's article on the colossal squid gives the distribution as in the Southern Ocean only.
It makes sense for many animals found in the Antarctic to not also be found in the Artic even if the environments are similar, simply because there's no way for the species to get from the Antarctic to the Artic. However if colossal squids can range more than a kilometer under sea level, then by that depth, the ocean should look the same in every direction: it would be so dark and cold that there's no easy way to tell if one is on the equator or under the North Pole. In other words the squid should be found in every ocean, not just the Southern Ocean.
What is wrong with this reasoning?

Possible reason might be ocean currents. They impact migration and availability of food. Also, (mainly indirect) observation seems to be rare. Can we really say they don't occur elsewhere (maybe in smaller numbers, which makes observation less likely)?


text:
Correlation brain size and muscle volume
I have 3 dogs that weigh ≈ 5 kg, ≈ 20 kg and ≈ 45 kg. The smallest dogs whole head would fit in the mouth of the biggest dog. Although I haven't measured it exactly but by just looking at the dogs I would expect the weight of their brain to approximately correspond to their body weight, that is the 20 kg dog's brain is 4 times heavier than the smallest dog and the 45 kg dog's brain is 10 times heavier.
Meanwhile, all three dogs seem to have similar intelligence.
What is all the extra weight of the brain of the bigger dogs used for?
You can expand this question and note that an average mouse brain weigh 0,5 g while an elephant weighs around 5 kg. Elephants might be smarter than a mouse but not 10 000 smarter. Besides, the brain of a human is much lighter than an elephant and we obviously are much smarter.
Why do bigger animals need bigger brains than smaller animals to accomplish approximately the same intelligence? Is it something along the lines that they have more muscle fibres and every single musle fibre needs a few neurons to control it?

No real expertise in neurobiology, but I know that there are factors to consider other than just mass.  For example, the proportion of the brain that is cerebral cortex varies considerably.  Also, the density of synapses (connections between neurons) is also not constant.  You may find this article helpful: https://mosaicscience.com/extra/does-brain-size-matter/

You may be interested in this question: https://biology.stackexchange.com/questions/61476 and the links therein.

Possible duplicate of Do smaller intelligent animals have a higher neuron density to account for their seeming intelligence? Otherwise, what?

Sorry to get philosophical, but if we do not understand consciousness, then how can we define 'intelligence' and 'smartness' in objective, measurable ways? Furthermore, we can assume abstract ideas like intelligence are physically real, albeit this does not mean we are necessarily correct.

I like the muscle_fiber/more_neuronal_mass theory. It makes a lot of sense having a better networked neural structure if you have more efferent processes to look at (in the form of more muscle fiber to actually move). After a quick search, it doesn't seem like this is a very thoroughly researched field. This review from 2014 states that:

there seems to be a positive relationship between whole brain volume and white matter volume and muscle size
grey matter (GM) volume had no direct relationship with muscle size, yet some areas of the GM were linked to muscle size (more specifically the right temporal pole and the bilateral ventromedial prefrontal cortex)
no relationship exists associating grip strength and whole brain volume
gait speed is positively linked to whole brain volume

The relationships between regional areas of the brain and their functions seem to be something dynamically non-linear enough to prove quite complex to classify properly.
The "extra weight", represented by a larger cerebral cortex, is where the neural integration happens and a study (and possibly others) confirms that cortical thickness is correlated with general intelligence in both hemispheres (samples = [children, adolescents, young_adults]).

References:
Kilgour AH, Todd OM, Starr JM. A systematic review of the evidence that brain structure is related to muscle structure and their relationship to brain and muscle function in humans over the lifecourse. BMC Geriatr. 2014 Jul 10;14:85. doi: 10.1186/1471-2318-14-85. PMID: 25011478; PMCID: PMC4105796.
Menary K, Collins PF, Porter JN, Muetzel R, Olson EA, Kumar V, Steinbach M, Lim KO, Luciana M. Associations between cortical thickness and general intelligence in children, adolescents and young adults. Intelligence. 2013 Sep;41(5):597-606. doi: 10.1016/j.intell.2013.07.010. PMID: 24744452; PMCID: PMC3985090.

A fast rummage through the web tells me (alot) that:
The most intelligent dog is a medium dog breed, the border collie.
Big dogs are generally more intelligent than small dogs, only 1/20 of the most intelligent dog breeds are small dogs.
bigger dogs have better short-term memory, able to focus better and have better self control, coordination end executive functioning.
They also have:
More surface area with nerves and skin cells
more muscle fibers.
Primate studies suggest that bigger brains have better executive functioning and not other types of intelligence.

I don't think the causality goes in that direction. Working dogs are smarter than other dogs, especially working dogs that need to interact with humans. Medium size is a good size for working dogs that should be handled by humans, while their size still makes them efficient in their function.

poodles are rated in the top 20 most intelligent breeds, and bulldogs are towards the less intel, I don't know about wolves and foxes, that's tricky to test for.

What is your point?

papillons and poodles are not related to working dogs and are higher on the intelligence tests than most workdogs. it's an just an oddity. https://en.wikipedia.org/wiki/The_Intelligence_of_Dogs

Poodles are working dogs. Papillons aren't exactly working dogs but have been bread to learn tricks that amuses humans so that is basically a working dog, although their works is play.


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How to interpret different results from Clustal Omega and Multalin?
I have been working on aptamers, which are nucleotide sequences. They bind to various targets, in my case a particular cell surface receptor. The people associated with the project performed SELEX and they have selected sequences that have affinity for the target. My advisor believes that the sequences could share a particular binding pocket (consensus sequence).
The sequences are mostly 40 nucleotides long but some of them are shorter or longer in length. I have to aligned the sequences in an attempt to identify sequences containing a consensus site. So far I have used both Clustal Omega and Multalin, but the results from them are pretty inconsistent.
Clustal Omega Alignment:

I also aligned a few sequences using a pairwise alignment method, but I found few similar regions among the sequences.
How do I interpret these results from Clustal Omega and Multalin?

Welcome to SE Biology. Please take the Tour (we can see you haven’t) and read about asking questions here. You have explained your problem well, but seem to want us to solve it for you. However we need to know what you make of it yourself. Do you know why alignments by different programs are different? You need to read about MSA and the particular algorithms behind the ones you have used. Which one do you think has aligned the sequences better? No reading there — use your eyes. And has the better alignment found a consensus site? Again, use your own judgment and that of your advisor.

I made some edits that I hope clarify your question, but it seems to me that you might want to ask a different question — "What alignment method would work best for finding a consensus from these sequences?"

You might want to look at partial order alignment.

@tyersome Should I delete the question and ask again?

I don't think that's necessary — you can just edit your post.  However, I encourage you to follow up on @WYSIWYGs suggestion — they show signs of having significant expertise in bioinformatics!


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Larva of Halyomorpha halys?
I just found these small insects on a Saponaria.
After search, it could be Halyomorpha halys, but I am really not sure.

Can anyone confirm? If so, should I kill them as they are considered as agricultural pest?
They are about 3-5mm. I am living in the south of Paris (48.814766, 2.334659)

This is an instar (nymph) of a shield or stink  bug (order Hemiptera, family [Pentatomidae])(https://en.wikipedia.org/wiki/Pentatomidae).
This appears to be similar to the 2nd (or possibly 3rd) instar of Halyomorpha halys.

European and Mediterranean Plant Protection Organization; Credit: Matteo Maspero
UTIA suggests the 2nd instar begins to develop an almost black appearance, where that blackness gradually shifts to browner shades in subsequent instars. According to Medal et al. (2013)1 the 2nd and 3rd instars have median lengths of ~2.75 and ~4.25 mm, respectively. According to WSU Extension, instar nymphs of H. halys are spiny (including on the shoulders) and possess light bands on the antennae.

 Source: WSU Extension
This University of Wisconsin Extension site provides a fairly similar photo to your specimens, which can be found at bugguide.com:

 Source: bugguide.com; Credit: Yurika Alexander

 Citations
1  Medal, J., Smith, T. and Santa Cruz, A., 2013. Biology of the brown marmorated stink bug Halyomorpha halys (Heteroptera: Pentatomidae) in the laboratory. Florida Entomologist, 96(3): 1209-1213. PDF


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When something "smells moldy" what are we really smelling?
When things smell moldy --  it could be clean clothes left in a heap, a damp basement, old books stored in elevated humidity -- they can smell moldy.
There are distinct smells for each of these.
Are we smelling the mold spores themselves, or are there other molecules released by molds that causes the "moldy smell" we perceive?

The vast majority of the things you smell are odorants, or volatile molecules; not spores. They are light compounds that have high vapor pressure (are airborne), and that interact with your chemoreceptors in your nose (can be smelled). The most-often reported microbial volatile organic compounds in living environments according to this study are as follows:

2-Methyl-1-propanol
3-Methyl-1-butanol
3-Methyl-2-butanol
2-Pentanol
3-Octanol
1-Octen-3-ol
2-Octen-1-ol
3-Methylfuran
2-Hexanone
2-Heptanone
3-Octanone
2-Methylisoborneol
2-Isopropyl-3-methoxy-pyrazine
Geosmin
Dimethyl disulphide

Geosmin is probably the most moldy-smelling and is detected very sensitively by olfactory systems of animals that want to avoid contaminated food. To me it smells muddy, or earthy, like soil after a rain shower. In our lab, about half the people find it a pleasant smell. It can be smelled in wine, it's the earthy taste found in vegetables, it's the smell of dead bacteria, and so on and so on. The term petrichor describes the odor and geosmin is a major contributing odorant for this.

Of course, this is just a shortlist of the major odorants. There exist hundreds if not thousands of other volatiles that are released by microbial life. And very often, the mixtures/proportions of odorants can be useful for the perception of smell; it need not be a single compound that makes things seem moldy.

Okay this is really interesting, I'll get a hold of the paper soon and give it a read. I've  about VOCs in the past in the context of air pollution and air quality, but this is the first time I've heard of MVOCs!

I believe geosmin is from bacteria, not mold, and at least the sources you cite are consistent with that. Therefore, geosmin doesn't really seem to answer the question, unless you can support a suggestion that "moldy smell" is unrelated to mold. Also the hypotheses I have heard about geosmin sensitivity are related to the importance of fresh water in a fairly arid environment, not detection of food contamination, hence the pleasant perception.

Geosmin is abundantly released by moldy fungi. It's microbial, not strictly bacterial in origin. I defer to any and every textbook on the topic, or a quick google search. I also work with it in the context of insect ecology :)

not sure if this is relevant but I just ran across it today by accident mVOC 2.0: a database of microbial volatiles.


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Why are there few quail any more in the Northeast of the US?
I currently live in southeast New Hampshire and was reading a history of my town and it describes the landscape as having a lot of quail and even partridges. The book said children going to school around 1920 would see lots of quail. The town itself has not changed much from 1920 except that there are fewer farms. The population is about the same. In fact, the population is probably lower now than it was in 1920.
I have never seen a single quail here, and certainly never seen a partridge. I have seen a pheasant on rare occasion. There are a lot of turkeys.
Is this like a Silent Spring thing, they all got killed off by DDT or something? Or is it because of insecticides killing all the crickets, maybe? I almost never hear crickets at night.

I don't recall ever seeing quail growing up in the rural northeast, yet partridges and pheasnts were fairly common.  Yet quail are very common where I live (just east of the Sierra Nevada).  I can see a dozen or so running around my yard most evenings.

Work in the early 1990s (https://pubs.er.usgs.gov/publication/5210546) (https://www.nwf.org/en/Magazines/National-Wildlife/1993/The-Case-of-the-Disappearing-Quail) suggests development (curtailing habitat), climate crisis (and associated water loss), and decline in insect populations (reducing food supply) as possible causal factors.
Insects are an important energy source for birds, generally. They help pollinate plants, which help feed birds, and they are also a food source, themselves. Their loss (https://en.m.wikipedia.org/wiki/Decline_in_insect_populations) particularly hits bird populations hard. Unless we change our agricultural practices, it is predicted that most insects may be extinct within a century. This would decimate many forms of life (ourselves, included with quail and other birds) that depend on them.

But that would not explain why they have apparently declined in the northeast, but are plentiful here in the west.  Might it be a change in land use?  Quail tend to inhabit open grasslands (and sagebrush scrub, hereabouts).  If the small fields & pastures of agricultural New England in the 1920s largely reverted to forest, there would not be as much quail habitat.


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How do bullfrogs eat?
I have a very small pond in my backyard and a bullfrog lives in it. I see him all the time, but I never see him eat anything. He either sits in the water with his head just above the water or he sits on a rock next to the pond.
He must be eating something, because he is getting bigger, but I never see him eating. Does he just eat late at night or early in the morning or something? How come I never see him eating?

Just because you did not happen to see it eating doesn't mean it is not eating. This is not even a controlled experiment. How much time have you spent in observing it?? You have been a member of this site long enough to know that questions like these are absurd. Moreover, it lacks adequate background (for instance, the species of frog).

I have discovered by further research that bullfrogs hunt primarily at night.
So, at night he is probably venturing into the lawn around the pond where there are various insects and smaller frogs, such as wood frogs, available to eat.


text:
Composition and quality of mushroom spores
Message to moderator(s):
This question was deleted since it looks similar to a question in another SE.
However, the question being asked in this SE is completely different. Would that be a strong enough basis to restore this post?

From this source, it states that:

Living spores have been found and collected in every level of earth’s atmosphere. Mushroom spores are electron-dense and can survive in the vacuum of space. Additionally, their outer layer is actually metallic and of a purple hue, which naturally allows the spore to deflect ultraviolet light. And as if all this wasn’t unique enough, the outer shell of the spore is the hardest organic compound to exist in nature.

With regards to a mushroom spore's electron density, having an outer metallic / purple layer, and the hardness of its outer shell, have these things been confirmed in biological experiments?

Were there any references associated with these claims?  Where have you looked to see whether there is any credible support for these statements?

@tyersome No, there were no references in that article, I also heard similar claims in a podcast that predates that article. I have looked into general websites regarding mushroom spores (don't have access to peer-reviewed biology publications), and they don't seem to have any information with regards to the composition and quality of mushroom spores.

Please don't cross post to multiple SE sites.

This post is not substantially different from the other one. See https://meta.stackexchange.com/questions/64068/is-cross-posting-a-question-on-multiple-stack-exchange-sites-permitted-if-the-qu - answers to both of these questions are going to touch on the same sorts of source, if the source even exists. Generally "is there support for this claim I found on the internet" questions are not acceptable here, either, without some additional research on your part.


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Is UV radiation more likely to cause mutations during mitosis?
According to Life: The Science of Biology (10th edition), UV radiation might cause the formation of pyrimidine dimers, which are the primary cause of skin cancer in humans.
Are mutations more likely in case a cell is exposed to UV during mitosis?
My TA (who is a stem cell researcher) implied that the answer is yes, as she explicitly said that the risk of getting cancer from gel manicure is non-trivial, due to the following reasoning:

During the treatment, small cuts are made (not on purpose) to the skin around the nails.
The exposure to UV occurs just after that, while the tissue is healing.
This significantly increases the risk of cancer.

However, I didn't find information about that by googling. On the contrary, I encountered studies about using UV to enhance healing of wounds, e.g., Is UV radiation beneficial in postburn wound healing?.

In addition, Wikipedia's scar page says (though I didn't find a reference for that claim in the Wikipedia page):

scars in the skin are less resistant to ultraviolet radiation

Also, people are instructed to avoid exposure to UV after laser hair removal.
Is these two related to mitosis? Or are they instead related to some property of scar tissue?

references:
Rennekampff, H-O., et al. "Is UV radiation beneficial in postburn wound healing?." Medical hypotheses 75.5 (2010): 436-438.

This question does not make sense. Human fingernails are inert, acellular, structures made primarily of keratin.  There are no living cells in them and therefore cutting or trimming the nails is not a wound.  Without a wound the term healing does not have a clear sense.  Fingernails “grow” at a constant rate, regardless of trimming.  Wound healing does require mitosis, manicures do not.  Ask your TA about the incidence of fingernail cancer.

@mdperry Thank you. I wasn't aware of keratinization. Quite fascinating. I might have misinterpreted her explanation (though she definitely said that the risk of getting cancer from gel manicure is non-trivial). Anyway, I sent her an email.

@mdperry She answered that during the treatment small cuts are made (not on purpose) to the skin around the nails. I edited my question accordingly.


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What does the MAF/MinorAlleleCount mean?
I'm not sure why reporting the second most frequent allele is helpful?
what is the Major allele?

Are you using a software that reports this? Where did you encounter this term? Please provide some context and explanation.

[W]hat is the Major allele [frequency]?

If the Minor Allele Frequency is $p$, then, for a bi-allelic locus, the major allele frequency is obviously $1-p$.

[W]hy reporting the second most frequent allele is helpful?

Most polymorphic loci of interest are bi-allelic. Hence, the MAF is an indication of genetic diversity. One could similarly report the expected heterozygosity instead ($2p(1-p)$).
It is common to consider only loci with a MAF greater than a certain value. There may be different reasons for that. Here are possible two reasons.
Sequencing errors
When sequencing your sample, errors are being made. Sure, error rate is pretty good (see this table from Molecular Ecology) but error still do exist. A polymorphic locus with a minor allele count of less than, says, 3 alleles might well just be caused by sequencing errors.
To avoid considering as polymorphic loci that are in reality not polymorphic, we often just disregard any data with MAF is below a given threshold.
$F_{ST}$
$F_{ST}$ is a measure of genetic differentiation among population. When computed on loci with low MAF, the statistic is biased (Beaumont and Nichols, 1996). Hence, it is usual to only consider loci with a MAF greater than an arbitrary threshold before computing $F_{ST}$


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Are your finger muscles and tendons interconnected?
Are finger muscles and tendons interconnected? If they are interconnected, then if i exercise one finger will it train the other fingers since they are interconnected and share the same muscles in the forearm? (correct me if im wrong)
I have done some research but i cant find the answer for example(if your thumb joint is injured you should avoid using stress balls to exercise the other fingers, why?)

Welcome to SE Biology.  It is expected that you will demonstrate that you have done some research on your own before asking questions here.  For details, please check out the tour: https://biology.stackexchange.com/tour and then this help page on how to ask questions on this site: https://biology.stackexchange.com/help/how-to-ask.  ------ For example, have you tried searching for "hand anatomy muscles and tendons"?

That's a really interesting question!  What might help you the most is reviewing hand and forearm muscle anatomy.  I have some examples that could help.  The flexor digitorum profundus and flexor digitorum superficialis are hand muscles that originate in the forearm region.  At the wrist they split into four tendons (so FDP has 4, FDP has 4) one for each non-thumb finger.  They help make a fist.  Then there are the intrinsic hand muscles.  One interesting example is the lumbricals, which originate at the FDP tendon and have a very specific action.
To answer your question, I don't see any reason why exercising the four non-thumb fingers is recommended against, other than the possibility that you could be inadvertently moving/stressing the thumb.  I don't believe there is any connection between muscles of the thumb and non-thumb fingers, other than proximity of muscle/tendons.


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What is this spiky fruit/cone?
I am trying to identify an unusual cone or fruit found today on Tayside in Scotland. Here is an image. Can you help?

Welcome to SE Biology!  Please insert images rather than making them links — this is for both the security and convenience of other users.  For details on how to use this site, please check out the tour: biology.stackexchange.com/tour and then the help pages on how to ask questions on this site: biology.stackexchange.com/help/how-to-ask.  Thanks!

Sorry it won’t let me upload photos. Will try another website. Thanks anyway

What happened when you tried clicking on the image icon?  Assuming you have copies of the images you should be able to use the "Browse" option to upload copies of your images ...

You have to reduce the file size (by reducing quality). You can use any photo editor to do that. I'll do that for now. Please take care in future.


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What is this soft cased worm-like creature?
Found this creature in the bathroom
Features which ought to help for identification:

Size = 1 cm
Soft casing
Can emerge from either end of its case and thus reverse the direction it crawls.
Many tiny legs.
Can walk pretty fast.

Found in the middle east

Welcome to Biology.SE!  Interesting creature, can you add more information about the local environment and specify where in the middle east you found this?  Also, what do you mean by "soft shell" — do you mean that the (sandy?) casing is flexible?

Looks like a plaster bagworm (https://en.wikipedia.org/wiki/Phereoeca_uterella)


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What's the difference between veterinary and human snake antivenom?
Recently, out of curiosity, I looked online if snake antivenom for humans were actually sold for individuals. I found out they aren't. Not only that, but bills can get really high on countries that don't provide them in public healthcare (i.e.: USA), as in 4 digit numbers. Makes one disappointed to realize the price of production of human-use antivenom is actually really small in comparison to what they are charged for[1]:

On the other side, veterinary antivenom is sold for treating animals attacked by some venomous snake. The brand I found for sale[2] is a polyvalent antivenom: A solution of specific equine immunoglobulins, purified by enzymatic digestion and lyophilizated (freeze-dried), obtained from hyperimmunized Equidae with Crotalus ("Cascavel" aka Rattlesnake), Bothrops ("Jararaca") and Lachesis ("Surucucu" aka Bushmasters) snake venom. I included the common-names in Portuguese since these are the 3 common vipers found in Brazil, where this particular antivenom is sold. Coral snakes (Elapidae) are also found here, but I didn't find any veterinary antivenom for those (and this one I found isn't recommended for bites from them).

Some veterinary-use antivenom shows more side-effects on animals than others, specially unpurified Equine Plasma antivenom, which can cause allergic skin reactions near the application site and peripheral lymphadenopathy 48h after application[3]. The same source comments on other types of veterinary antivenom, but I'm not sure which the one I found classify on (if any, because of the targeting snakes being slightly different). The description of F(ab’)2 antivenom resembles the one provided by the brand I found: Both are purified, enzymatically cleaved/digested, lyophilized and obtained from horses.
Technically, what is the difference between the antivenom for human usage and veterinary antivenom? In an hypothetical situation that one gets bitten far from medical help, how big would be the risk of applying a veterinary antivenom? Obviously injecting drugs that are not FDA approved is not recommended, and considering the number of snake-bite related deaths is relatively low in some continents[4] it would be unwise to even give people the idea of using unapproved drugs to treat bites. I was just wondering if, after assessing a situation and realizing medical help won't come (or come in time), having one of those in hand could save a person's life after a viper bite.

UPDATES:
There's a scientific article published in the British Journal of Clinical Pharmacology, entitled "Adverse reactions to snake antivenom, and their prevention and treatment"[5], that brings light to the adverse reactions to snake antivenom. Severe systemic anaphylaxis rates can be as high as 40%, specially in places where the antivenom manufacture quality is dubious. Antihistamines and hydrocortisone didn't prove effective in controlling the antivenom acute reactions, and only adrenaline seemed like a decent prophylatic treatment to anaphylaxis. The management of antivenom acute reactions is as big of an issue as the treatment of the envenoming itself. And I'm still talking about antivenom approved for human-usage.
Speculation: Polyvalent antivenom could be more problematic than specific antivenom, because more unnecessary foreign proteins must be injected to treat the same amount of venom. Not only that, but probably the companies that manufacture veterinary antivenom are not as worried about their quality (and purification process) as ones that are more tightly regulated to produce human antivenom. For that reason, acute anaphylaxis would be more likely while using those.
Whether the risk of anaphylatic reaction is compensated by the risk of untreated envenoming is still not clear (one might say it's a question that won't have a definitive answer, or even opinion-based). I'll keep adding any new information that brings more light to the issue, but answers from people more knowledgeable in the area are very welcome!
References:
[1]: https://www.washingtonpost.com/news/wonk/wp/2015/09/09/the-crazy-reason-it-costs-14000-to-treat-a-snakebite-with-14-medicine/?noredirect=on&utm_term=.b4855c4e100c
[2]: https://www.dechra.com.br/produto-detalhe/102/master-soro-plus
[3]: https://vetgirlontherun.com/veterinary-continuing-education-update-antivenom-treatments-animals-raegan-wells-vetgirl-blog/
[4]: https://animals.mom.me/snake-bite-death-statistics-worldwide-2431.html
[5]: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4767202/pdf/BCP-81-446.pdf

You inject a horse with the venom and in return you get in its blood anti-venom antibodies. Those antibodies will be poorly tolerated in humans and shall produce an allergic reaction, even more if the individual already received horse antibodies in the past (that's how anti-(goat-IgG) antibodies are made). They will be also less efficient due to differences in the constant region of the horse antibodies, not binding well to the human Fc receptor.
One solution is to cleave the horse IgG with pepsin or papain protease to separate the F(ab’)2 or Fab fragments. But still it won't bind to Fc receptors and the renal clearance will be also faster. The good point is that such antivenom can be administered more safely to any species.
For human use the best solution is to use sequencing, plasmids, in-vitro culture, to make recombinant antibodies merging the human constant region with the variable region of horse anti-venom IgG but that's a more expensive biotechnology. And the obtained recombinant IgG will pose the same allergy problem as the whole horse IgG in other species.
It is shamely common for drugs that the manufacturers don't give enough information to tell what is what. It may very well happen that the FDA approved expensive vials are old whole IgG and that a much cheaper internet veterinary antivenom is using the recent technologies.
https://vetgirlontherun.com/veterinary-continuing-education-update-antivenom-treatments-animals-raegan-wells-vetgirl-blog/
https://www.mdpi.com/2072-6651/14/9/606/pdf


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What is a deep exhalation/inhalation?
I tried to find the academic definition of deep exhalation/inhalation but found nothing special.
I speculate that the correct definition is as follows:

• Deep Exhalation: Exhaling the air with effort as much as possible,
  after a normal "inhalation".
• Deep Inhalation: Inhaling the air with effort as much as possible,
  after a normal "exhalation".

The corresponding volumes of the air which is being moved inside respiratory tracts would be:
Vdeep exhalation = Tidal Volume + Expiratory reserve volume (ERV)
Vdeep inhalation = Tidal Volume + Inspiratory reserve volume (IRV)

But, in case we define them as below, the previous conclusion regarding the volumes turns wrong and consequently should be revised.

• Deep Exhalation: Exhaling the air with effort as much as possible,
  after a normal "exhalation".
• Deep Inhalation: Inhaling the air with effort as much as possible,
  after a normal "inhalation".

Vdeep exhalation = Expiratory reserve volume (ERV)
Vdeep inhalation = Inspiratory reserve volume (IRV)

I think it's impossible to assess without any subtle definition. I'm really confused.
Any help would be highly appreciated.

You should investigate the concept of a collapsed lung. I think that may allow you to answer your question.

@TheNate Thank you. I'll give it a try. In the meantime, possible to let me know if there's a more active biology forum to ask questions? It seems Stackexchange is not too crowded by biologists as much as by developers!

Deep inhalation and deep exhalation are informal terms and cannot be defined by lung volumes, because saying deep by itself does not tell how deep.
In the first part of the question deep refers to maximal:

Deep inhalation that means inhaling the air with effort as much as possible = maximal inhalation
Deep exhalation that means exhaling the air with effort as much as possible = maximal exhalation

According to Physiology, Residual Volume (StatPerls):
The volume of air in the lungs after maximal expiration is called residual volume (RV).

Residual volume (RV) is the volume of air that remains in the lungs
  after maximum forceful expiration. In other words, it is the volume of
  air that cannot be expelled from the lungs. This volume remains
  unchanged regardless of the lung volume at which expiration was
  started.

The volume of air in the lungs after maximal inspiration is called total lung capacity (TLC).

TLC is the total volume of the lungs at maximal inspiration.

According to Merriam-Webster dictionary:
Expiratory reserve volume = the additional amount of air that can be expired from the lungs by determined effort after normal expiration.
Inspiratory reserve volume = the maximal amount of additional air that can be drawn into the lungs by determined effort after normal inspiration.
Lung volumes:

Image source: Wikipedia, Creative Commons License


text:
Holder for 75 mm x 25 mm glass slides that can handle vibration
Hello Biology Stack Exchange,
I have an application where I have cells on a glass slide (dimensions: standard 75 mm length x 25 mm width  x 1 mm thick).  I want to vibrate/shake the cells rapidly while viewing through a microscope.
I have a piece of equipment that can produce vibrations, I just need to connect it to the glass slide somehow.
Are there any holders for glass slides out there that:

Firmly hold the glass slide
Enable me to somehow connect vibration equipment with the slide?  (Ex: screw into the holder, glue onto the holder, clamp onto the holder)
And still view the slides contents under a microscope?

Thank you in advance!

Welcome to Biology.SE!  I'm skeptical that you will be able to image actively vibrating cells, but that clearly depends on what sort of frequencies you are interested in (and your cameras frame rate/shutter speed).  Can you add more of that sort of detail to your question and maybe why you want to do this?  Also, have you considered using ultrasound to produce the vibrations?

@tyersome thank you for pointing out ultrasound!  Not bad thinking.  Per imaging active cells, I have previously adhered vibration motors directly onto glass slides, and I was still able to make out what was happening on the slide, even though it was very chaotic.


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Protein structure prediction using PSSM? Or not?
I have been studying protein structure prediction algorithms. A lot of recent work uses something called the PSSM, the position-specific scoring matrix.
I think that what a PSSM does is to build a 2-D matrix of all possible residue pairs in a protein, then scores how likely it is that the two residues mutate in tandem. Co-evolution of two positions which are far from each other in the primary sequence are an indication that they are in contact. When one residue in a contact pair changes, that generally destabilizes the protein, and the other residue in the pair is under selective pressure to compensate. Knowing this gives you a good start on building the protein contact map.
Do I have that right?
If that is correct, then this technique of protein structure prediction depends on having many examples of proteins in a homologous family. You need nature to do a lot of sampling for you. And you need to dredge up massive numbers of homologs from genomics projects. I've read that creating the multiple sequence alignments for PSSM work is computationally intensive. If I understand the process correctly, I can see why.
My main question is: what can protein structure prediction models built using PSSM do, when there isn't a PSSM?
For example, the Top7 protein is a fully-novel protein fold that does not have any homologs in nature. It was created in 2003 using RosettaDesign software. Rosetta's protein structure prediction algorithms predate PSSM as far as I know. Sixteen years later, there are exactly six variants of Top7, all of which have been made in the laboratory. That hardly sounds like enough data for a statistically-valid PSSM, and in any case, the variants were not naturally selected.
If you don't have a PSSM, is it even possible to enter your sequence into a model that expects one?
Thanks for your input.

I think you are making PSSMs out to be much more sophisticated than they really are.
A PSSM is merely a scoring matrix — it gives position specific scores for each residue at a given location.
There is no explicit pairing of interacting residues though that does sound like an interesting approach ...
You can learn more about PSSMs from many sources on bioinformatics including NCBI.

Thanks for your quick reply, tyersome.  If the PSSM is an N x 20 matrix, you're right, it can't really do what I thought it does.  So is the PSSM distinct from the "co-evolutionary methods" that I'm reading about in this recent post on Google's AlphaFold? (https://moalquraishi.wordpress.com/2018/12/09/alphafold-casp13-what-just-happened/)  I don't have enough characters to post a relevant quote from the article in this comment, so I'll continue in another one.

Quote from (https://moalquraishi.wordpress.com/2018/12/09/alphafold-casp13-what-just-happened/): "CASP11 began to show life because of the introduction of co-evolutionary methods, but just barely because most FM targets had shallow multiple sequence alignments (MSAs), which are required for co-evolutionary methods. CASP12 was when the power of these methods finally got demonstrated, and CASP13, even when excluding AlphaFold, showed further progress due to the widespread adoption of deep learning in co-evolutionary methods."


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Meaning of units in ELISA based tests?
For some ELISA based antibody tests (e.g. h-tTg antibody test), labs report units as RU/mL or U/mL. Also different labs have different cut off (normal range) values.
I understand that different kit manufacturers recommend different ranges because the units are not standardized (e.g. IU/mL) for enzyme activity concerned. But I didn't understand the difference between RU, U and AU
Question
Is there a difference between RU/mL, AU/mL and U/mL? Are the figures comparable across reports from different labs (which may be using different kits)?

No actually. U is definitely not IU. I am referring to ELISA tests where there is no international standards yet. For example, IgA tTg antibody test. I know AU is Arbitrary Units. RU is either Relative or Reference Unit. U is simply unit. Doubts is what's the difference between these.

Thanks for informative comment. I am not from biology background so your comment helped. Now what I meant by standardization is that what conjugate to use and incubation times are not standardized for some tests. Because of this, extinction coefficients are not known. So the lab depends on calibrators given in the kit. Calibrators have specified units and using that curve is fitted. Based on fitted curve sample's concentration is derived. Now, from what i read, manufacturers give their own units. But some give RU some U some AU. For tests where standard reaction conditions are defined IU.

The ELISA kits are calibrated to meet the requirements of
  internationally certified laboratories such as Center for Biologics
  Evaluation and Research (CBER) associated with FDA. In most cases, the
  presence and specific concentration of an antigen is the target for
  the measurements. Such measurements take place through the absorbance
  measurement. According to the Beer-Lambert law, concentration of a
  compound in a solution is proportional to the quantity of light
  absorbed at its specific wavelength and at a constant optical
  path-length. Following absorbance measurement, a simple calculation
  leads to the concentration of the analyte via equation below:
A = εlc
where A is absorbance of the solution at the particular wavelength, ε
  is the molar absorptivity, l is the path length or deepness of the
  solution (which for common spectrophotometers is 1 cm or less if a
  well plate reader is employed), and c is the concentration of the
  substrate in the reaction solution (M or mol/dm3). Majority
  of ELISA microplate readers correspond to this method for the
  calculation of the analyte concentration. Introducing standard
  solutions with known analyte concentrations can be the basis of such
  calculations for the instrument. Measurement unit are typically
  expressed in gram per liter (g/l), mol per liter (mol/l) and copies
  per milliliter (copies/ml) for nucleotides, plaque forming units per
  milliliter (pfu/ml) for infectious viruses, colony forming units per
  milliliter (cfu/ml) for cells and phages, as well as unit per
  milliliter (u/ml) for specific enzymes. These measurement units can be
  also reported over time (i.e. ng/ml/h). Relative units (RU/ml) or
  equivalent units (Eq/ml) are normally used if no international
  standard references exist for the conversion.

Source: Enzyme-linked Immunosorbent Assay (ELISA): From A to Z (SpringerBriefs in Applied Sciences and Technology) by Samira Hosseini, Patricia Vázquez-Villegas, et al. | Dec 31, 2017; ISBN-13: 978-9811067655; ISBN-10: 9811067651. Page 65.
Contrary, Units Per Millilitre (U/mL) are normally used when there are international standard references, agreed upon by scientists and doctors.
Please find the following information on Arbitrary Units (AU):

The WHO Expert Committee on Biological Standardization (ECBS) is the
  scientific body that establishes WHO biological reference standards
  which serve to define an internationally agreed unit to allow
  comparison of biological measurements worldwide. WHO International
  Standards (IS) for biological substances are recognized as the highest
  order of reference materials for biological substances and they are
  assigned potencies in International Units (IU). International
  Standards are used to quantify the amount of biological activity
  present in a sample in terms of the IU, allowing comparisons between
  assays from different laboratories.  Calibration of assays using
  System of Units (SI)units is not appropriate given the variability of
  the specific activity of a biological material. Use of an arbitrary
  unit makes it possible to better define parameters such as the
  analytical sensitivity of tests or clinical parameters such as
  protective levels of antibody.

Usually, arbitrary units are defined within a particular study. For example:

A human serum pool positive for anti-dsDNA IgG antibodies (DNAPo) was
  prepared by mixing equal parts of serum from 10 patients with SLE who
  had a positive CLIFT test ≥ 1:640. The DNAPo was arbitrarily designed
  as having 100 arbitrary antibody units (AU) per ml. Artificial serum
  standards containing different AU/ml were prepared by diluting the
  DNAPo with phosphate-buffered saline (PBS) containing 0.1% Tween 20
  (PBS-T). A human serum pool negative for anti-dsDNA IgG antibodies
  (DNANe) was prepared by mixing equal parts of serum from 10 healthy
  persons who had a negative CLIFT test and no clinical evidence of SLE.
  The DNAPo and DNANe pools were used as positive and negative controls
  in the ELISA and CLIFT reactions.

Thus, the U/mL figures are comparable, while RU/ml or AU/ml are not.

Thanks for the answer. I thought when there are international standard references, IU/mL is used. In any case what does AU mean?

@Dayne, thank you! I have updated my answer on AU (arbitrary units).


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Can exposure to blood make pathogens resistant to the immune system?
If a drop of my blood is dropped into a pool of pathogens. Does that act as "reverse-vaccination" for said pathogens?
I see this it as a potential risk for bacteria/viruses to compete or get acclimated with the weakened/dormant/key-specific of the immune system.
Please correct me if I'm wrong.

You have got the concept of vaccination a bit wrong. Pathogens have to evolve to acquire resistance to immune system (or antibiotics). Technically, the white blood cells also evolve to acquire resistance against pathogens if they don't have a strong innate immunity. Development of immunity after vaccination is also not instantaneous. The pathogen population has to "grow" in the blood for at least a few generations to become resistant. A drop of blood would probably not give the pathogen enough time to evolve. Moreover, your white blood cells will die quickly outside the body unless they are cultured in a controlled environment. Therefore, the selection pressure to evolve would also not be there.