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Need biological system with specific reset process
I need a biological process that can be described as a stochastic process in statistical physics. I am familiar with some processes such as birth-death or gene expression, but now I need a process where a specific reset process occurs. In this reset process, there is a counter that counts and increments an observable as the system evolves over time. The reset occurs randomly after a certain amount of time has passed, during which the counter does not count anything.Is it possible?
Thanks for your attention.

Not that I know of; most biological processes go from one state to another without reversion. What sort of reset are you after? Hard reset - counter increments up, then returns to 0 immediately or counter counts back down, or something inbetween?. If one of the latter two you might be able to use paired enzymatic reactions, such as between a DNA polymerase and a DNase.

if there counter is triggering the reset then it can't be random if it is based on a counter counting time,  maybe I am confused about what you are asking for

I guess telomere shortening is kind of like this, but I'm not sure based on the description (it's also probably noisier than what you have in mind)

stochastic processes are everywhere; I think the tricker bit is how you've specifically setup this "reset process" as being completely independent of its count accumulation. I think the best example is probably spontaneous neuron firing, but there's some controversy in the field as to just how "spontaneous" this is

I think bacterial chemotaxis may qualify, depending on how the phenomenon gets aliased into the signal and time-counter variables.
The bacterial flagellar rotor can turn in two directions. Because the flagellum is chiral, clockwise and counter-clockwise rotor directions produce two different types of movement. One type is running in which the motion is roughly linear, the other is tumbling in which the bacterium basically rotates.
It's easy to show that random switching between these modes leads, over time, to a random position in space. So, if one (say) puts a single bacterium at the center of a 2D playpen, its coordinates after an interval are random.
The ratio of runs/tumbles is set by a kind of olfactory system, so that when the bacterium is moving towards an attractant there are more runs to close the distance, and less tumbles to scramble the bearing. But even when traveling straight to an attractant, tumbles still occasionally occur. This is summarized below in a figure and its caption from 1 (with minor edits, and my boldface):

Attractants bind to the receptor-transducer proteins ( Tar, tsr, Trg, Tap) in the membrane. The receptors also mediate the response to certain repellent. This activates a CheW-dependent change in the rate of autophosphorylation of CheA and the proteins that are phosphorylated by CheA (CheB and CheY). Attractants reduce the rate of autophosphorylation, and repellents increase the rate of autophosphorylation. The phosphoryl group is transferred from CheA-P to CheY and CheB. CheY-P interacts with the switch proteins (FilM, FliN, FliG) to cause clockwise rotation of the motor and tumbling. Thus repellents increase tumbling because they increase the level of CheY-P, and attractants reduce tumbling because they reduce the level of CheY-P. CheB-P is a methylesterase whose activity results in demethylation of the receptor-transducer proteins. As CheB-P goes up, methylation goes down. Thus repellents reduce the level of methylation because they increase the level of CheB-P and attractants increase methylation because they reduce the level of CheB-P. CheB-P autodephosphorylates. CheR is a methyltransferase that methylates the receptor-transducer proteins. The more highly methylated receptor-transducer protein does not transmit the chemoattracant signal to CheA. Hence adapation to a chemoattracant is due to increased methylation of the receptor-transducer proteins. Adapation to a repellent is due to undermethylation of the receptor-transducer protein. The relative activities of CheA-P determine the level of CheY-P, hence the frequency of tumbling [3].

When a run is initiated, the protein CheY is in a dephosphorylated state. The phosphorylation of this protein is a second stochastic process driving the chemotaxis. When it is eventually dephosphorylated again, also a stochastic process, this comprises a reset of that timing system.
As a result, the time in current run or tumble is a stochastic variable that near-instantaneously resets. It could be appropriate to act as the "counter" time-index variable that could be paired with the bacterium coordinates random variable.

Thanks for your complete answer. I must read more about it. thanks.


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Can Sleeping With Reptiles Reduce Excess Body Heat from Your Partner?
I'm an engineer and biology is my weakest point, so please forgive if this question is dumb.
My wife always complains that I set the air temperature too cold at night. She's exothermic in a number of good ways, but she also radiates too many literal Watts. It's like sleeping with a space heater. She wants to get a pet and has been asking me what kind of dog I want, and that got me thinking...
What if a pet could solve our sleep problems?
Sure, they might strangle you in your sleep and then eat you, so this probably isn't the most practical solution. But snakes and other reptiles might make the perfect heat absorbent bedding!
All kidding aside, I'm truly curious. My incredibly shallow bio class gave me the idea that warm blooded animals are exothermic and cold blooded animals are endothermic. But is that right? And if so, does it follow that sleeping with reptiles would cool your bed down to some temperature more hospitable than Mordor?

Reptiles are generally ectothermic or "cold-blooded", not to be confused with exothermic. This means they largely use environmental heat sources to get their heat, rather than generating it themselves
The same limits apply here as you might find in any other system - once they reach your body heat, they won't get any warmer and will not appreciably draw any additional heat. They will likely also get more active with the additional heat, which I suspect is not exactly what you want in the middle of the night. This might depend on whether you have a nocturnal species or not.
you'd also need to consider the mass of reptile you might need in the bed to provide any substantial cooling - a wee gecko ain't gonna to do much, but you also probably don't want a Komodo dragon hogging the bed covers for a variety of reasons.
I'd suggest you get one of those bed-covers (duvet/comforter/quilt/doona) that is capable of holding two different insulating thicknesses, or simply have a lighter cover for both with an additional blanket for your wife. You can also put a standard two-person insulating duvet and a single inside the one cover.
On second-thoughts, perhaps you are on to something here. Get the all new RepiCoolTM It's 100 finest quality Tokay geckos in one easy to use system of convenient mesh pockets. Too Hot??? simply add an extra gecko or two for that great cooling effect; too cold? simply take geckos out as you need and allow the fantastic warming effect of the bags to keep you "just right" all night long!!! But that's not all!! Also included at no extra charge; fall asleep to the soothing sounds of the gecko and you'll never have problems sleeping again! geckos not included, get geckos for a one-off additional payment of only $99.99, each sold separately

100 geckos making that sound at night (lol) would also affect (soothe?) the sleep of the neighbors. I am always curious why people don't use the blankets with different levels of warmth on either side, or just use an extra blanket on one side.

@anongoodnurse Deliberately chose that species for that feature; most aren't quite as noisy, but plenty do make similar noises and are nocturnal. I'm glad it amused someone.

It sure amused me! I'm certain it has amused/will amuse others who haven't/won't post a comment. I'm a bit chatty. :)

source: Stack Exchange

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

sort: votes


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Do the EDAR sinodont mutation affect brain size or intelligence?
I am reading on wikipedia that a certain mutation in the "Ectodysplasin A receptor" known as rs3827760 or 370A is responsible for the sinodont dentition pattern in East Asians as well as affecting breast size, causing thicker hair and "reduced chin protrusion".
Question: In what way, if any, does this mutation affect brain size and intelligence?
Does this mutation cause any other evolutionary advantages?
One would expect that humans have gone through a series of mutations affecting our skull, making it less robust and causing us to have weaker jaws than apes, but then making room for a larger and more well developed brain.

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


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In what sense is Syringammina single-celled?
In what sense is Syringammina single-celled? For example, if it's true that all cells have membranes (is it?), then how do you identify its membrane? Or does unicellular simply mean that it has only one lipid bilayer (presuming --- since I don't know one way or the other --- that the crucial ingredient of any cell membrane is a lipid bilayer (is it?))
I'm not a biologist, so please excuse my possibly annoying question.


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What are all the possible abnormalities in our body that will result in ataxia?
So I know that ataxia is caused by loss of proprioception.I only know that dorsal column medial leminiscal pathway carries proprioceptive fibre to the cerebellum.So in theory damage to either this pathway or to the cerebellum will cause ataxia.Is there any another way that will result in ataxia?

Welcome. What makes you ask this question? Some background on the motivation of the question can help. The problem with this kind of question is that it is a very specialized topic (our community is relatively small, yet we cover a fairly big chunk of science), but the question itself is really broad (is there any one other cause of X?). I doubt you will get a satisfactory answer with the question in its current state.


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Would using positive numbered glasses while using a computer help prevent myopia?
There are multiple web pages linking screen-time and myopia. While this is not necessarily proven, for example as shown on the NIH page here https://pubmed.ncbi.nlm.nih.gov/31943280/ , it seems logical that exerting our eyes to look closer than "infinity" for long hours might cause that (myopia).
So I was thinking, what if we use reading glasses, glasses with positive prescriptions, while using computers, effectively changing the screen distance to be our "infinity" distance. Would that help alleviate the strain on our eyes and therefore myopia, or its worsening?


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What can lymphocyte-produced antibodies do that 'innate' opsonins can't?
I have a conceptual misunderstanding relating to immunology which I'd be grateful if anyone could help me clear up.
My A Level textbook says that at the start of an immune response, opsonins bind to antigens; these opsonins are "a type of antibody" that then increase the probability of the pathogen being phagocytosed by a macrophage or neutrophil.
Macrophage phagocytosis then leads to antigen presentation; the macrophage migrates to the lymph node and then the hope is that a lymphocyte with the specific receptor binds to the antigen on the macrophage APC. Clonal selection/expansion/differentiation follows, and the B plasma cells produce large amounts of antibody that are released into the blood.
But why is this necessary, if the opsonins at the start of the process which tagged the pathogen for phagocytosis already exist in the body at the start of the response, before clonal selection? What can the very specific lymphocyte-produced antibodies do that the more generic opsonins can't?


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What is the meaning of NF-kB (transcription factor) "activity"?
This article discuss about the NF-kB activity and its mathematical modeling Understanding NF-κB signaling via mathematical modeling. The NF-kB is a transcription factor mainly involved in the regulation of inflammatory genes. However, I do not really understand this: what do we mean by NF-kB activity ? For instance, if we consider this graph (that is figure 1A in the paper that I linked):

by NF-kB activity on the vertical axis, do we mean the number of RNA molecules produced by the target gene regulated by the NF-kB over time ? Or it depends on the kind of experiment ? In the article it tells: this prediction was confirmed by using EMSA on wild-type cells. What does EMSA effectively measure ?
P.S. The idea that by activity I mean the number of RNA molecules produced comes from the fact that I read some thesis works about NF-kB activity in which Cignal Lenti Reporter System (QIAGEN) is used for the experiment and I read in  Reporter Gene Assays that a reporter gene assays are typically used to measure the regulatory ability of an unknown DNA-sequence. This is done by linking the unknown promoter sequence to an easily detectable reporter gene whose product can be easily detected and quantifiably measured. However I do not really understand how EMSA can experimentally give us information about NF-kB activity (maybe because I did not understand how it works).
I thank you in advance.

The word activity has at least two meanings in biochemistry. One is chemical activity as in the effective concentration of a chemical. This comes up a lot because biomolecules often behave non-ideally.
The other sense, relevant here, originates in the description of enzymes. As catalysts, enzymes accelerate the rates of chemical processes. Enzyme activity characterizes the rate of an enzyme catalyzed reaction, so these activities are quantities that include time dimensions (Cornish-Bowden, p. 81).
This leads to a definition of the activity of a transcription factor, a biomolecule that catalyzes the initiation of transcription. The activity of a transcription factor is its enhancement of transcription (which, since uncatalyzed transcription has an effective rate of 0, is the same thing as the observed rate of transcription).
Usually this is only indirectly measured, and usually the absolute activity (in, say, transcription initiations per cell per hour) isn't needed, only the relative activity. That's why activity is often illustrated on axes with normalized/absent units; the raw units are often arbitrary. So, yes: activities in this case could be literally measured by the number of mRNAs transcribed when NF-κB is activated. But anything proportional to that mRNA population is also suitable as a measure of activity.
From the reference in question:

NF-κB enters the nucleus, denoted by the suffix ‘n' (k1). This leads to synthesis of IκB mRNA transcript, denoted by the suffix ‘t' (tr2).

So, synthesis of the IκB transcript is the main response variable they're interested in tracking in term of NF-κB activity. But that's not the definition of activity, just a convenient measure of the promotion of transcription. NF-κB promotes many transcripts, not just IκB!
In 5, electrophoretic mobilility shift assays are referred as follows:

As time-course data, derived from electrophoretic mobility shift assays (EMSAs), indicated that the three IκB proteins had differential dynamic control, we set out to construct a mathematical model of NF-κB signaling to study the specific roles of each IκB isoform in regulating the temporal control of NF-κB (Hoffmann et al, 2002)

A biomolecule has a certain mobility in this experiment and the mobility shifts when the shape or charge distribution of the biomolecule changes. So here the raw signal is the migration distance of a given band (somewhat arbitrary as a measurement, but proportional to activity).
I have not yet checked the Hoffmann et al 2002 paper. But if we assume that, here, "EMSA" summarizes experiments 1) comparing nuclear and whole cell extracts (key for deciding that NF-κB is activated) and 2) using Western blotting for confirming protein bands, perhaps the "confirmed by EMSA" phrases are less opaque.

Thank you very much for your answer! I have one question: I like that you give a formal definition of activity of transcription factor as The activity of a transcription factor is, narrowly, its enhancement of transcription. However, can I find this definition in some literature material or is something that you can know only by reasoning about what a transcription factor does ? And second question: by "titrated" you mean bound to DNA sequence of target gene ?

I've added some explanation but will find references too

Wow, congratulations on your education ! So I wait for references, thanks.

My answer now has some references and I think should help with your direct concerns about activity. I took out the unnecessary language about titration, and explained it directly. I will improve the EMSA part.

Thanks now the answer is very helpfull ! So I would enjoy also the EMSA part.


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How good is the vision of diurnal birds of prey really?
Diurnal raptors (especially eagles and hawks) are commonly thought to have incredible visual acuity, up to 5 or 8 times higher than a typical human. However, I haven't been able to find any scientific evidence of such measurements, beyond popular science websites and unsourced Wikipedia articles. The actual scientific estimates I've seen (such as this, see the results referenced in part 9) indicate that their vision is not really overwhelmingly better than our own, with even exceptionally large raptors like the wedge-tailed eagle only having twice the visual acuity of an average human, and many small sized raptors like falcons having actually substantially poorer vision. I understand that eye size is important (even with their proportionately large eyes they're still not larger than ours, and that places a maximum limit on spatial resolution)
They also have lower achromatic contrast sensitivity than a human (although their ability to distinguish chromatic contrast is far higher).
So are there any actual bird species with 5 times better vision than a human or is it just a pop culture/folklore myth?

Helpful paper https://www.sciencedirect.com/science/article/pii/S1084952119301004. part of the problem is "acuity" is not a perfect term, some eagles can see things from 5 times the DISTANCE humans can.


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What happens if you don't comply with BSL standards?
I understand that if you work with agents regulated by the FSAP, you are required to comply with biosafety standards by federal law and there are inspections to enforce this.
But for those not working with select agents, I'm wondering what keeps them compliant.

Do all labs at least try to follow these standards? Are there any that just choose not to?
For those that do comply, what is their reason? Is it required to get funding? Or they're just being responsible?

Are you confusing the meaning of agent, agent means a type of material, if you are using ANY pf those materials you must comply with BSL standards under penalty of law (there is a list of exceptions for special circumstances). A list of those substances can be found here. https://www.selectagents.gov/sat/list.htm

I'm not confident enough to answer this, but I don't think there are any direct legal mechanisms to enforce BSL standards where no select agents are involved. If an employee got sick and died, the organization responsible would face wrongful death, so self-interest will promote internal enforcement.

I’m voting to close this question because it is a legal question, not one about a problem in biology.

I’m voting to close this question because, as I wrote previously, it is not about a problem in biology as clearly explained in the [Tour].

What has British Sign Language to do with biology?

You will likely get a better answer from the Law SE. I notice you didn't say which country you are in, but this will impact on which penalties there might be. I think in some cases there are international agreements that many countries have signed up to (e.g. the Select Agent Program is part of one I think), but these are for high risk things in general.
However, in general, if you don't follow the law, there are punishments, just like there are for any other law breaking. What those punishments are depends on the jurisdiction you are in.
It will depend also on the severity of the infringement. In my country small infractions might get a notice to rectify, larger/continued infringements might result in personal fines (to the infringer) as well as fines for the institution and/or biological safety committee/officer, shutting down of parts (or all of the facilities at the institution), potentially even jail time for persons committing the infringements.
Of course there are people that disregard the law, just like there are people that disregard any laws you can think of. Do they get caught - YES; people and institutions get caught for this sort of thing all the time - if you search you can even find lists of more severe infractions, as these are often published for clarity.


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bilateral symmetry: word for clockwise rotation on right and counterclockwise on left
It seems like there should be some terminology for bilaterally symmetric organisms that could be used in descriptions, where a clockwise rotation on the right is equivalent to counterclockwise rotation on the left. Is there a name for this type of rotation?

I'm a little confused by your description - do you mean mirrored motions - like if you swim the breast-stroke or butterfly (or bird's wings flapping etc?). If so there are so many motions possible, there isn't a single term.

radial symmetry?


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Does vaccinating people with cowpox give people immunity to smallpox?
I've just recently learned about the body's defense mechanism about how lymphocytes from memory cells that are specific to a pathogen after being infected by a pathogen for the first time, but then I saw that vaccinating people with cowpox can give people immunity to smallpox, which is similar to cowpox. Why can this happen? Shouldn't the memory cells formed in this case be specific to only cowpox?

cowpox and smallpox are nearly the same disease, much like how the bat strain of covid and the human strain of covid are very related diseases. https://journals.plos.org/plosone/article?id=10.1371/journal.pone.0007666

As suggested by John, I think it is worth interrogating what you mean when you say that cowpox is "similar" to smallpox. What is similar between them? What is different between them? What would make the memory cells be "specific" to one or the other? Possibly, look into the history of smallpox vaccination: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9709930/

I think the key point here is to note that pathogens are assembled from multiple subassemblies, which are themselves composed of various proteins. It's these subassemblies of proteins which B cells develop antibodies for, in which case we call that subassembly an "antigen." The antibodies then attach to those antigens, which tags the pathogen for removal by other cells, destruction by proteins (in the case of membrane attack complexes), or otherwise prevents that part of the pathogen from doing whatever it would normally. There are also T cells, which have their own kind of antigen receptor (T-cell receptors). Have fun looking into those! You might check out "The Red Queen: Sex and the Evolution of Human Nature," by Matt Ridley, which is all about the Red Queen hypothesis, and dives into the major histocompatibility complex.
So, in the case of smallpox and cowpox, they share common antigens. That's what's being referred to in papers like "A comparison of the antigens present on the surface of virus released artificially from chick cells infected with vaccinia virus, and cowpox virus and its white pock mutant." Smallpox and cowpox are both orthopoxviruses, which you can learn more about from ViralZone's description.


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Do both a separate B and T lymphocyte need to be activated during the immune response?
Isn't it very unlikely that there will be both:
a) a B and a T with a receptor complementary to the antigen, and
b) that they will come into contact with the right antigen-presenting cell?
What would an immune response look like with only a B lymphocyte or a T lymphocyte activated? Is there any way for one class of lymphocytes to 'transfer' the complementary receptor to the other class?


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What's the grade of D-glucose that can be used in glucose assimilation test in bacteriology?
Background information
Carbon assimilation test is based on the ability of a bacterial species to utilize an organic compound (e.g. D-glucose) as a sole carbon source.
This means that for carbon assimilation tests, any compound that is a potential source of carbon is considered a contaminant (e.g. Maltose for glucose assimilation test).
Question
What D-glucose grade can be used in glucose assimilation test in bacteriology, specifically, Acinetobacter species bacteria?
For example, this product (DEXTROSE MONOHYDRATE Extra Pure)
https://www.alphachemika.co/chemical/2120/DEXTROSE_MONOHYDRATE_Extra_Pure.html
says that it has 0.01% maltose, is this significant?


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Does the smoke produced by tobacco affect mitosis in vegetables (plant cells)?
There is a plethora of literature and research studies on the effects of tobacco on the human body and other animals.
I am interested in knowing whether the rate of mitosis in plants is affected by the smoke produced by burning tobacco (e.g. a vegetable under study would be put in a chamber filled with tobacco smoke).

Just a word of caution: there is no such thing as "mitosis speed" without careful consideration of meaning. Plants are composed of a lot of differentiated cell types. Some in the soil, others above ground, some internal, others external, some compose growth cones at the shoot/root tips, others simply structural and inert. Some cells are old, young, in sexually or asexually reproducing specimens, some cells would exhibit readily easier exposure to a 'general smoke' experiment than others. Both biotic and abiotic factors are known to affect cell division, but the particularities matter.

You can ingest tobacco as inhaled smoke and observe heightened co-incidence of lung cancer, but that doesn't mean that all cells may experience "faster mitosis" or shorter cell cycles as a result of tumor growth (uncontrolled cell proliferation). Nor for that matter "slower mitosis" or longer cell cycles (as a result of toxicity, hypoxia or indirect effects). Also, beware of false attribution fallacies: smoke (particulate matter in the air, like soot) is NOT carbon monoxide, but we consider it part and parcel of smoking, which isn't smoke per se. Remember to think about Qs carefully!


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Chronic-stress of predation risk in vertebrate prey
Prey must be vigilant when their predators are around.
Predators may affect mortality (and morbidity, i.e. loss of quality of life) through these mechanisms:

Direct attacks, including injuries sustained if the prey manages to escape.

Changes in the prey's foraging/hunting behavior which may restrict access to high-quality food sources.

A chronic stress response, which in humans has been documented to increase mortality.

Have the health effects of chronic stress in wild prey populations been documented? Can the strength of effect (3) be comparable to (1) or (2)?

How would one do that, given that: the animals are wild, thus not under our supervision; our supervision (including observation, and capturing for bloodwork) would be stressful in itself; which animals are more stressed and which are less stressed? How to prove correlation/causation? There are some experiments or studies one can do with wild animals. This doesn't seem to be one of them. However, is there a reason to think, knowing this happens from humans and animal studies, to think it doesn't in wild animals?

@anongoodnurse: The best way, besides some sort of implanted real-time monitoring system, is to use "sluggish" biochemical markers (similar to how A1C is a three-month moving average of sugar levels). Most likely such a study would "piggyback" on other studies which need to take samples.
One hypothesis is that novel predatory risks cause more chronic stress than the predators a prey is "used to". Similar to humans not being adapted to the different type of stress we face in modern society. Selection pressure hasn't had the time to weed out the harmful long-term stress effects on the body.

Do you know of any such markers? how would one know what caused the stress? Your desired info is very specific.

Not specific to this, but somewhat similar studies of baboons by Sapolsky did look at chronic stress (related to social status).


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Why don't hamsters exhibit a fear response when other hamsters nearby are under attack?
There is this live feeding video on youtube that displays 30 live hamsters being eaten by 4 bullfrogs. You can find it here: https://www.youtube.com/watch?v=rz4Or3o-jHA
What struck me as extremely odd was that none of the hamsters exhibited any kind of stress when one of them was being eaten alive.
The first one got eaten head first at 0:28 https://youtu.be/rz4Or3o-jHA?t=208 yet none of the other hamsters tried to run away. Instead, some of them even approached the attacking frog and started sniffing its eyeballs. Then somewhere after 3:25 https://youtu.be/rz4Or3o-jHA?t=206 another hamster is attacked from the side which causes it to scream out in pain. Yet the other hamsters are still unfazed by it. Some are even cleaning their fur as the carnage around them unfolds.
So how does this work. Why do all these hamsters seem so comfortable?
EDIT: At the end a few of the hamsters do seem to freeze a bit, but no real panic. There is another live feeding video that shows a single bullfrog eating a group of mice. You can find it here. https://www.youtube.com/watch?v=9RDwz8mjOIw These mice do exhibit real fear. Since both hamsters and mice are part of the same larger family called Muridae, it's very strange that hamsters react so differently.

This does seem odd indeed. I don't have time to look into and research an answer, but I can't help but notice that "The entire laboratory and pet populations of Syrian hamsters appear to be descendants of a single brother–sister pairing." (Wikipedia) representing one heck of a bottleneck. Inbreeding  may play a part.

Maybe the hamsters are instead pretty clever and realized they're confined in a death trap and have simply accepted their inevitable fate


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What kind of bubble this？

This is the MARC-145 I cultivated. Recently, many bubbles appeared in the cells. I don’t know why.

Late stage apoptosis. Specifically what you are seeing here is cells that have undergone the blebbing stage and are releasing or have released apoptotic bodies.


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DnaA binding energy to E coli genome
I have been told that DnaA binds strongly to DnaA boxes on the E coli genome, but binds weakly to 8 out of 11 sites near ori. I want to know more quantitatively what strongly and weekly mean. Are there order of magnitude estimates of binding energies of DnaA to various locations on the E. coli genome?

I would suggest searching the literature for answers, I didn't instantly find binding energies but I could readily find dissociation constant estimates.

@MaximilianPress Thank you, this is helpful. I had done a quick search and hadn't found anything, but I wasn't searching for dissociation constants, which is equally useful. Feel free to post this as an answer, and I will accept it.


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Could trophy hunting lead to deer evolving to lack antlers?
There was a recent paper in Science which showed that elephants are quickly evolving tusklessness because elephant hunting imposes selective pressure against having tusks:
Shane C. Campbell-Staton et al., Ivory poaching and the rapid evolution of tusklessness in African elephants.Science 374,483-487(2021). DOI:10.1126/science.abe7389
Is it plausible that trophy hunting among deer (particularly bucks) for their antlers could lead to a similar evolutionary process? Or do the differing population sizes and selective pressures make such a thing unlikely? Are bucks' antlers relatively beneficial to their mating success, compared to the increased risk of getting killed by a hunter?

There's a big difference between hunting for a trophy and killing anything that has antlers; as elephants are killed for ivory - the poachers don't care about how much, just in getting some. Trophy deer tend to be much older (i.e. already sired young), so the genes passed on already. I have no scientific backing for this, just a little deer hunting experience.

@bob1 -- thanks, and please feel free to make this an answer!

thanks - i'll decline as I don't have any references to back it up, though I am sure there is literature on this somewhere in the scientific annals.


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What is regional homogeneity in neurology?
newbie to.neurology here. For context, I'm studying this article (https://www.nature.com/articles/s41598-021-89166-8#Sec14) which relates the gut microbiome to brain structure in schizophrenia patients. The paper uses the term "regional homogeneity" so often throughout the paper without explaining what it means, and my attempts to research it only leave me more confused. I only understand it as some measure of
brain activity with other stuff related to synchronization. That's kind of a problem since so much of my project depends on knowing what it means exactly. Any help is greatly appreciated.

4th paragraph of the introduction (Alterations in brain function...) and the 4th paragraph of the method section titled "MRI data collection and preprocessing" (The ReHo index was calculated...) tell you what it means. You probably need to read the cited references for a deeper understanding, or at least search Kendall's coefficient of concordance.

@anongoodnurse Then one needs an explanation of voxel and connectome, not regional homogeneity. Regional homogeneity similarly can be simply understood from the separate meanings of those two words, but what's relevant for this paper is how it's calculated which is very clear in the methods.

@BryanKrauseisonstrike: Thank you for pointing me in a general direction, but I can't afford to go down the rabbit hole of researching and understanding what functional connectivity and friends mean. Do you understand this concept at all, and if so, would you be willing to walk me through it?

@Specs_Goldfish Hi, I'm sorry, but, your comment is not correct. In fact, you can't afford not to go down that rabbit hole if you want to use this technique for anything at all. Your project depends on you going down that rabbit hole, and really, understanding functional connectivity at least at a level sufficient to understand this technique is not a "rabbit hole", it's one of the principal methods used to study human neurobiology. Ignoring it would be like leaving telescopes out of astronomy.

@BryanKrauseisonstrike: You're right, I absolutely need to read everything to get a formal understanding, but for a dense high school student with a presentation due in two days, any sort of oversimplified explanation will do. I apologize for showing up so unprofessionally.

@Specs_Goldfish I'd start with at least the Wikipedia article on resting state fMRI. You might also search "functional connectivity" here or on Psych & Neuro StackExchange. Taking shortcuts due to a short deadline is a strategy you should quickly learn to avoid - one strategy is to be better prepared further in advance of the deadline.

You state, "...my project depends on knowing what it means exactly..." Then you need to know exactly, which can't be explained in a couple of sentences. You're asking professionals to help you out of a jam (a time crunch) that you created for yourself.

Good question! The brain is composed of billions of cells, and not all of them are doing the same thing at the same time. Some areas of the brain may be more active than others at any given moment. However, within specific regions, the cells (or neurons) are expected to be working together -- or, in other words, they should be synchronized.
When we use fMRI to scan the brain, we're creating a 3D image, and each tiny cube or box within that 3D image is called a voxel. I.e., "volumetric pixel," just a box instead of a square like a pixel. Each voxel represents a tiny portion of the brain, containing a large number of neurons. In an fMRI scan, the intensity of the signal we receive from each voxel can tell us how active that part of the brain is (based on, for example, how much blood is being used in the region).
ReHo is a measure of how similar the activity is within a cluster of voxels. If they are all behaving very similarly — if they're all increasing or decreasing their activity at the same time — then we say they have high regional homogeneity.
To calculate ReHo, we use Kendall's coefficient of concordance to tell us how well the activity across a cluster of voxels is synchronized.
You can imagine that some disorders would disrupt brain connectivity/communication between neurons, resulting in more disorganization. Or you could imagine that excessively high ReHo might indicate some altered state of mind.

From my reading, your answer is correct but very simplified. I don't know just how much detail the OP needs (for example, how much volume is in a voxel, and approximately how many neurons in that voxel, how many voxels in a cluster, and how Kendall's coefficient tells us how well activity in a cluster is synchronized.) But what I really don't understand is your last sentence. I think you need to provide some support for it. Thanks.


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Does This Rock Contain A Fossil?
A couple of months ago I came across a rock which has suspicious insertions in it. It was found in southern Spain, more specificaly hiking near Zahara de la Sierra (coordinates are provided: 36.830427, -5.416054). I am curious if it could contain some sort of fossil as some of the structures are bone-ish. The rock is 40 x 40 x 10 cm (16 x 16 x 4 inches) in volume and weighs around 10 kg (22 lb) Thank you beforehand

There seem to be inclusions in a sedimentary rock, but without a clearer picture, there's no hope of identifying anything. Could you provide a few other angles including the underside - in as high resolution as possible.

think of uploading some close ups to fossil id forums

Seconding @JiminyCricket. You can't tell with this quality of photo - would need closer up of the "fossil" bits and some different angles; but look like inclusions or intrusions of some sort to me.

the stuff in the upper center of the photo is the only stuff that could possibly be a fossil, so providing a close up of that might be enough.

I added an extra picture I had in my gallery, but soon you'll get some more closeups and different angle shots. Sorry!


text:
How does $\ce{H2CO3}$ form in the blood with a ratio of 1:20 with $\ce{HCO3-}$ if there are not enough $\ce{H+}$ ions
I have recently been studying about the bicarbonate buffer in the blood and have a doubt regarding the concentration of carbonic acid in the blood plasma.
My understanding of the buffer system is that about 85% of the total carbon dioxide in the blood diffuses into the red blood cells. In the RBCs, $\ce{CO2}$ reacts with water(catalysed by Carbonic anhydrase) to  form carbonic acid($\ce{H2CO3}$), which dissociates into $\ce{HCO3-}$ and $\ce{H+}$. The $\ce{H+}$ binds with haemoglobin, and the $\ce{HCO3-}$ is released into the plasma by a chloride shift.
The doubt is how does $\ce{H2CO3}$ form in the blood from $\ce{HCO3-}$ to have an equilibrium with it and to form the buffer system.
I initially thought that some $\ce{HCO3-}$  would bind with the auto-ionised $\ce{H+}$(aq) ions to give $\ce{H2CO3}$, but the concentration of $\ce{H+}$(aq) is miniscule(about $4*10^{-8}$ molar) as compared to the concentration of $\ce{HCO3-}$(between 0.022-0.032 molar when in equilibrium with carbonic acid) and thus would not react adequately with $\ce{HCO3-}$ to give the concentration of $\ce{H2CO3}$(0.0011-0.0016 molar) required for the buffer to function.
Therefore my question is how can there be a 1:20 ratio between $\ce{H2CO3}$ and $\ce{HCO3-}$, if there is hardly any hydrogen ion concentration for $\ce{HCO3-}$ to form carbonic acid.
I have looked at multiple articles regarding the transport of $\ce{CO2}$ in the blood as well as the bicarbonate buffer system, but none of them explain how exactly does the carbonic acid form in the blood.
Some of the articles/videos that I have looked at before posting the question:
https://courses.lumenlearning.com/wm-biology2/chapter/transport-of-carbon-dioxide-in-the-blood/
https://www.ncbi.nlm.nih.gov/books/NBK532988/
https://www.khanacademy.org/test-prep/mcat/chemical-processes/acid-base-equilibria/a/chemistry-of-buffers-and-buffers-in-blood
https://youtu.be/QP8ImP6NCk8
https://chem.libretexts.org/Bookshelves/Physical_and_Theoretical_Chemistry_Textbook_Maps/Supplemental_Modules_(Physical_and_Theoretical_Chemistry)/Acids_and_Bases/Buffers/Blood_as_a_Buffer
https://youtu.be/gjKmQ501sAg
https://youtu.be/5_S5wZks9v8

Bicarbonate and its conjugate acid buffer the blood due to their intrinsic behavior (pKa/pKb) of donating $H^{+}$ if there is too few (high pH) or taking up $H^{+}$ if there is too much (low pH).
You will not run out of $H^{+}$ because of the intrinsic property of $H_{2}O$, that defines pH; $H^{+}$ is readily created by dissociation of $H_{2}O$ [source].
Taking up $H^{+}$ simply reduces reformation of $H_{2}O$ from $OH^{-}$ + $ H^{+}$  [source], but you will not run out of $H_{2}O$ as its in excess in the blood.
Temporarily, $H^{+}$ may come from other molecules (e.g. buffers), but can be imagined as being later "reimbursed" from (excessive) water.

It has to do with the buffering activity of Hb and $\ce{HCO3-}$ leakage.
$\ce{H2CO3}$ dissosiates inside the RBCs and the resulting protons, $\ce{H+},$ bind to Hb, decreasing proton pressure caused by the free $\ce{H+}.$ This shifts the reaction in the direction of forming more $\ce{H+},$ in turn forming more $\ce{HCO3-}.$
$$\ce{H2CO3}\rightleftharpoons\ce{HCO3-}+\downarrow\ce{H+}$$
At the same time, $\ce{HCO3-}$ formed inside the RBC is exported out in a chloride-shift similarly decreasing its concentration and pressure inside the RBC.
$$\ce{H2CO3}\rightleftharpoons\downarrow\ce{HCO3-}+\ce{H+}$$
That's the reason plasma concentrations of $\ce{H+}$ are low while of $\ce{HCO3-}$ are high relative to that of $\ce{H2CO3}.$ In short, the dissociating $\ce{H2CO3}$ overwhelms the $\ce{HCO3-}$ associating with the little free $\ce{H+}$ in plasma.


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Calculation for underlying genetic value of a phenotype given parents genetic values
What is the most accurate way to calculate a child's genetic predisposition to a phenotype, given both parents' genotypic predispositions?
Assume trait X is 50% heritable and controlled by an arbitrarily large number of SNPs. The trait is normally distributed in the population. Parent 1 is in the 80th percentile of genetic predisposition to trait X. Parent 2 is in the 60th percentile of genetic contribution to trait X. Will the child's predisposition be on average the 70th percentile?
Due to regression to the mean and given 50% heritability, will the best estimate of the child's phenotype be in the 50 + ((70-50)*0.5) = 60th percentile?

Update
OP specifically drew my attention to the use of the genetic prediction, rather than phenotype.
I think that the answer remains more or less the same, except that instead of the actual phenotype distribution, you have the distribution of genetic predictions.
I don't think that quantiles are appropriate for prediction tasks.
Original answer
I believe that the answer is "no" because the percentile is a nonparametric description of the distribution. I believe that the form of your calculation is right, but the values you've plugged in are wrong.
For example, 1.755m is ~50th percentile male human height (from here), 1.78m is ~60th, 1.795m is ~70th, 1.815 is ~80th, and 1.85 is ~90th. Note that the intervals between those quantiles is not regular, so your estimate will be accordingly biased if you act like the quantile matches the value of the heritable trait.
(Sorry about the dumb rounding, I was working from the calculator, which is somewhat imprecise.)
So your midparent estimate for height would be something like 1.755 + (.0425 * .5) = 1.77625m
In other words: use the actual phenotypic measurements (or whatever transformation the heritability estimate comes from), not quantiles.

are you sure? I'm referring to percentile of genetic risk, not the observed phenotype, when I say percentile, until the last step

@BigMistake- ah, I see. I think that my answer remains the same, except that the phenotype in question would have to be whatever the genetic risk value is. It's still a quantile of the underlying distribution, it's just that rather than the phenotype you have a genetic risk measurement. Depending on the structure of the prediction task, there may well be additional biases that require a different form for the prediction, but I can't comment on that.

Does this change if we assume the population genetic predisposition for the phenotype normally distributed? I think in this case, the percentile might yield the same result

@BigMistake not sure that I understand. When you perform a quantile transformation of data (percentile is a 100-quantile transformation), you fundamentally change the shape of the data to a uniform distribution. Normal -> uniform data transformation will not preserve underlying normality, so you will not preserve the moments of the underlying distribution, not even the mean. It will only work if the underlying data is also uniformly distributed. I'd suggest playing with some data to investigate this if it doesn't make sense.

Exactly. Under the assumption that the data is already normally distributed, transforming it into percentiles (now uniformly distributed) doesn't affect the calculation's validity

@BigMistake- still not sure that i understand. If you perform the calculation on the normally distributed data and the uniformly distributed data and compare, you will find 2 different answers. IDK what your goal is here, but getting a different answer sounds bad to me. Not least because your 50th percentile is not the mean! you don't actually know what percentile your mean is. That seems like an issue for making a prediction about the expected value of a phenotype with regression to the mean.


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Mushroom identification in in a balcony planter in Bavaria
I've seen the following mushroom pop up in a balkoney planter in Bavaria (Germany) in June. They were growing pretty quickly (just in a few days)
Description
So that others have a chance to find it via Google / text search:

Dimensions: The whole "body" is maybe 3cm high. The "cap" has probably a diameter of 1cm (I can measure it in the evening).
Stem: The stem is smooth and has a bright color.
Cap: Looks like a cocktail umbrella. It's beige on the top. On the bottom it has dark "stripes" going from the stem to the outside

Photos

A picture from the bottom:

My research
Google Reverse image search / https://tineye.com/: Parasola plicatilis - however, I think mushroom are pretty easy to confuse. As this is growing next to food plants I mainly want to know if they are poisonous / how careful one needs to be.
The cap is not transparent as What is this mushroom attached to the terrarium with transparent cap and black strips?


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What are common culture temperatures?
In literature, authors sometimes refer to 37°C as a common culturing temperature. As I understand it, those are temperatures that are conventionally used for incubators in laboratories. For mesophilic bacteria, I found that common culturing temperatures are 28, 30 and 37°C. However, I was wondering whether that can be translated to Archaea, Fungi and/or algae research. What are the temperatures that people typically use in the laboratory to investigate mesophiles from these taxa?


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Need to Identify This Bug
When I woke up this morning I found 10 or more of these tiny little red and brown bug on the window to above the kitchen sink. They must be attracted to the light as the sun was just rising. I killed as many as I could but they are very small and hard to see. They are mostly bright red. Have 6 legs and antenna.
Does anyone know what they are? Are they dangerous?
Thank you,
Hersh

Please add some information on the location where these bugs where found.

Specifically where in the world you are based - nearby major city or state will help.

This question is more about zoology than biology.

Can you explain your need to identify it? (what exactly is your need? do you need species, genus, family?) If you cannot explain your need here, please adjust your title to be more informative/specific about your post.

(these are aphids, btw... but genus and species is not obvious and would need geography to have a chance to identify)

Hello all, I am in Swedesboro, NJ USA. I want to know what the bugs are to know how to deal with them in my house.

This is an aphid, so it could be at most dangerous if you were a plant. ;)
You can recognize them by a soft, often colorful body, relatively long antennas and legs and the so-called cornicles.


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What is the best way to learn about gene regulation?
For those of you who already have a decent knowledge of how gene regulation works, how should someone new to the topic acquire a detailed overview?
Is there a particularly good and up-to-date resource?
Is it better to learn from the primary literature? If so, what are the main sub-topics within gene regulation to cover?

I would not learn from the primary literature, the terminology will likely be confusing and there will be a tendency to conflate whatever the current methods are with the concepts.
I'd suggest going for a basic introductory course in the topic, or a textbook. Here is a resource from NHGRI which may be helpful as an introduction.
Here is an online textbook section that might handle the topic at a very basic level. Here is an online version of a traditional standard text at the undergraduate level.
Probably the best somewhat more technical introduction to the basic concepts, without a lot of the fuss, is Mark Ptashne's classic 1986 book on phage lambda.
I saw Ptashne give a talk in the mid 2010s in which he declared (somewhat pompously) that we still didn't understand anything in gene regulation other than phage lambda. No one contradicted him, and I don't think that anyone would contradict him if he said the same thing today.


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Arguments against incest
Incest is forbidden in most countries because if there is a genetic disease in the family the child of a incestuous relationship will be at least holder of the gene of that disease. But lets say the members of a family dont  have a genetic disease and are not holders of any gene related to a genetic disease then theoretically would a child of a incestuous relationship not suffer from diseases by birth?

@JiminyCricket. Editted.There are dominant genes and less dominant genes for every trait of a human person for example lets say for the color of the eyes if someone inherits the gene which translates to the brown eyes from his dad and the gene which translates to the blue eyes from his mum then because the gene which translates to the brown eyes is more dominant than the gene which translates to the blue eyes , the kid will be born with having brown color eyes,yet he will be a holder or a carrier of the gene for blue eyes.

evolution is about probability, the probability of your hypothetical assumption is breathtakingly low. That's why an avoidance instinct exists, not because it it always holds true.

There is more to it than just the biological risk, there's also morale issues and the fact humans developed a family structure. (That's better discussed on a different site, or in chat.)

Incest doesn't necessarily mean that the partners are having unprotected sexual intercourse. It simply means sexual intercourse between closely related member of a family. In case of protected sexual intercourse, it doesn't matter whether or not the family has history of some genetic disorder.
But let's say they are practicing unprotected sexual intercourse. In that case, it does depend on the genetic history of the family. If either or both of the parthers has gene that result in a disorder, then thier offspring who gets that gene expressed in his/her body will suffer from that genetic disorder. And if it is not expressed, they become a carrier for that gene.
Now, coming to the case you mentioned, Yes, if neither of the partner have gene that causes certain genetic disorder, then the offspring will not suffer from the said gentic disorder.
But it only works if there's a no history of incest wihtin that family. In case they do have history of incest within thier family, they are likely to suffer from inbreeding depression. Inbreeding depression 'exposes' deleterious recessive genes by making them homozygous. This causes drop in fitness of the offspring and reduced fertility. Increased homozygosity is what causes issue, which increases chances of a harmful recessive gene getting expressed.
So it's not a big worry, if they don't have any such gene that cause obvious harm by resulting in a certain genetic disorder. But continuous incest in family may result in problems later on.
Anyway, it is possible to be able to determine compatibility of two people by checking thier genetic information [we may become even more advance in near future]. We can selectively edit a gene to make it so that it won't be present in the offspring. Gene editing at advance level will get really popular.


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Why is loud music much louder after pausing and resuming it?
If I pause a sufficiently loud song (in headphones) for several seconds, then resume it, I perceive it as deafeningly loud, even painfully. Yet, if I first lower the volume, resume, and then gradually increase it over a span of as little as two seconds, there's no problem.
Like turning on lights when someone's sleeping, but for ears that were awake six second ago.
Why does this happen?

This is probably a good hint that listening to loud music in headphones is bad for the ears!

Hearing is capable of sensory adaptation such that prolonged constant stimulus is perceived as less intense. In hearing, the adaptation to loud sounds is called acoustic reflex and is mediated by two muscles: the tensor tympani muscle and the stapedius muscle. Both of them involuntarily and quickly contract when a loud sound comes to the ear in order to minimize any possible hearing damage.
However, they do not respond immediately, which you observed yourself. Depending on the loudness and the frequency of the sound, the response time generally ranges from several tens of milliseconds up to several hundreds of millisecond1,2. Therefore, gradually increasing the loudness gives the reflex enough time to respond and decrease the sensitivity of your ear.

1 Bell, A.
A fast, "zero synapse" acoustic reflex: middle ear muscles physically sense eardrum vibration (2017)
2 Narayanan, R. Characterization of Acoustic Reflex Latency in Females (2017)

@chivracq There are many more than just five senses. The classical five are only a few; there's also your sense of balance, your kinesthetic sense (i.e. your sense of where your body parts are relative to each other--how you know that your arm is at your side and not raised up, for instance), your sense of hunger, the sense that tells you when you need to use the restroom, and most people consider "touch" to be a combination of several senses, including your sense of pain and your sense of temperature. And there's your sense of humor! (that last one was a joke, just in case yours is impaired.)

@Hearth, alright, I actually wanted to add "physical + psychological" to the word "Perception" that I used in my previous Comment... OK, I understand (a bit)... Thanks for your explanations/clarifications, and I'll stop "polluting" this Answer, the "System" is complaining about "extended discussion + moving to chat"...

Oh...!?, "good"... Some High-Rep User removed the "Like many other senses" I was "complaining" about, => +1 from me for both the Qt + Answer. // There is a Typo btw in the Answer: "several hundreds of millisecond[+s]" (missing 's'). Hum, and in the Qt also: "six second[+s] ago" (also a missing 's').

Based on this answer, I got that it needs some time to adapt to loud sound, but how about the reverse? Does it need much time to adapt to no/quiet sound at all? Or otherwise, will pausing only for a very short time (either voluntarily or musically) not amplify the subsequent loudness?


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Efficiency of molecular motors vs. human-made motors
On the wikipedia page for "Molecular motor", it says "In terms of energetic efficiency, this type of motor can be superior to currently available man-made motors." without any references to back it up. Is this true in general and how would we go about comparing for example a diesel engine with the F1-ATPase, in terms of efficiency?

I think that statement is misleading because it is too vague. Yes diesel and gas engines are inefficient, however electric motors typically average between 80-95, depending on the range of rotation speed and torque, (i,e. slow speed and high torque out of design range), they can get hot and waste 20-50% efficiency. The best EV motors are currently hitting >95% efficiency at a high range of rotation speeds.
Molecular motors have been claimed to reach nearly 100% based on limited studies (ATP synthase), however most of them are in far lower ranges than electric motors " Henry Hess of the University of Washington explains that
cytoskeleton motor proteins “convert their chemical energy with >50% efficiency into mechanical energy."
https://guava.physics.uiuc.edu/~nigel/courses/598BIO/498BIOonline-essays/hw1/files/HW1-sankar.pdf

The efficiency of F1-ATPase has ben measured at so close to a hundred percent that the margin of error of the measurement  exceeds the difference.  BUT these measurements were also taken around 1999- 2000 before the highest efficiency EV existed, so the statment was true back then. of course the step right before F1-ATPase, F0-ATPase only runs at around 50% efficiency.

It is referencing an out of date study poorly.
The efficiency of F1-ATPase has been measured at so close to a hundred percent that the margin of error of the measurement, exceeds the difference. BUT this margin of error was almost 10%. The statement was accurate when the measurements were taken, around 1999- 2000. Before the highest efficiency electric motors were common knowledge, so the statement was sort of true back then. Of course the step right before F1-ATPase, F0-ATPase only runs at around 50% efficiency.
It can be really hard to measure the efficiency of individual components of a biological process, the process as a whole from sugar to ATP is around ~40% efficient. which is still high for anything that consumes a fuel.
https://www.cell.com/fulltext/S0092-8674(00)81456-7


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Explanation of QPCR's "mixing curves."
I just started using qPCR (learning the logic and the basics, actually). I am trying to create a standard curve for ecoli and Pseudomonas syringae. I started by making some DNA dilutions of 10%, 1%, 0,1%, and 0.01%, and I amplified them along with the non-diluted DNA (let's call it zero dilution) and three replication of each DNA.
In my output (just an example), I got a curve in which some dilutions are a kind of mixing, let's say: zero dilution comes first, followed by 10%, then 0.1% (instead of 1%), then the 1%, and lastly, the 0.01%.
Actions made:
I checked the CT values (I got cts for all my amplifications)
I loaded the amplification products on agarose gel, and I got zones in all of them.
Question:
Why do I have the least diluted DNA solution before the more diluted one?
Thank you in advance.
PS I am not a microbiologist, so my knowledge is limited :P. Of course, any suggested paper that explains this issue is highly appreciated.

The obvious thing is that you have made a mistake of some sort. Exactly what that mistake is is difficult to say - possibly technical (e.g. reaction efficiency) or possibly something wrong in your set-up. Get someone experienced to show you how to do this.

Probably easier to help diagnose a problem if you upload a screen shot of the amplification curves and/or melt curves. One issue that a lot of people run into when starting out is that the dilution process is going to be very sensitive to contamination. So, you need to be mindful of what DNA templates have been handled near your workstation in the past and always change tips between each dilution step. Even the smallest droplet of your neat DNA (your "zero dilution") could contain enough template to dramatically change the Ct values in the 3rd or 4th dilution of a 10-fold series. This also can apply when loading your template dilutions into your plates.
One simple way to check is to plot your Ct values against the log of your relative template concentrations and run a simple linear regression. The points should all fall on a straight line with slope around -3.32 and r-squared of 0.98 or better (obviously they won't at first in your example case). If you swap the values for your out-of-order samples (1% and 0.1% in your example) and the regression line straightens out, you probably just mixed up those dilutions when loading your reactions. If you swap them and you still don't have a straight line, you probably made a mistake in the dilution steps. Either way, do it again to confirm.
This all assumes you're have a well validated primer/probe set, adequate starting template amounts, appropriate master mix, and appropriate controls. If your starting template is on a plasmid, it should be linearized or digested to avoid supercoiling, which can make for weird qPCR signals. If you're not using filtered pipette tip, use them. Never handle amplified templates in the same area you set up your plates, and never use the same pipettes for both.
This link has a collection of papers on qPCR that might be helpful for getting started.
https://bitesizebio.com/62143/qpcr-papers/


text:
Is this a spiders net or a wasp net?
I have found something scary on my attic (Bavaria, Germany - found in June):

Size: The small one is a bit bigger than a ping-pong ball. The big one is smaller than a soccer-ball... maybe the size of a small handball ball?
Is that a spiders nest, a wasp nest or something different?
I could not see any alive wasps or spiders ... and I didn't want to get too close to that thing.
I'd be very happy if anybody could give me more information about that thing. I'll probably get a bit closer tomorrow (when it's hopefully very bright ... )
My research
I looked up wasps nets and spiders nets. To be honest, this makes me feel pretty bad (especially the thousands of spiders ... less the wasps).
We do have wasps once in a while in the house and I haven't noticed spiders in the house at all so far. I do see some dead wasps on the picture. My hope is that this is a "dead" wasp nest.

It looks like a wasp nest to me, but it is hard to see the texture of it in this photo (is it paper-like?) Needs better focus to be sure. Whatever it is, it looks old and abandoned and dusty.

You make me happy :-) I hope I find the courage to approach it tomorrow. Then I'll make a better photo :-)

It is probably a European Hornet nest but I'm not an expert nor an entomologist.

This looks pretty much like a paper nest of a Vespinae, the subfamiliy where wasps or hornets belong to: typical is the ball-like, gray construction with the entrance on the bottom (latter is not visible on the OP's photo) which is built from chewed wood fibers.
Here is a Vespula vulgaris queen during the construction of her paper nest (image source: Murmelade     CC-BY-SA-4.0):

Wasps and hornets are both protected in Germany - in consequence, removing a nest is only allowed under certain circumstances (although I doubt that this law is ever executed). Still, wasps and hornets are beneficial insects that are usually relaxed, but always foraging for their colony (what makes them kind of stubborn once they have found a food source). The Süddeutsche Zeitung has just published some recommendations on living together with these insects recently.

I've been a second time up there. It's definitely a wasp net, as there were several dead wasps around. I'll now wait until winter to be sure they are give e

Your answer would be improved by explicitly indicating why you believe the OP's nest belongs to a wasp. Right now you just speak authoritatively without providing any explicit evidence for your opinion. Answers should preferably be able to answer the question convincingly without the need to go to external sources. You should cite sources, but you should also summarize relevant portions of citations directly in your post so as to provide clear evidence for support.

Thank you for your comment, I added some more details...

Very good. Thanks!


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Mass Spectrometry Artefacts: R-deamidation / Oxidation?
Context: I am a student-researcher. I expressed GST-tagged protein (Pyruvate Kinase) in the yeast Saccharomyces cerevisiae on synthetic drop-out media. I then purified the GST-tagged protein, ran it in a polyacrylamide gel and sent the band containing the purified proteins for Mass Spectrometry. The proteins were subject to trypsin digestion and subsequently LC-MS/MS, and analysed using ProteinPilot software (SCIEX). I am quite unsure of the analysis parameters using the software as it is not up my alley.
Generally, is R-deamidation considered an artefact of MS? Deamidation usually occurs on asparagine or glutamine residues. However, I observed a large amount of peptides with arginine deamidated, and I am wondering whether arginine deamidation is biologically significant or simply an artefact of trypsin digestion / MS preparation. I also wondered if it could be the S. cerevisiae way of mimicking protein citrullination, a PTM observed in humans, since yeast has no known enzyme with arginine deiminase activity. However, I have my doubts about this, and and I would just like to clarify if anyone knows about the significance of R-deamidation for proteins.
Additionally, I am aware that oxidation may be an artefact of the GST protein purification process. Would there be any way to tell a functionally relevant oxidation modification from an artefact generated through purification without testing every single modification observed?
Thank you so much! I apologise in advance if I was unclear with anything.


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What this shape name? (concave laterally and straight medially, cross section shape of crayfish rostrum)
What is a shape name for upper surface (colored black) of the cross-sectional shape in the attached image? It is a cross-section through a crayfish rostrum. It is horizontal and linear medially, but concave laterally. By shape name, I'm thinking of words along the lines of emarginate, cuspidate, etc:

In what way is this a biology question?

This is a shape I see in a crayfish rostrum.  It would be nice to describe it succinctly if possible.

Then please edit the question and include this information in it, possibly with an image.

@crayman9 it would help if you could label the parts of the image or even use a drawing tool to make a better drawing. For instance are the 2 left and 2 right asterisks parts of the body or the claws? Is the line the ventrum of the animal? Which part of the animal was the section through.

Ok, I added a drawing.  I didn't realize it was as simple as drag and drop.

Laggingly/tardily concave is the best I could think of. Imagine it takes time to become concave.


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Why is the anterior pituitary not considered part of the diencephalon?
According to the wikipedia page on the diencephalon, the posterior pituitary gland is considered part of the diencephalon, but the anterior is not. Is there a reason that these two lobes of the same gland are considered different enough not to be part of the same brain region?

Worth going to the wikipedia page on the pituitary:

In all animals, the fleshy, glandular anterior pituitary is distinct from the neural composition of the posterior pituitary, which is an extension of the hypothalamus.

The anterior pituitary arises from an invagination of the oral ectoderm (Rathke's pouch). This contrasts with the posterior pituitary, which originates from neuroectoderm.

The posterior lobe develops as an extension of the hypothalamus, from the floor of the third ventricle.

In other words, the different parts of the pituitary are, developmentally, entirely separate. The posterior lobe is actually part of the hypothalamus. The anterior lobe is not even part of the brain.
Lumping them together with one label happened because the anatomists who originally named the thing didn't know much about it, which is not surprising because anatomical names are quite old and understanding of the functions of any parts of the brain is quite new. Old names stick.


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Why Triceratops' frill reabsorbed the triangular epiossifications on the edge of the frill?
Why Triceratops' frill reabsorbed the triangular epiossifications on the edge of the frill?
Juvenile and even sub-adult Triceratops had triangular prongs on the edge of the frill, called "epocciptials" or "epiossification". However, in very mature specimen the frill lacks those triangular prongs and transitional specimens show how the epiossification fuse with the frill to form a wave-like edge and later even a smooth edge.
A scientific description of this ontogeny can be found here:

Horner, John R; Goodwin (2006). "Major cranial changes during Triceratops ontogeny". Proceedings of the Royal Society B (273): 2757–2761. doi:10.1098/rspb.2006.3643.

Short summary by Horner: https://www.youtube.com/watch?v=m2_Fcp6W7U4
The question is: why? What benefit did this modification (the smoothening of the frill's edge) give to Triceratops?

General Images

Figure 1.1: this Triceratops exhibits prominent triangular epiossifications. Source: https://en.wikipedia.org/wiki/File:Triceratops_skull_frills.jpg

Figure 1.2: growth serie of Triceratops.
Source: https://en.wikipedia.org/wiki/File:Triceratops_ontogeny.jpg

Figure 1.3: a skeleton of adult Triceratops in New York's AMNH. The frill shows a smooth edge.
Source: https://en.wikipedia.org/wiki/File:Triceratops_AMNH_01.jpg

Triceratops horridus

Figure 2.1: Triceratops horridus Marsh, 1889, shows scalloped edge https://www.si.edu/object/triceratops-horridus-marsh-1889%3Anmnhpaleobiology_3383580
Figure 2.2: https://commons.wikimedia.org/wiki/File:Triceratops_horridus_skull_in_the_Gallery_of_Paleontology_-_Paris.jpg
Shows transition from scalloped to wavy edge.

Figure 2.3: Triceratops horridus showing wavy-to-smooth edge.
https://en.wikipedia.org/wiki/File:Triceratops_Hendrickx2.jpg

Figure 2.4: a skeleton of adult Triceratops in New York's AMNH. The frill shows a smooth edge.
Source: https://en.wikipedia.org/wiki/File:Triceratops_AMNH_01.jpg

Triceratops prorsus

Got a couple of different species there. Bottom photo is Triceratops horridus; top two photos are T. prorsus I think, though could be other ceratopsids. Fusion of bones is common with age - our skulls do it.

As Bob out the bottom image is a different species. So the comparison is faulty.
as for why bones fuse with age, that is very normal, it happens to bone in thousands of species our own included. The parts are separated by growth surfaces, when growth slows down aka adulthood, those surfaces fuse for strength. This is so predictable in humans the fusion of different bones can be used to age a skeleton. We see this in dinosaurs too but without living one to correlate fusion times with it can't be used to age specimens well.
As for why the angle of the epocciptials change , that's easy, the number of epocciptials do not change so as the frill gets larger the epocciptials need to get wider. They can either grow in all dimensions or just get wider making the angle shallower. Whatever function the epocciptials have must not be impacted by getting shallower so that's what they do saving bone and horn. considering how much mass they would add if they grew in all dimensions its not even that surprising.
https://www.sciencedirect.com/science/article/abs/pii/0305440388900829
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6427487/
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3864909/

That bones fuse with age, I know. The question is why the triangular epiossifications reabsorbed and disappear and not merely fuse but retain their shape. The scalloped frill of a Triceratops has a defensive advantage and probably also a display value from the prominent epiossifications in other ceratopsids).

They don't, you are looking at two different species. if you count the number of epocciptials they stay the same in the same species throughout its life. in Horridus the epocciptials are tiny, so they are just really hard to see in the adults as their width is drastically greater than their length.

I added Figs 2.1-2.4 consisting only of Triceratops horridus (however, I could not determine from the images what was the age of the animal it came from).

@Triceratops from my skimming of the literature it seems you are not alone here - the problem is that formerly there were a bunch of species, all classified on the frill edges. However, with the recent clumping, there is now diversity in the frill edges within each species - so some have it and some don't within the same species, this means that it likely isn't age dependent, so your premise fails to some extent there.

@bob1 if there is a variation within a species it is likely sexual dimorphism. but if you look at the series in fig 2 the epocciptials do not disappear. the only figuire without epocciptials is 2.4 which could be not collected, a diffrent species, or even destroyed it is a very old specimen. If you think they disappear you will need to demonstrate that.

@John I'm no expert on dinosaur systematics at all, so I don't know that they disappear or not, just that there is some diversity in size/shape across a species. Sexual dimorphism is definitely a possibility, that hadn't occurred to me.


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When do invasive species become native species?
Until when an invasive species is considered an "invasive species" and when it is starting to be considered a "native" species, i.e. a species that is an integral part of the local fauna/flora?
I ask this because the expansion of species to new territories also occurs in nature and without human involvement. And in some cases, a newly-arrived species drive out the local species and causes its extinction. However, today it is regarded as native.
Many of today's fauna are the result of different species coming from different areas. Maybe in the next century, species that were considered invasive today will be considered native or an integral part of the fauna/flora.
The criterion may be time passed since that species was introduced or the time when the invasive species reached an equilibrium with the ecosystem.

On a human timescale or a geologic timescale, on a human timescale never.

A time in years. It may be a century (probably a human timescale) or a millennium (human or geologic timescale?) or at least 50,000 years or even million of years (the last is surely a geologic timescale).

It seems to me that this is simply a problem of some people allowing themselves to extend the label "invasive species" to include anything not transported (directly or indirectly) by humans, as the term ordinarily indicates.

2 issues. 1) Inconsistencies/disagreement about how to define "invasive" and 2) well, time, and the [narrow] subjectivity in which we typically observe/analyze it. I don't think this question can easily be answered, and - quite frankly - I think it more of a philosophical question more than a biological one.

There are two uses of invasive,

species introduced to new territory by humans, theses are considered invasive essentially forever. So to answer your question, they don't.

species that enter a new territory via a natural pathway like a landbridge or storm drift and destabilizes the local ecosystem. there is no specific cut off for these as it is more about the context than anything else.  Bison are considered native today but paleontologically they were originally invasive. This is more about how they got to north America. Often once the biosphere restabilizes with the new species they often stop being referred to invasive but this is not a hard and fast rule and could take millions of year or a lot less. On a long enough timeline all linages could be considered invasive.

Invasive species is defined by the USDA as:

non-native (or alien) to the ecosystem under consideration and,
whose introduction causes or is likely to cause economic or environmental harm or harm to human health.

Under this definition, a species that was labeled 'invasive' will lose the label when it stops causing harm. Although I can think of no examples, in theory an ecosystem could stabilize into a new state after an invasive species causes significant disruptions, which would cause the invasive species to lose the label.
Personally, I really like this definition because it differentiates between non-native species that integrate into an established ecosystem (e.g. coyotes in Eastern US) and non-native species that disrupt an established ecosystem (e.g. rodents in New Zealand). While the former is a natural and healthy biological process, the study of which dates back to island biogeography in the 1800's, the latter is a damaging process almost always caused by humans.

In any field, some terms may be defined within the context of a particular research study. The same goes for conservation biology, where definitions may reflect the specific goals of a conservation plan.
NPS defines "native species" as, "All organisms that have occurred, now occur, or may occur as a result of natural processes." (Source). So if something is introduced by humans or because of human activity, it's never considered native by NPS. Also, Non-native species are not necessarily considered invasive (most are probably not).

Essentially nothing since the start of the anthropocene: any invasive organism that owes its transportation and dissemination to human intervention remains forever precluded from acquiring the status of endemism.
There are over 40 million flights per year and 50,000 cargo ships with 11 billion tonnes of goods affecting places like the Galapagos, New Zealand, Madagascar, Hawaii, not only places that were joined during ice ages, so biologists use chronology to label endemism.
From microscopic fungi that decimate forests, tics and mosquitos, the black death (yersinia pestis), covid19, to hippos, pythons and trees, ecosystem breaches are going on at a massive rate of 1000's per century, causing extinctions and ecosystem degradation which is of particular interest to biologists.
Biologists specify times when a species migrates to a new ecosystem, so invasive vs native is a simplified concept of recency. Bears in America 3 million years ago, Dingos in australia 5000 years ago. *quote: The brown bear appeared in eastern Beringia only 50–70,000 years ago.


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Does anyone know what kind of bug is this?
i found these tiny little bugs today all over my windowsill, the walls around the window, and on my chargers in the plugin near the window. they’re like microscopic i can’t even see them. i used a spider and ants spray to kill them, it’s all i had for now. i’ve also been cleaning and wiping my walls down but there’s still a few left. i’m scared they’ll all come back again by tomorrow. does anyone know what they are and how i can get rid of them?

Welcome ca.bus. Could you tell us where in the world you are, what if anything is visible that they might view as a food source. Looks to me like a type of thrip instar, but more info needed, and ID isn't easy anyhow. A close-up picture from on top and another from the side would help if you can get them. Use the [edit] facility to add detail.

Likely related (but awaiting better picture to confirm) : https://biology.stackexchange.com/a/85321/16866

any shipping plans? (asking for a friend)

This is a mite: it has eight short legs and only one body part (in comparison to spiders, which have two body parts). No idea which order or even species though.
Here is an article about indoor mites - maybe "yours" is among them - with some recommendations to manage them.


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Is Acer Palmatum Diecious, Monoecious, or another variety of ecious?
I am compiling information about plants in my garden, and studying botany for interest, and was wondering if anyone knows whether Acer Palmatum (and more broadly Acers in general) are monoecious, diecious, etc.
I found some info stating that Acer Rubrum can be either effectively but not sure for Acer Palmatum. I have not read the journal article yet admittedly, as I am looking for a way to access it that doesn't bust the bank.
Additionally, what is a good source for searching for this information, and other botanical info that might be slightly too niche or specific for general gardening practitioners?
Thanks in advance!


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Which plants are best for experiments about plant growth?
I was assigned writing a term paper about optimizing plant growth using control systems. This assignment is part of a class on sustainable energy usage, which means it's primarily on physics and technology.
I will have to conduct experiments comparing the growth of plants under different conditions and whether or not using control systems are effective (and sustainable) at improving plant growth. More focus will be put on the  technical and energy aspects of this problem but getting the experiments with plants right is important, too.
Unfortunately I don't know much about experimenting with plant growth and most of my decisions would be blind guesses. The experiments should be short term (a couple of days would be ideal, the fewer the better. I do still have three months) and on a small scale in general.
The following are some of the questions I have.

What specific plant or species is well suited for what I am describing here?

What are representative and common measures of plant growth?

What kind of light should I use? I will conduct the experiments indoor to keep the conditions about the same each time.

Additionally, I would be glad if someone could point me to good resources on this topic.

With all those questions, you're essentially asking us to design your experiment for you. You should be talking to whomever gave you the assignment for guidance. We don't know exactly what they want. Also, if you want to measure plant growth over two or three days, you would do well to find a plant that grows, oh, inches a day.

why don't you search some experiments for plant growth science, using related words, and see which cress, elodea, tomatoes, grass, and other species they use for different circumstances.

@bandybabboon First of all thanks for your suggestions  <3. I found it quite difficult to find something on this topic because a lot of what I found was targeted at kids, middle-schoolers and suchlike.

as a pre formal researchg you can try gpt frankly, it's pretty detaild if you make it double check and explain.

Arabidopsis is a common model organism for classroom lab experiments, used because of a rapid growth cycle (days is probably too short, but a couple weeks would work).
It would be suitable for proof-of-concept. However, extrapolation to other plants is going to be problematic. There is no substitute in biology for the "real thing", we don't have laws like physics where you can scale using an equation.

I don't know much about experimenting with plant growth and most of my decisions would be blind guesses

The way to answer all your other questions is to read published papers in this area. You'll want to focus on the methods section - something you may have previously trained yourself to ignore, but it's often the most important part of the paper because it is necessary both to understand and contextualize the results and because it is necessary if you want to build on the work done.
If you want a useful project that goes beyond a classroom-level term paper, you should collaborate with someone who does know much about experimenting with plant growth. If you go on alone, you'll probably learn useful lessons about experimental design, but I'd give it maybe a generous 25% chance that you actually answer something useful to your intended research question. Instead, most likely after 3 months you'll have some failed experiments that taught you about ways that experiments can fail which you can hopefully avoid the next time around.


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Recent developments in the diagnosis of Parkinson's Disease
I was reading a research paper titled - "Discovery of Volatile Biomarkers of Parkinson’s Disease from Sebum" by Drupad K. Trivedi. I am Providing a short summary of it.

Discovery of Volatile Biomarkers of Parkinson’s Disease from Sebum

Parkinson's disease (PD) is a neurodegenerative disease that is difficult to diagnose early. However, a "Super Smeller" individual was discovered who can detect PD by odor alone. Early studies showed that the odor was present in the sebum (skin oil) of PD subjects. In this study, the volatile metabolites of sebum samples from control subjects and PD subjects were analyzed using thermal desorption-gas chromatography-mass spectrometry (TD-GC-MS) and validated by a separate group. The results identified a distinct volatiles-associated signature of PD, including altered levels of perillic aldehyde and eicosane. The odor of these compounds was confirmed by the "Super Smeller" to be highly similar to the scent of PD. Additionally, the study used machine learning approaches to validate the biomarkers. Further analysis showed that the compounds eicosane, perillic aldehyde, hippuric acid, and octadecanal were consistent and differentially expressed between PD and control samples. The presence of these biomarkers was confirmed by the "Super Smeller" through qualitative smell analysis. The study also demonstrated that these biomarkers were not associated with medication use in PD subjects. The findings suggest that analysis of volatile metabolites in sebum could potentially be used as a non-invasive screening method for PD. However, further research with a larger sample size is needed to validate the results and understand the underlying mechanisms of PD-associated odor.
I have read several research papers on this topic, but I am still unclear about the accuracy of these compounds for detecting Parkinson's disease and whether they have been validated in other experiments. I would greatly appreciate guidance from someone with more knowledge on this subject. As part of my college club, I need to write an article on this, and it would be helpful to have more insights.

So - you are at college and you have done the relevant literature search and looked at the paper's references? And what did they say?

Have you searched for relevant papers which cite the Trivedi et al. paper?  A basic such search is easy to do with Google Scholar.  Was the Sinclair 2021 Nature paper of any help?

A small point: the problem with PD isn't so much with the diagnosis as the treatment, although clearly, any approach to treatment may be enhanced by some understanding of the possible implication of these volatile substances in the pathogenesis of PD itself: "the underlying mechanisms etc.''.  So, the matter is certainly worth pursuing from that angle.  Why don't you write to Trivedi himself if only to broaden your perspective?


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Covalent modification of Pyruvate Kinase in RBCs
Human body has 4 isozymes of PK and I am particularly interested in the RBC isozyme.
It is capable of being covalently modified through phosphorylation catalysed by Protein Kinase A which is in turn activated by increased cAMP levels in response to Adrenalin or glucagon.
There is evidence of increased cAMP levels in response to adrenalin stimulation in RBCs as seen in this article: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2269310/
However, this seems counterintuitive because phosphorylation inactivates the enzyme and since glycosis is the sole energy source of RBC's it would deplete it of energy.
Can someone clear this up for me?


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The meaning of atoms sign in protein structure
There are some atoms sign of protein structure in paper, like Nε2， Cε. I know this sign is for information about atoms position, but I don't know the exact meaning. The below is original words in paper, which is about structure of type3 copper proteins.
I need more information about this atom sign system.

This is the "numbering" of the atoms in the amino acids. For this purpose, greek letters are used. This follows the convention that the Cα is the carbon atom next to the carboxylic group. Cβ is the next one and so on.
ε1 and ε2 mark the positions at the end of the ring, which are carbon and nitrogen.
See this picture (from here), which shows all the positions in Histidine:

So here, ε1 is abbreviated as ε. Cε is same as Cε1.

@CharlieXiong Yes.

Examples and references for the atom names are here: https://bmrb.io/referenc/nomenclature/


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What is total body water and why is it inversely proportional to fat content of body?
In my textbook "Physiology" by 'Linda S. Costanzo' its written that total body water is the amount of fluid present in the body. So my question is that is it just the water content it means by "amount of fluid" or it means amount of liquid content within the body (I.e. water, oils etc.)
Secondly, i have no idea that why is it inversely proportional to fat content. Is it because the decomposition of fat release relatively lots of water molecules and thats why its inversely proportional.

Total body water is the total amount or percent of one's body that is comprised of water. It isn't the same as total body fluids, but on careful examination, it's close. For example, the average adult has a blood volume of about 5 liters (there are formulas to calculate more accurate numbers.) Blood is a fluid. It is normally about 55% plasma with the rest being mostly red blood cells. Plasma (also a fluid) is ~90% water and red blood cells   are about 70% water (estimates vary slightly), So while blood is mostly water, blood (fluid) is not equivalent to water.
Most cells have a fairly high percentage of water. The exception is fat cells/adipose tissue. Whereas muscle is ~70% water, adipose tissue is only ~10% water.
Therefore, if, say, 70 pounds of lean human tissue is (say) 70% water, and 70 pounds of (white) fat contains only 10% water, a 140 pound lean/muscular athletic male with 10% body mass comprised of fat will have more total body water (TBW) than a sedentary male of the same weight but with more adipose tissue. That's why the more fat your body is composed of, the lower the TBW.


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Does dopamine suppress serotonin production?
In a youtube video in spanish, I heard that dopamine suppress serotonin production. Is that true?


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What is meant by 20 ul final concentration of polyacrylamide?
I am performing a phenol-chloroform extraction in which precipitation is enhanced by linear polyacrylamide. The SDS for linear polyacrylamide mentions that it should be used such that its final concentration is ~20 ug/mL.
The protocol I am following mentions 20 ul/mL. Page 21, 3rd line of the second paragraph under precipitation.
Am I misunderstanding one or both of these instructions? 20 ul/mL seems like a lot, especially given that it is sold in 5 mg/mL solution (i.e. ~5 ul/mL).
Are they referring to different concentrations, i.e. one is 20 ug LPA/mL extraction volume, and the other is 20 ul 5 mg/mL LPA solution/mL extraction?
Is there a typo in this paper?
Thank you.

Questions here should be standalone, so, ideally you shouldn't have to follow a link to understand what is going on. You should add the quote to your question - that is one massive paper and the link takes you to the webpage, which doesn't have page numbers etc, so you then have to download.

The simplest answer here is that they have made a typographical mistake in the paper and it should be 20 ug/ml.
The other possibility is that they have a stock concentration of this reagent, which they add at 20 ul per ml of precipitation volume - in which case this stock will be 1 ug/ul (1 mg/ml), assuming they use your standard concentration. When writing the paper, they forgot to convert this into standard concentration, probably (in my experience) through familiarity with it noted this way and forgetting to change it.
I note that polyacrylamide is mentioned exactly twice in the paper you linked - once in the text and once in the references, but curiously enough, not in the methods section, only in results. For completeness; the referenced paper1 adds 4 ul (20 ug) to a reaction.
Ref:

Andrea K. Bartram, Calvin Poon, and Josh D. Neufeld. Nucleic acid contamination of glycogen used in nucleic acid precipitation and assessment of linear polyacrylamide as an alternative co-precipitant. BioTechniques 2009 47:6, 1019-1022

Confirmed by the author it was a typo. ug was meant not mL.


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At what point does the capability of sexual reproduction diverge in evolution?
I am asking this question as a layman in biology: What the title is supposed to mean is, as a species evolves, say humans and chimps from its common ancestor, at what point and why are humans or chimps not able to reproduce with it's common ancestor anymore? I'm asking this because two very different looking dogs can still reproduce, so how long would we need to keep breeding dogs until the resulting dogs can't reproduce anymore with the "older" dogs?

Your analogy here is a bit flawed - it is more like current dogs unable to breed with current dogs - which already happens. Very large dogs can't physically breed with very small for instance. The small males can't get up that high physically and the small females can't carry or birth the cross-breed pups as they are too large.

Does this answer your question? How many generations does it take for one species to become a new one?

Zooming out a bit, biologists are usually interested in what practically stops gene flow, not whether gene flow is technically possible or not.  A good example of this is chipmunks on the north and south ridges of the Grand Canyon, USA.  A human could pick up a few chipmunks from the northern side, bring them to the southern side, and they'll breed perfectly fine with the local population.  But in real life, chipmunks cannot naturally cross the canyon and so there is actually no gene flow.
Now to answer your question about when it's literally impossible for two different populations to mix and have children, it's always genetic.  There is simply too much genetic difference between the two species to have a viable offspring. A great example is mules, the offspring of horse and donkeys.  Horses have 64 chromosomes, and donkeys have 63, which is a different number.  For the first generation of mules, it just so happens to not matter. But the dissimilarity prevents mules from breeding and having offspring.  Between any pair of species, there will be genetic differences, and at some point, the genetic differences just become too great to allow reproduction.  For example, you could never cross a horse with a plant because they are simply too incompatible.  However, there is no one compatibility issue that is always responsible.  Different species will have different issues.  It is not always having a different chromosome number.

worth noting chromosome number is not enough several species have different chromosome numbers within the species. like everything in biology its messy and blurry.


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

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

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

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

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

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

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

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


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What's a name for this type of setae on a crayfish
What's a name for this type of setae? It's found an the base of the antennal peduncle of a crayfish. They are roughly cone shaped. They look like spines but are flexible. Would they simply be called conical setae?


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Identification of Bone like subject found on Beach in santa cruz ca
I found this at the Beach in Santa Cruz California, it is about 2 inches long and at its widest it is about 1.5 inches wide and it weighs 3 grams, and I'm not sure what it is, Google Image search suggests a dehydrated ducks Foot, it looks more like a fin from a fish or something or at least part of one. Does anyone have any ideas of what it could be? (All images are of the same subject)