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How can combusted methane from landfill samples be quantified?
Background:
For my studies I'm wanting and attempting to make a landfill greenhouse gas emissions (GHG) model that predicts the amount of greenhouse gas equivalent emissions ($GHG_{eq}$ [tonnes/year]) by analysing a series of landfill core drill samples and extrapolating the data to predict how much GHGs would be produced if the samples can be representative of the landfill as a whole and allowed to naturally degrade. Note that this comes with the assumption of minimal heterogeneity which I know is not the best assumption for most landfills but I'm hoping to get a LOT of data (it's better than nothing).
As the most notorious GHG from landfill is methane, I'm going to simplify this question to just predicting the amount of methane which would be produced from the (combustible) material in landfill assuming it would just sit there forever.
Note that I have cross-posted my question from the chemistry stack exchange.
The Data:
I have this data which is the average of 3 landfill drill core samples and shows the type of waste which has been calculated from sorting and weighing different types of material found in landfill (Table 1) and the chemical composition and high heating value (HHV)/calorific value of the material (Table 2) which I've had tested in an independent lab. For Table 1, an assumed "type" of plastic, rubber, wood (etc.) is made with a constant chemical composition to simplify the model (although I do recognise that there are many different types of plastics and woods etc.).

The Method (?):
I've seen the generic methanogenesis combustion reaction as:
$$CO_2 + 4H_2 \longrightarrow CH_4 + 2H_2O$$
I've also seen an elemental formula for hydrocarbon combustions along the lines of:
$$C_xH_y + (x + \frac{y}{4})O_2 \longrightarrow xCO_2 = \frac{y}{2}H_2O + Heat + Light$$
I know how to calculate the conversion rate going from any GHG such as $CO_2$ or $CH_4$ to $GHG_{eq}$ but it's this first step - the predicting of the GHGs themselves with what formula - which I'm lost at.
The Questions:

How can I calculate $CH_4$ from landfill samples with the attached data and which reaction should be used?
(Bonus) What other considerations should be accounted for with any of the other data? (e.g. the Sulfur going into $SO_2$ emissions (etc.)).

If this doesn't work on biology, try [sustainability.se] or [earthscience.se], though it's unclear to me where this question fits best. Please take the tour, read the help centre before posting etc..

Sounds like an interesting project. Is your aim simply to utilize existing models to predict methane production from this landfill, or to test different models with empirical experimentation? After a quick web search, I found several reports on methane production from landfills or municipal solid waste. Several of them cited the IPCC First Order Decay (FOD) method, which should be accessible online. Also saw at least one cite the LandGEM model, accessible on the US EPA website.

Hmmm, I suspect this will be much much harder than you think. You would need to know the decomposition rates of each of the different carbon sources, and the biological utilization under the different conditions. You might be able to get some sorts of models for some plant-based waste from industrial composting studies. You should also note that paper ~= wood, as it's almost entirely made from cellulose derived from wood, and how do these differ from "organic"? To a chemist organic means carbon-based - including plastics! It has no special meaning in biology other than in farming/production.

@MikeyC I saw the LandGEM model and some other (licenced) ones online but I'm really looking to make a model from the ground up to be honest, that way I can fully understand what's going on. If it indeed becomes too challenging then I'll try and look for another model.

@bob1 Yes I'll need to make some assumptions certainly, great points. But rather than focusing on the scope of the whole landfill site as it's certainly too broad, what about the specific landfill drill core samples themselves on a case-by-case basis? Then I can process multiple samples and plot the heterogeneity.

Why would you reinvent the wheel? Real people doing real work with landfills in the real world are using existing models. It seems your first step should be not to build from the ground up but to understand the existing models, and only propose changes if you can find an improvement.

I’m voting to close this question because it is cross-posted across the network here ansd here with an upvoted answer at Chemistry.SE.

Good point Bryan. @AliceD I have not declared any answer as correct yet, this question is not solved. I also upvoted the answer here? Im still processing answers. There have been brilliant other insights I've had from posting on other stack exchanges which you are limiting by closing this thread for unsubstantial reasoning. You are preventing dialogue and thus critical thinking capability.

Cross-posting across the SE network is discouraged network wide. FWIW: I flagged the other cross-post as well for mod attention. In the future, please post a question only on the most suitable site. The community will then decide whether it's appropriate. If not, it can be migrated.

Why then did the mods from chemistry stack exchange request me to post to other stack exchange websites? Logic doesn't add up.

Methane production in landfills is a biological process that is carried out in 4 steps: hydrolysis, acidogenesis, acetogenesis and methanogenesis. In the first step, organic matter (for the sake of the this argument, let's consider carbohydrates, fat and proteins) is hydrolysed into less complex compounds (monosaccharides, fatty acids and aminoacids). In the second step, these compounds are fermented into fermentation products (FP) such as acetate, propionate, butyrate among many others; in the third step, the FP are converted by acetogens into acetate, which is converted into methane by methanogenic bacteria in the last step.
Each of the 4 steps mentioned are carried out by different bacteria and they also release other gases such as H2 and CO2 that can be used to produce methane, or are simply released to the atmosphere. Because protein contains nitrogen and sulphur, other gases can be produced (e.g. NH3, NO2, NO3, H2S, SO2, etc..). The process as while increases in complexity when others less prevalent organic compounds are considered, or simply by taking into account other materials that you mention in Table 1.
To answer your questions, I don't think you have enough information to build your model. Considering that more than 50% of your waste is organic, I would find a way to fractionate it into the 3 major components. From there, in the literature, you can find plenty of data regarding the conversion of waste into methane and what you could expect in a landfill with similar composition. Of course, ideally, you would even get actual data from similar landfills to feed your model. A similar process could be done to the other materials that are dumped into the landfills you are studying. The more you fractionate and the more you can estimate how much methane comes from each fraction, the less error your model with have in the end.
As for the sulphur, as far as I know, most of it will come from the metabolism of protein, so if you can measure the amount of protein that is dumped to the landfills, then you will be able to know how much SO2 is expected to be generated (again, there should be literature available regarding how much it is expected).
Good luck with you project.


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Does the body make alterations to fatty acids before their storage?
I was wondering if you would be at all able to help me with some questions I can’t find the answers to. I’m a first-year uni student doing some research for the fun of it but I’m really struggling to answer some of the questions I’ve thought up and would greatly appreciate any help!
I’m trying to research how the body stores the fat it consumes. I understand that fat is stored in adipocytes as triacyl glycerides (TAGs) but I’m trying to find some information on which fats the body stores.
For example, if you were to consume some olive oil (oleic acid), would the body synthesise TAGs from the oleic acid or would the body convert the oleic acid into another fatty acid before this step (like palmitic acid)? Does this have any impact on the body’s ability to store fat (or the energy density of the fat?)? Does the body have a preferential approach to the storage of saturated vs unsaturated fats and are these fats stored in different places preferentially?
I’ve read through 9th Edition Biochemistry by Berg, J et al. (2019) which is where I raised these questions from. I’ve also looked through 3rd edition Molecular Biology and I’ve read a few papers on Google Scholar but none of them had the answers I was looking for.
If anyone would be able to offer any help, I would be eternally grateful Thank you in advance!
Mason

The books you have consulted may be good for certain things, but not for mammalian energy metabolism. Older books such as Lehninger are more suitable. Looking at the really old literature (1965) some fatty acids will be oxidized to acetyl CoA, whereas others would appear to be utilized directly. If this is your research project you need to start with this older work (https://link.springer.com/content/pdf/10.1007/BF02636928.pdf) — use your university library to access it — and search for more sophisticated recent studies on Google Scholar using a query like "fate of dietary fatty acids".

source: Stack Exchange

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

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Where in the cochlea are frequencies below 200 Hz detected?
I understand that different frequencies are detected in different positions along the cochlea.
I'm also aware that the range of human hearing is roughly between 20 Hz and 20 kHz.
However, looking at the below diagram, the lowest frequency, at the end (apex) of the cochlea, 200 Hz is the lowest frequency.
Hence the question: wwhere or how are the lower frequencies (between 20 Hz and 200 Hz) detected?

The answer is two fold, each related to the two ways pitch is encoded in the inner ear. These two mechanisms are place coding and rate coding.

Regarding place-pitch; given that there are hair cells tuned to frequencies lower than 200 Hz, it's not surprising that your linked image is incorrect. Below are 2 (random) figures drawn from the internet showing the human tonotopic map that do show the lower frequencies:

Regarding rate-pitch: at low frequencies, say from 1 kHz and below, the auditory nerve is more and more able to phase lock onto the stimulus. Because of the refractory period of auditory nerve fibers of a few ms or so, this process becomes more pronounced at frequencies below, say, 500 Hz. In guinea pigs phase locking (e.g., Stronks et al., 2010) becomes apparent at higher frequencies than in humans. This rate pitch coding still is most pronounced at the place where the frequency of the tone stimulus matches the characteristic frequency in the cochlea, yet because of the high frequency tail (see the other answer from Bryan Krause), it may occur at other places as well at high stimulus levels. Phase locking is thought to contribute to pitch perception, although it's a matter of debate.

In cochlear implants, for instance, rate coding could be easily implemented, yet in most systems speech coding is based only on frequency mapping based on place-coding by placing electrodes at the corresponding frequency bands in the cochlea. Cochlear implants, in a nutshell, bypass the degenerate hair cells in severe-to-profoundly deaf ears by directly stimulating the auditory nerve. They consist of an implanted array of electrodes in the cochlea (for place coding), and an external speech processor converts speech into a number of frequency bands equal to the number of electrodes to be able to place-code different frequencies along the tonotopic cochlear map.
Reference
- Stronks et al., Hear Res (2010); 259(1–2): 64-74

Fig. 1. Human tonotopic map. source: Cochlea.eu

Fig. 2. Human tonotopic map. source: Abdulla, Audio Watermarking for Copyrights Protection, 2007

A figure like this is likely representing the best frequency for hair cells. In actuality, cells respond to a broad range of frequencies. Perceptual specificity comes thanks to lateral inhibition. Tuning curves look something like this:

image from: http://www2.tulane.edu/~h0Ward/BrLg/AuditoryTransduction.html
The y-axis here is in units of threshold, so a small number means the cell is detecting quieter sounds at that frequency. For example, cell D here has a best frequency around 300 Hz, but was still somewhat sensitive to the lowest frequencies presented (looks like about 180 Hz). You won't see many experimental tuning curves that go below that because a typical speaker doesn't go down that low.
If someone says humans can detect sounds down to 20 Hz, that doesn't necessarily mean any inner hair cell has a best frequency at 20 Hz; if it did, it would probably be somewhat sensitive to some even lower frequencies, too, and you'd have to report a different number. If humans can hear 20 Hz sounds, that just means that for some cell, 20 Hz is on the far left end of its tuning curve, such that a loud enough sound at 20 Hz can be perceived.
You can assume the cells most sensitive to the lowest frequencies are at the apex.

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


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Is it possible to crystallize proteins so that the crystal has a normal concentration of potassium chloride?
I've been learning about protein crystallography, and how crystals are made.  A lot of the crystallization processes involve gradually changing variables (protein concentration, pH, salt concentration, precipitant concentration etc) for example through vapor diffusion in order to drive the process forward.  One of the things I noticed is that it is very rare to see sodium, potassium or chloride ions in the finished crystal structures.  The crystals tend to have a lot of water in them (both in channels between the proteins, and bound to the proteins and visible in the crystal structure) but much fewer than expected visible ions.  Back of the envelope, 0.15M KCl should have one K+ and one Cl- per 11 nm^3 or per 370 waters; in reality there seems to be almost no ions visible in the structures, except strongly bound ions as cofactors like Ca2+, Mg2+, zinc, iron etc. It is hard to tell if that is because the ions are there but not in a periodic structure, or because they are not there; and also hard to tell what the final concentration of ions is.
Is it possible to crystallize proteins so that the crystal has a concentration of potassium chloride similar to that inside of the cell?
Does having KCl (or NaCl) at normal physiological levels prevent proteins from crystallizing at all? (regardless of other conditions)  Or, is this something that is possible but not done usually? (eg in favor of much higher/lower concentrations, or having different ions around)  Or, is this already the usual state for prepared crystals? (but just not visible in the structures because the ions are always disordered)
Additional question: If the effective concentration of KCl in crystals is very different from physiological, does this significantly change the protein structure?  Has there been any study of the change in structure vs type and concentration of ions?


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Do the neurogenic chemicals in mushrooms get transmitted to milk?
In a recent video by SciShow they discussed several studies showing that several compounds in lion's mane mushrooms encourage neuron growth. Do we know if these chemicals get passed into milk if a lactating female consumes them? I'm curious about both human breast milk for supplementation purposes (and possible safety concerns about whether this could cause overgrowth in an already rapidly developing infant brain) and ruminant milk (cows, goats, and sheep for possible commercial applications).
List of sources SciShow used:

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3924982/
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3449638/
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4583117/
https://hrcak.srce.hr/file/52615
https://www.mdpi.com/1422-0067/20/4/859/htm
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5237458/
https://www.jstage.jst.go.jp/article/biomedres/40/4/40_125/_pdf/-char/en
https://www.jstage.jst.go.jp/article/bpb/31/9/31_9_1727/_pdf/-char/en


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Special food for big cat cubs?
For house cat kittens there is special 'kitten food', containing more nutrients than normal cat food in order to compensate for the fact that at pretty much any time of the day kittens spend a gazilion times as much energy as an adult cat would.
I know that most differences between cat foods are mainly marketing aimed at humans, but here there seems to be at least something 'real' about the difference, given that the vet told me not to let the adult cats eat from this high energy kitten food, as it would only make them fat. Also, of course, the claim that kittens spend more energy than adult cats is easily verified by just looking.
So my question is: does this 'special food for kittens because of them being so energetic' have any analogue for big cats such as lions, leopards, lynxes etc? Is the part of the meat that a lioness gives to her cubs qualitatively different (e.g. another body part) than the part she keeps for herself?
(To be clear: the question is really about big cats. When I want to know more about food for house cats the internet is full of information, but I found it hard to find anything detailed on what cubs of big cats eat and how it differs from the food of their adult peers at all.)

The problem with pet food is there is no variety. Humans expect to be able to just give the same thing over and over again. That means a third possibility is the lioness just gives a different part each time (and not necessarily from the same prey species either) with no distinction between adults vs kids. After all, it's not like the cub, or even the lioness, eats every part of the entire animal every time.

Also, wild cats actually need to expend energy to get their food so I don't think it's a fair comparison to compare activity levels of cubs that can play in captivity to adults that don't/can't hunt in captivity. You don't waste energy hunting to eat in excess. It's a lot of pointless work.

https://pets.stackexchange.com/questions/tagged/big-cats

Cat food has a specific a composition, because the suppliers have to keep their products consistent and they are designed to meet the nutritional needs of indoor cats. I do believe that kittens have a higher energy need, but I would argue it's mostly due to development/growth and energy loss (higher surface-to-volume-ratio with a higher loss of heat energy) than their activity. Kitten food is mostly high in fat content (source) to increase the calories, which is the reason it shouldn't be fed to adult cats, who don't need these calories.
In the wild big cats prey on different kinds of animals and eat all kinds of parts of the carcass. The nutritional composition of their food will therefore vary more than for house cats. Adult wild cats will definitely need more calories that a lazy house cat, as they have to hunt, fight and survive. So, a higher energy density would also be beneficial for adults and no difference between them and their offspring has to be made.
I couldn't find any source that lion/tiger/cheetah cubs would eat only specific parts of the prey. Also, mother cats usually don't "feed" their cubs. You would rather see the cubs feeding on the carcass alongside their mother. Several cubs would be spread around the carcass, eating different parts.
I think there is a little misinterpretation in your question and that's the assumption wild cats would pamper their young and rather take less quality food for themselves. If we take lions for example: they have been reported to have a hierarchy in feeding on their prey. The male first, then the females and their cubs. The cubs are last. As they are least important for the survival of the group in times of scarcity in food, mothers will rather let them starve to death than not eating themselves (source1/sci-hub/page 315, source2/sci-hub).
What sounds cruel to us is a survival strategy, since a surviving pack can reproduce again, when food is more abundant, while well fed cubs are doomed anyways, when their mothers are too weak to hunt. As an extreme form of this the parents might turn to cannibalism, which is more frequent in fish (source/sci-hub), while mammals with smaller litter sizes might abandon some of their offspring to take better care of the rest (source/sci-hub).


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chip sequencing
I understand the concepts of steps in Chip-seq up to DNA purification, but I don't get how one can then amplify the purified DNA samples that are once bound to the proteins.... Since sequence-specific primers are needed for qPCR, but you don't know where exactly the protein of interest binds to in the genome (that's why you do a chip-seq experiment), theoretically, how can you design primers to amplify?

Specifically, I am referring to this graphical representation of the steps in ChIP-seq
Image source: https://compgenomr.github.io/book/measuring-protein-dna-interactions-with-chip-seq.html

This question could be reduced more generally to "how does whole-genome shotgun sequencing work?" The problem of translating a high-complexity mixture of naked DNA fragments to a sequencing library is shared by many techniques. I would strongly suggest reading more on the topic of library preparation. Here is one resource.


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What is the actual molecular mechanism for muscle relaxation?
A number of my students asked what happens to the sliding filaments when muscles relax. For example, in an individual sarcomere, do all myosin heads release all at once or one/few at a time?
More generally, what is the process/mechanism by which muscle relaxation occurs? What is actually happening to cross bridges themselves at a molecular level step-by-step from the point of full contraction to full relaxation?
Background to prove prior research: I know that AcH will be removed from the synaptic cleft of the NMJ, ceasing action potential generation due to stopping the influx of Na+. And I know that this causes calcium to stop being released by the sarcoplasmic reticulum (and that calcium pumps are even activated to transport Ca2+ back in). Finally, I know that without Ca2+, troponin moves tropomyosin back over the myosin binding sites of actin.
My question is really focused on what happens next. Some myosin heads must still be bound to actin during and following this process. How are they released? One at a time? All at once?.... What triggers this? (I know ATP will bind to each head causing it to release, but does the body intentionally flood/saturate the sarcoplasm with ATP to cause this to happen quickly, or is there some controlled regulatory mechanism?).
Does an individual sarcomere have a controlled slide back, or does it "snap back" into relaxed state all at once?

You have it pictured correctly. Myosin unbinds spontaneously from actin when it binds ATP which is maintained at near-constant levels regardless of the contractile state. It's the sudden drop of Ca2+ (from pumping into the sarcoplasmic reticulum) that causes troponin to change conformation and (with tropomyosin) occlude the myosin head from rebinding. This is the "steric blocking hypothesis" for how troponin-tropomyosin inhibits contraction. A good reference for this is Ebashi from circa 1960 (mentioned in the Lehman review below).
You have a related and more subtle question about the coordination of this process at the scale of a sarcomere. Because the Ca2+ concentration is globally coordinated between sarcomeres, and because tropomyosin is an elongated protein that connects multiple regulatory regions, the thin filament (actin plus troponin-tropomyosin) switches its regulatory states rather cooperatively, so that the whole muscle fiber switches on and off rather uniformly. This is more subtle and recently characterized structural biology.The most direct evidence for cooperative switching comes from a series of papers from McKillup&Geeves (also mentioned in the review below).
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5479050/


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Black flying bug infestation

What is this black bug in my house. There is literally an infestation. They are everywhere. The size of a small tick. They fly and just keep coming. Im from pakistan, lahore.
I've never seen these before in my life and have lived in this house for over 10 years.

Have you noticed anything about their behavior? Are they attracted to anything in particular? Light, water, food, windows, each other?  Do they stay airborne a lot, for long periods of time, or just "buzz" a short distance before landing and walking around again?


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Does the current phylogenetic system classify only Algae as Thallophytes?
I am studying the current system of division of plants.
While studying Thallophytes, I came across some sources which said that Thallophytes consist of Fungi, Algae, and Lichens. Some others (https://asm.org/Articles/2021/January/Three-Reasons-Fungi-Are-Not-Plants), however, stated that Fungi are no longer considered plants.
My question being, which statement is the truth?
It would be quite helpful if I could get an answer, as none of the sources I have visited are intercepting this problem.
There may also be shortcomings in my knowledge, for which I apologise in advance.


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Does a gene need to be transcribed for every single protein made?
There is one set of DNA in the nucleus and one instance of any particular gene. That gene is transcribed into mRNA and then it is translated by a ribosome. A cell has millions of ribosomes. So it seems strange to me that the cell relies on transcribing this one gene over and over again to get mRNA to supply its excessive amount of ribosomes. I feel like there should be some way to replicate the mRNA after transcription. Otherwise, it seems like it is way too slow and having millions of ribosomes makes no sense.

mRNA is not destroyed immediately after it is translated once. There can be multiple ribosomes translating a single strand of mRNA, as well. Depending on the regulation of the system, a single transcription event (producing one mRNA strand) could produce tens to hundreds or perhaps even thousands of protein molecules.

Image from here, which also provides much more in-depth information and calculations.


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What is the oligomeric state of Leptospira LipL32 protein?
Does anyone know the oligomeric state of the mature and functional lipoprotein lipL32 in Leptospira?
It's an outer membrane-bound protein. In its mature state, the signal peptide (residues 1-20) is removed, and the cysteine (resid 21) reacts and binds with the head group of a lipid. I've looked through many articles, from x-ray to western blots, and although I understand its structure in terms of the single protein, the results from the x-ray crystal data (as per the protein data bank) are my cause for confusion.
These are the results from LipL32 in the PDB. Three different structures, a multi-mer, and two different dimers.
Are these different geometries the result of the experiment, or is the protein's quaternary structure as one would expect in the organism?

If you are going to reference an outside resource, please provide the actual URL so people can see exactly where it goes. Do not use URL shorteners.

@MattDMo done - enjoy.

@AnthonyNash what MattDMo was referring to was to not use 3rd party shorteners. You can still shorten the link using standard formatting: your text (or using the "add link" button in the formatting panel, that way the mouse over works and you can see the link is actually heading to RCSB, and not some dodgy website, which is obscured when you use the 3rd party sites.


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Can the concept of fisherian runaway be explained using simple models?
I want to understand the concept of fisherian runaway. Dawkins' book tells about this, but it's not clear enough. It can be seen that the essence of Fisher's idea is that when a male peacock with a large tail leaves offspring, these offspring receive not only large tail genes, but also genes of “love for big tails” in females. But it is not clear how positive feedback follows from this.
Let's consider a simple model. There are 100 males and 100 females in a peacock population. 80 males have long tails, 20 males have short ones. 80 females prefer long tails, 20 short ones. Further, obviously, 80 first males and 80 first females will give offspring with long tails, and accordingly 20 males and 20 females - with short ones. Thus, in the next generation, 20% of cubs will be born with short tails, and since having a short tail is beneficial from an utilitarian point of view, over time, these 20% will crowd out the remaining 80%.
Now suppose that peacocks are not monogamous, but polygamous. 1 male with a short tail will fertilize 20 females, and 4 males with long tails, respectively, 80 females. So far, nothing has changed.
Now suppose that polygamy is even more pronounced, and instead of 4 males with long tails, the harem belongs to one. And here the principle “for everyone who has will be given more, but the one who does not have, even what he has will be taken away from him”, which Dawkins mentioned, can work. Since this supermale with a long tail has 80 females, the fact of his popularity serves as additional advertising for the remaining 20 females. It works that, when all other things being equal, it is better for a female to choose a male that other females have already chosen (such a principle, on average, does more good than harm). Accordingly, this supermale will have additional females from among the remaining 20.
Is this really all that Fisher's model suggests? This argument seems to me not very convincing. Can someone apply my approach (counting the number of males and females) to correctly explain Fischer's ideas?

Remember that Fisherian runaway is an explanation for a thing that happens; in particular, it explains why it's stable when it happens. It's not a claim that this always happens for all traits.

I don't think the last statement of your second paragraph holds true necessarily. The long tail is obviously useful in that it attracts females, therefore mating, so it won't get out-competed by short tails.

Dawkins and Weinstein discussing the topic.

your numbers don't add up, 80 males have long tails, 20 males have short ones. 80 females prefer long tails, 20 short ones. means way less than 20% of the next generation have short tails, because males don't encounter every female but only a small percentage, a large portion of your short tailed males may never encounter a short tail preferring female. thus many will fail to reproduce, likewise female may fail to reproduce or settle for long tailed males because that is all they encounter.

Now consider the simplest form of this, mating calls, making noise that attracts mates also attracts predators, but not finding a female mean your genes die out so even risky behavior that also increases your chances of finding a female will have huge gains as long as the chance of encountering a female without it is low.


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Odd bugs in terrarium. Harmful?
I noticed these bugs in my terrarium, there is a springtail in the photo for size reference.
I've seen 3 or 4 so far, I'm worried about it out-competing my springtails or possibly being a parasite that will spread to other tanks.  It is shaped like a tick. It's really hard to see but I think it has 6 legs and 2 antennas.
I live in Central Illinois.
I have an African Bullfrog who I occasionally feed live mice, but he is on the other side of the room.
I was thinking that it was probably a mite of some sort. According to an article by the IDPH, the only pest mite in Illinois would be the Clover Mite.  It doesn't look like a Clover Mite, but it does look similar to a predatory mite, like the Amblyseius Cucumeris.

Shaped like a tick; it'll be a mite (also in the Acari with ticks). Which mite would take microscopic examination, unless it were the red velvet mite, which are quite obviously red usually.

Do you have birds or rodents in or nearby the terrarium? Even perhaps outside a nearby window?

@theforestecologist: I have an African Bullfrog who I occasionally feed live mice, but he is on the other side of the room. To bob1: I was also thinking that it was probably a mite of some sort. According to an [article] (https://dph.illinois.gov/topics-services/environmental-health-protection/structural-pest-control/occasional-invaders.html) by the IDPH, the only pest mite in Illinois would be the Clover Mite. It doesn't look like a Clover Mite, but it does look similar to a predatory mite, like the Amblyseius Cucumeris.

Welcome to the site; in the SE model, the answer box is only for answers, this isn't a "forum" site where posts make a long chain from oldest-to-newest or vice-versa. The best way to respond to comments asking for clarification is to [edit] your post to include it.

It's definitely a mite. My questions were trying to determine if it was a bird mite or related. Without better picture and more info, it's unlikely you'll get an accurate and more precise answer


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What is the the meaning of Coordinated effects in genetics?
I want to find the definition of Coordinated effects
in the paper enter the matrix link the author defines "Complex biological process" as

coregulation or coordinated effect of multiple molecular species resulting in one or more phenotypes. Examples can range from activation of multiple proteins in a single cellular signaling pathway to epistatic regulation of development.

I gathered that coregulation refers to the Transcription coregulator link

In molecular biology and genetics, transcription coregulators are proteins that interact with transcription factors to either activate or repress the transcription of specific genes.

But the term coordinated effect eludes me. Does it refer to the Coordination complex? And what is the context in biology? Several papers mention the coordinated effect but fail to define what it is.
Biology and genetics are new to me; I need more understanding of the general field. Naturally, the term might be standard, but it is just puzzling.

You deliberately omitted the second half of the author's definition: "Examples can range from activation of multiple proteins in a single cellular signaling pathway to epistatic regulation of development." If you are right, that the term is only used by these authors, then what is your problem? Within this paper, just stick to the author's definition.

Quite the assumption that I deliberately did that. That I would say is quite presumptuous. Moreover examples are not definitions. They might outline key factors but this is no definition

You're right, examples are not definitions, they're usually better than definitions.

It's the definition the authors use in their glossary, which itself is defined to be a collection of definitions (https://en.wikipedia.org/wiki/Glossary). Ergo you only provided half of their definition, which is a misrepresentation. I didn't say that you deliberately misrepresented the authors, simply that you deliberately omitted part of their definition. I don't see how you can argue against any of this.

Interesting point. My questions was not the term "Complex biological process" but the term coordinated effect. Even with brain krause comment an example is better than a definition. my argument still holds that the term coordinated effect is not defined in the paper and merely an example was given. Finally, arguing that examples are better do not help the reader understand the term. @acvill actually explained the term in the context

Coordinated, here, does not connote any special meaning above that of its English definition, nor is it referring to coordination complexes. Consider one of the definitions of coordination from OED:

Harmonious combination of agents or functions towards the production of a result

In your linked paper, the authors are using coordinated effect to refer to the cooperative or synergistic influence of multiple molecules or processes on a phenotype. I think this is most easily understood in contrast to the simple models of genotype-to-phenotype mapping that are often taught in introductory genetics courses, i.e. a single gene variant encodes a single factor that produces a fixed phenotype. A complex biological process is one in which the abundance, activity, and localization of different molecular components have an effect on the magnitude of a phenotype.

cheers! very well put. clear, concise and nicely outlined with comparison to the English dictionary. There are still concept that need to be explored but an overall great outline.


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Cut plasmids with unknown sequence only once
Is there a way to linearize plasmids in a sequence-independent manner?
The circular plasmid should be cut ideally only once. It does not matter where. But as soon as it is linearized, it should not be cut any more.
We are talking about plasmids up to about 20kb.

Do you have any information on your plasmid?

The method should not be dependent on the host/origin or on any other characteristics. It should work for bacterial plasmids, constructs, etc. So basically as long it is circular double stranded DNA the approach should work.

When you write "it does not matter where", does that mean it can cut in the insert of a recombinant, or is it necessary that the cut be in the plasmid vector itself?

@David Yes, it can cut the insert as well. It really does not matter where in the plasmid.

Ok. Well, I think my answer is ok. If it had to cut the plasmid you might have to engineer a DNAase attached to a protein that specifically binds to the origin of replication or the like — a major undertaking if it doesn’t already exist.

I was going to write a facetious comment asking if the poster believed in fairies, but I restrained myself. Why? 1. because it would not have been nice, 2. because it occurred to me that there was a hack you might be able to use to do this:

Let Nature do the work for you.

Long, long ago, I used to do DNA cloning myself, and so I frequently ran plasmids on agarose gels. I have lost most of the photos, but I happened to contribute a chapter to a text book in which I presented an example, so I reproduce a photo below:

What this shows is that in practice (at least they way I did it) a plasmid preparation does not consist of just a single band representing supercoils of the double-stranded closed circular DNA. Typically, and to varying degrees, there are two more species produced by shearing (or perhaps slight nuclease contamination) — relaxed nicked circles and doubly-nicked linear species.
The linear species would appear to be what the poster wants. (He doesn’t say what he intends to do with it, so I can't be sure.) If so, the band in the gel could be cut out, placed in a dialysis bag in suitable solution, and subjected to an electric field, when the DNA will be removed from the gel into solution by electrophoresis. (I can’t remember the details of the latter. I used to do it routinely, so it should be well documented on the Internet, and there may well be modern, more efficient ways of retrieving DNA from agarose gels.)
But if you wish to improve on Nature…
The proportion of linear species in the gel above is relatively low, so one might wish to go one better. In fact my original thought was to use low concentrations of DNAase calibrated to produce just the two cuts that would generate linear species, before I realized that there was probably no need to go to the trouble of calibration as plasmids contained nicked linear species already. There are many commercially available non-specific endonucleases such as bovine DNAase I that I imagine one could use. I am not quite sure how one would terminate the reaction and inactivate the DNAase. Heat perhaps; one could check how this is done in other procedures like footprinting.
It is possible that the nicking is caused by physical shearing, in which case one could perhaps vortex the plasmid to increase this instead of using DNAase.
The general idea of calibration to obtain the ‘right’ incomplete reaction is seen in the chain-termination method of DNA sequencing, for example. Any incomplete reaction will always give a range of species, of course.


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Is there such a thing as 'genetic memory'?
I have come across the concept of genetic memory in two books I recently read:

In the book 'Call of the Wild' by Jack London, a dog called Buck has memories of a primitive hairy man who presumably domesticated one of Buck's ancestors.

In the book 'Congo' by Michael Crichton, a female gorilla called Amy draws pictures of places from 'genetic memory'. The author goes on to say,

Genetic memory was first proposed by Marais in 1911, and it has been vigorously debated ever since.

To me, this sounds a bit like Lamarckism, which we know is incorrect. So is there such a thing as 'genetic memory'?

"The Call of the Wild" was written in 1903, at which time little or nothing was known of genetics. Presumably the author was extrapolating from the idea of animal instinct. "Congo" was written later (1980) but as a science fiction novel. And fiction it certainly is: the idea that memories can be passed on in one's DNA is complete nonsense.

I want to emphasize that actual memories passed on genetically are pure fiction as far as we know. However, there are genetic markers such as methylations, induced as a part of stress responses, that are thought to be inheritable, but they do not cause actual memory, just induce different cellular responses in the person inheriting them.

Certain innate animal behaviors could be rationalized as a kind of genetic memory, just not in the sense described in these passages. Domesticated dogs may instinctively fear strange people approaching their social unit, leading to aggressive displays towards strangers. Drawing pictures of specific places may seem far fetched (and was certainly fictionalized in this case), but there are some complex behaviors driven by genetic instinct. Food caching (and recovery), nest building, courtship displays, parental care, some migration patterns, and even communication behaviors.

You may want to read this

It's probably worth mentioning that genes are precisely "memory", but in a different sense to what is implied by the common usage. Genes are memory of all the past evolution.

I recommend looking into "transgenerational epigenetic inheritance", see for example here. It's possibly the closest thing to what you mean, but it isn't "memory" in the way that you mean.

There is an accepted form of "genetic memory" known as "epigenetics (wikipedia)", provided the concept is applied in accordance with scientific guidelines.
For example, from this study, we learned that

Epigenetics is the branch of genetics that studies the different
mechanisms that influence gene expression without direct modification
of the DNA sequence. An ever-increasing amount of evidence suggests
that such regulatory processes may play a pivotal role both in the
initiation of pregnancy and in the later processes of embryonic and
fetal development, thus determining long-term effects even in adult
life.

In simple words, a mother's (especially, during pregnancy) experience may  "carry on" to, and affect  her child's future (through epigenetics). But nothing so specific as a hairy man or a scene etc.
Further detailed information can be found in a vast amount of literature e.g., in this review, the author concluded

In C. elegans, the transgenerational inheritance of
temperature-induced changes in the expression of heterochromatic genes
was associated with altered trimethylation of H3K9 over fourteen
generations. In addition, H3K9me3 is critical for establishing
heterochromatin and essential for normal meiosis. Gestational
exposure to bisphenol decreased H3K9me2 and H3K9me3 in germ cells of
the neonatal testis., suggesting a possible role for these marks
during early developmental stages.

Please cite one specific molecular aspect of a mother’s “experience” that is passed on in the manner you state, describing the mechanism.

@David I found some more illustrations, but I believe the reader would benefit more from reading the original research articles (many of which were published on high profile journals like Nature and Science) listed in the review.
I've read over a few pages and concluded that the QA format on Stack Exchange is not suitable for scientific publications.


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What kind of bug is this? I’m not sure if it’s a cockroach
Found this bug in my home. Is this a roach?

Welcome to the site. It is almost impossible to say from your photo as the main features are obscured, the subject is badly lit and the body is distorted (crushed?) If you had better photos we might be able to tell. Would also need a location in the world to help ID.

Rove beetle possibly.  Not sure though, and if so it's not clear what kind of rove beetle - it's a large and varied family, and the picture is a bit smudgy.  They seem to usually be harmless/not a pest species, and occasionally wander into houses from outside.  https://en.wikipedia.org/wiki/Rove_beetle
Doesn't look like any of the types of cockroach I found pictures of on a quick search.  It seems that there are several unrelated species called "cockroaches", but all of them seem to have plain antennae, not "beaded" ones like the insect in your picture, their heads are a different shape, and most of them aren't visibly segmented like that.  https://en.wikipedia.org/wiki/Cockroach
You might have more chance of finding out whether it's a cockroach just by typing "cockroach" into a search engine and looking at some of the image results than by posting here.  I mean, you've got the insect (or had at the time) and we haven't, so you can see it better.

My impression is also Rove Beetle of some kind.  The big beetle head and mandibles. the smallish partially deployed wings, exposed abdomen and "hunchbacked" look lean in that direction.  However, it's not clear if some of these apparent points are simply artifacts of the squashing it underwent, so that's just an impression.


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Inferring mother's allele probability based on father and children
I am currently in the process of analyzing our family's genome. I do have access to his, mine and our father's genome, but not to our mother's (deceased). I was wondering how I could combine our 3 genomes to infer information about our mother's.
With regard to two different genes I am faced with these two situations:
Gene 1:

Father: GG
Brother: GG
Me: GA
Mother: Likely AA, less likely GA but most likely not GG or otherwise I would also have GG?

Gene 2:

Father: GG
Brother: GG
Me: AA
Mother: No idea, if she had GA I would have at most GA, if she had AA my brother shouldn't have GG. Does this mean a mutation is involved?

Thanks in advance!

Gene 1: Mother was almost surely GA (she couldn't had been AA because then both children were GA). Gene 2: Mutation or some other non-Mendelian inheritance or ... well ... different father.

In a basic biology class one of the first steps in understanding Mendelian inheritance is always building Punnett squares. I recommend you play around with those, with all your different guesses about mothers, to figure out what makes sense and doesn't. You'll learn more that way than asking someone else to give you the answer.

need to consider haplotype  (https://www.nature.com/scitable/definition/haplotype-haplotypes-142/)


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What is the share of body energy that the brain consumes? Is 20% reliable?
"20% of the energy at only 2% of the weight" is a frequently regurgitated factoid. More precisely, it should read: 20% of oxygen consumption.
The problem starts when one looks into the source experiment. The Wikipedia article on the brain offers Mink et al. 1981. Unfortunately, that paper merely summarizes the data of others and itself references the ancient 1957 paper by Kety, The general metabolism of the brain in vivo (reference 50). Alas, Kety again only summarizes the data of yet others from the 40s and 50s (see table 1). So, we have a horrible case of he said, she said.
Does anybody know of a more recent and more reliable study that estimates the % of energy consumed by the brain?


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What is the latest possible point during a pregnancy when a fetus can merge with another fetus?
Background
A Chimera is an organism that is composed of two or more zygotes.  There are several documented incidences of this happening in humans as shown in the cited link.
Since chimeras primarily arise early in pregnancy when one fetus absorbs another, I wanted to know....
Question
What is the latest point in pregnancy at which a human fetus can absorb another human fetus?


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Bone found on uk beach
I found this bone on a uk beach. Looks like a hip or shoulder.
It has saw marks in so didnt die of natural causes. Anyone know what its from? Maybe cow or pig

Please update with more info. [Edit] your post to include dimension measurements, more precise info about the location you found it (e.g., more specific beach, surrounding landscapes/habitats/land use, where on the beach it was found), and also include more photos. This additional info is needed to receive a more accurate answer

It's the right hip joint from a cow pelvis that has been well worn by the stones on the beach.
A cow is a mammal often used for milk which lives in fields, they have 4 legs and 2 horns and say moo.

+1 for clarifying cow.


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Does centrifuging and filtering supernatant confer an advantage compared to just filtering?
We are trying to isolate bacteriophages from environmental soil samples. One of the first steps is elution, centrifugation and filtering of the soil samples.
One protocol suggests to:

Elute the soil 1:1 with buffer solution. (e.g. Phosphate buffered saline)
Manually shake the tube a few times.
Let it settle overnight at 4°C
Centrifuge 3x 10 min, 5000g at 4°C
Prefilter supernatant with 16 um cellulose
Filter with 0.22 um PES filter

The suspended soil will settle somewhat overnight. In the paper they state:

In this optimization protocol, any filtration attempt with pore size < 16 μm was impaired if the single (Fig. (Fig.1,1, route 1–4) or united (Fig. 1, route 5–6) supernatants were not centrifuged thrice at 5000×g for 10 min beforehand.

When we do this same protocol, we find that in most samples the supernatant can be pushed through a 0.22 um syringe filter  without clogging even before centrifuging. Since centrifuging does take a while when processing many samples, we are considering skipping this step.
Now, is the purpose of centrifuging the eluted sample solely to make filtration easier or are there any other advantages to centrifuging when attempting to isolate bacteriophages?

This is the sort of thing you need to use your own common sense for. You have soil you want to get rid of. Centrifugation will do that efficiently and in bulk. But perhaps it is a problem in the field, and in any case you need to filter smaller particles. If you can kill two birds with one stone, fine. If clogged membranes are a pain, not fine. That’s my take, knowing nothing about isolating phage. But I’d try what was most convenient and see if it worked. The main thing is to think about what is going on.

After having read up on this subject and successfully isolated phages from soil I can say fairly confidently that centrifugation can be skipped unless the sample is very dirty and clogs the filter.
For example, here is a direct isolation protocol from soil that does not use centrifugation but lets the sediment settle for 10 minutes before filtering the supernatant.


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Is there non-coding DNA common to all living things?
I saw the question asked about proteins common to all life, and was happy to see there are proteins common to all living things. Similarly, I wonder if there are portions of non-coding DNA that are common to all living things too.
PS  This was NOT a homework question as the feedback indicated.  I was curious to know and didn't know where to turn so I asked Stack Exchange.  I am not a student, just a person who wants to understand life better.

Relevant link https://en.m.wikipedia.org/wiki/Conserved_non-coding_sequence

There is an answered question about such conservation in eukaryotes here: https://biology.stackexchange.com/questions/2607/ . An intelligent reading of the answer suggests why this is unlikely to extend to prokaryotes.

@Jon unfortunately on SE.biology there is a confusing close vote reason which uses the term "homework" to really mean 'under researched'. I know that is confusing and irritating when your post gets closed using that reason when it is not a homework question. My advice would be to google around for an answer, show what you found and what you didn't understand, and then hopefully the question can be reopened. perhaps start with the wikipedia link I shared in the comments.

Thanks for explaining.  I did google around but just missed the answer I guess.  Anyway, no need to reopen since your comment pointed me to the answer.  Thank you!


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Please identify hard hollow structure found on beach
This washed up on the shore in NJ last week. It looks like a molar but I cannot find anything similar
1.75” across about 1/2 high. It has a weird indent too

Most likely a shell. We would need some sort of scale for size and photos of other surfaces for full ID.

StackExchange works differently from other sites: the answer box is for answers only, it's not a forum with a string of posts replying to an original. If you need your accounts merged you can use the "contact us" link at the bottom of the page or https://biology.stackexchange.com/contact If you have new content to add use the [edit] feature.

Is it actually bone? all kinds of weathered junk washes up on NJ beaches

IT could be an old ceramic tube like a piece of a clay bottle, a weight for a net from an indian.

The most defining thing is the holes on one side, it has a hole in the top too. Use reddit or FB fossil ID or what's this fossil or fossil forums they specialize in weird beach finds.

https://www.reddit.com/r/fossilid/


text:
Is atmospheric nitrogen chemically necessary for life?
It is my (very basic) understanding that neither plants nor animals utilize the nitrogen in the atmosphere.  Humans do not make use of atmospheric nitrogen through respiration and plants do not extract nitrogen from the air, but rather from the soil.  First of all, am I correct in this understanding?
If I'm right so far, then what role (if any) does the nitrogen in our atmosphere play, biochemically speaking?
I understand that it plays a significant physical role, contributing to air pressure, allowing light to permeate, allowing liquids to exist on the surface, burning up incoming meteors thus protecting life, and basically being a physical gas that is not oxygen or carbon dioxide thus keeping the concentration of those gasses low.  But I'm interested in the biochemical use of atmospheric nitrogen if any.  So, is nitrogen a necessary atmospheric component for life, in terms of its chemical reactions with living things?  Or is the atmospheric nitrogen essentially unused in the chemistry of life?

Nitrogen is a necessary part of amino acids which are building blocks for proteins. Animals get this nitrogen from eating plants, plants get them from symbiotic microorganisms and those germs get nitrogen from the atmosphere. So we do need atmospheric nitrogen in order to make meat.

https://en.wikipedia.org/wiki/Nitrogen_fixation

@slebetman. Nicely put, but there is also the Haber process (industrial N2 fixation) without which agriculture as we know it would be very different. As the quoted wikpedia article puts it: "With average crop yields remaining at the 1900 level the crop harvest in the year 2000 would have required nearly four times more land and the cultivated area would have claimed nearly half of all ice-free continents, rather than under 15% of the total land area that is required today"

To get soil nitrogen in the first place, nitrogen fixation is necessary which takes atmospheric N2 and converts it into biologically useful forms.
Nitrogen fixation is performed by bacteria and archaea. You may occasionally hear about nitrogen fixing plants, especially peas and beans in an agricultural context, but these involve symbiotic relationships with bacteria that do the actual work.

There could be a planet with life based on non-atmospheric nitrogen compounds - but I suppose life would eventually "realize" it could get a whole bunch of energy by "burning" them to get gaseous nitrogen, thus filling the atmosphere with it?

@user253751 I haven't yet found any other planets with life so I'm stuck with this one for observations about how these things work.

@user253751: No, the reduction of nitrates to nitrogen and oxygen is endothermic and does not gain energy by itself. But some lifeforms can use nitrate to oxydise something else and gain a bit of energy this way.

@jk-ReinstateMonica And yet, life does finds a way to burn non-atmospheric nitrogen compounds to get energy and nitrogen gas: anammox. https://en.wikipedia.org/wiki/Anammox
One can, however, imagine an anaerobic, hydrogen-rich world where nitrogen is mostly in the form of ammonia/ammonium, and perhaps there's no energetically favorable reason to transform it to N2. In such a world, you'd be unlikely to come across nitrate, and if an organism did find or generate some, it would be more energetically rewarding to use it to oxidize hydrogen to form water and ammonia.

@BrendanFurneaux: Ammonium Nitrate is a quite unusual compound (even an explosive) consiting of reduced and oxiydised nitrogen in one salt. Of course you can use nitrate to oxydise ammonium and gain energy, this is no contradiction to my previous comment.

I'm surprised: Are you saying that without life, there would not be a substantial amount of nitrates on Earth? (I'm not skeptical but merely ignorant ;-). )

@Peter-ReinstateMonica There are other sources, like lightning, and nitrates for fertilizer are made artificially using Haber–Bosch, but yes my understanding is that most nitrate on Earth has a biological origin, though it's also used by biology, so it's quite possible there'd be as much or more nitrate from other sources if there was no biology - this I'm not sure about.

@BryanKrause Nitrate (dissolved in water, not as concentrated nitric acid of course) is thermodynamically favored compared to a blend of oxygen and nitrogen gases in the atmosphere, so in the absence of life and over geological time, we would expect all of the oxygen in the atmosphere to react with nitrogen to form nitrate.  However, I expect the nitrate itself would further react to oxidize other compounds dissolved in the ocean.  But the elephant in the room is that the free oxygen was generated by life, and most/all nitrate on Earth is generated by a reaction involving free oxygen.

@jk-ReinstateMonica Your statement started with "No", in response to user253751' s question about whether life would "burn" non-atmospheric nitrogen compounds to form nitrogen gas; I provided an example of that actually happening, which is furthermore a major part of the nitrogen cycle on Earth.  You focused specifically on nitrate, rather than ammonium, but that's not what the original comment asked about.  As for ammonium nitrate being an unusual compound -- as a pure salt, sure.  But it's not so strange to find the two ions dissolved in the same water.

@BrendanFurneaux Yes, that's a pretty big elephant. I'm a bit suspicious over whether geological time is really long enough, though. Yes, conversion to nitrates is energetically favorable, but breaking that triple nitrogen bond is not trivial. Biological fixation of nitrogen goes through a reducing pathway even, not oxidation, just like with the Haber process. Without knowing too much more about the detailed chemistry, I'm a bit skeptical that the oxidation pathway you propose would occur fast enough over geological time, even with a high (i.e., modern) oxygen atmosphere.

@user338907: By nitrogen I mean elementary nitrogen N$_2$, indeed.

@BryanKrause I was expecting things like lightning to be part of the mechanism over geological time; but you are probably right that it would be an extremely slow process.  Chances are, in the absence of photosynthesis to replenish it, the atmospheric oxygen would be depleted in many other ways before it had a chance to oxidize much of the nitrogen.

Also, birds poop (en masse) was historically a good source for nitrogen rich fertilizer. Like others say, there was historically a big problem gleaming on the horizon about acquiring it and being able to feed quickly increasing population of people, before Fritz Haber (quite controversial character) made a breakthrough! To dive deeper into the whole story, I very recommend this youtube video by Veritasium: "The Man Who Killed Millions and Saved Billions" https://www.youtube.com/watch?v=EvknN89JoWo

While atmospheric nitrogen is definitely necessary for keeping up the ecosystem of Earth as we know it (as Brian Krause has already pointed out), it is not really a necessity for some life form on earth, especially among the extromophiles species and even complete ecosystems can be found that do not rely on atmospheric nitrogen at all.
Atmospheric nitrogen also helps keeping up the atmospheric pressure, without any nitrogen in the atmosphere, water would boil at about 27°C.

Could you explain how the extremophiles obtain the nitrogen atoms in amino acids etc. if it is not ultimately from molecular nitrogen. At present your answer is just an assertion and for the large number of users who are familiar with extremophiles, the Wikipedia link does not clarify the matter.

They can be taken from nitrate which is readily accessible and the most natural form for nitrogen in the lithosphere.

And how does the nitrate arise?

Well, the nitrogen has to be somewhere, and under oxydising conditions nitrate is its stable form. Under reducing conditions it would be ammoniak. Elementary nitrogen is only metastable under either condition. Without biological activity, it vanishes rather quickly.

You are kindof right, Atmospheric N2 is bound with a triple covalent bond, which is the strongest of all simple diatomic molecules.
If you have a vivarium with helium/argon breathing gas and the soil has a ready supply of dissolved nitrogen for fixation into NH3, then the animals and plants will live just fine for a very long time, but many plants that fix N2 that depend on nitrogen fixation symbiosis may fare worse.
N2 is nearly not soluble in rainwater, so ultimately, all plants and animals that depend on nitrogen in the soil require atmospheric N2.
If there was no airborn N2, the forests would be in trouble because they would yellow and have diminishing reserves of nitrates and nitrites...
Nearly all the biospheres would perish unless you keep on fertilizing the soils, them most plant species would be virtually ok growing hydroponically in an atmosphere without N2.


text:
What is the solubility of rotenone in ethanol?
I’m trying to kill SH-SY5Y cells with rotenone, but the rotenone does not kill. I saw an article where rotenone is soluble at 5mM in ethanol. I dissolved 1.7 mg in 1 ml of ethanol to obtain a 1ml of 5mM solution. I also tried DMSO but it’s viscous when dissolved in DMEM. Is there something I am doing wrong?

How much DMSO are you adding to how much volume of media?

Also, your solution is only 4.3 mM, not 5. Please [edit] your question and add more details, including how old your rotenone stock is and how it's been stored, how old the solutions are and how they've been stored, the concentration you're using to kill the SH-SY5Y cells, how long after the addition of rotenone you're waiting before checking for cell death, and the manner in which you are looking for cell death.

Please clarify your specific problem or provide additional details to highlight exactly what you need. As it's currently written, it's hard to tell exactly what you're asking.

This sort of question, although related to practical biology, is not really suitable for this site, because it is, in effect, a question about the properties of a molecule that anyone can find by searching the web. And if you finish the [Tour] and read the Help on asking questions you will see that this is what we expect from posters. I know nothing about rotenone, am not familiar with organic chemistry databases, but was able to find that NCBI has a PubChem site documenting compounds. Look here: https://pubchem.ncbi.nlm.nih.gov/compound/Rotenone#section=NSC-Number .

Actually, as written, it looks more like a Chemistry.SE question.


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Is deleting two or three consecutive nucleotides and inserting exactly two or three back more common than two or three consecutive SNP?
I am looking at cancer mutations. I found that some of the mutations are e.g.

c.1251_1252delGGinsTT
c.151_152delGGinsTC
c.351_352delCAinsTT

I wonder if these are indeed two consecutive single nucleotide polymorphisms, such that they are indeed:

G>T, G>T
G>T, G>C
C>T, A>T

I would like to know which scenario is more biochemically plausible. I would like to distinguish them because I am looking for grouping them into mutation categories. I am not sure if I should treat these as indels or SNPs.
Thanks!

I believe it is SNPs, though they can be di-nucleotide polymorphism (DNP) or TNP. I saw this on some common oncogenes, e.g. TP53.

Thanks for your clarification,  I think you'd better include all the information and ask again in bioinformatics stack exchange ( , you will receive immediate feedbacks).

Please also refer to SNP and indel definitions:  https://genome.sph.umich.edu/wiki/Variant_classification, (https://snp.gs.washington.edu/SeattleSeqAnnotation154/HelpIndelAnnotation.jsp)


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

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


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Can someone help me identify this caterpillar?
I was in Colorado Springs in mid-October when I noticed something floating in front of my face. I tried dodging it, but it landed on my sunglasses. When, I initially saw it, it was attached to a single ~1-foot long strand of (what I believe was) silk. Now, I BELIEVE it was using this silk to float on the wind (as I've seen some species do on nature documentaries), but it is possible it was dangling from something I walked under, and I just failed to notice. Considering where I was when I noticed it, I believe the former is more likely. The creature, I believe some kind of caterpillar, was a bright, almost translucent green. It is incredibly small, approximately 1/8 to 1/16 of an inch.
I tried to see if I could find the caterpillar online. Caterpillaridentification.org has a list of caterpillars found in Colorado that you can filter buy color. The one I believe it looks closest too is the "cabbage looper", but Google says those caterpillars are about an inch and a half long, considerably larger than what I saw. This makes me believe that I probably ran into a newly born caterpillar.

Cabbage loopers are indeed about 1 in long, and quite fat - you will find them in your garden commonly. May not be the larva of a butterfly that you are finding.

I think this is an early stage Oak Leaf Roller caterpillar. They are green and have a black/brown tip, as can be seen in your first photo. Fully grown are about 1" (25 mm) long.
They are known to dangle down from trees on silk threads when dislodged.


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What are these micrographs of?
There are some images floating around the Internet that were supposedly taken with a microscope, built in the 1920s, that was supposed to achieve resolutions that would normally be ludicrous for an optical microscope, then or now, due to being smaller than the wavelength of light (and is caught up in a complicated conspiracy theory).
By the way, there seem to be strong indications in the surviving documents that it was actually an ultraviolet microscope as well as or instead of a visible-light microscope, so that might have some bearing on what's plausible in the way of resolution.
Not sure whether this question belongs here or at Physics.SE, but it seems like here might make more sense since the question is what these micro-organisms are.
There are about twelve or thirteen of these pictures floating around.  Some of them, on investigation, turn out to be magnified only 5000x or so, which, from what I've seen, seems to be considered impressive for a light microscope but not unheard-of.  These are some of the ones that I'm still puzzled by.
(Can put more details/refs of the microscope in the question if you like - wasn't sure whether you'd object to things being discussed on your site that are connected by association with a conspiracy theory  :-D  )
Question - I'm not a microbiologist, what do people here who are more used to microscope images think these images show, and at what magnification?
These three were published in a Smithsonian Institute annual report in 1944, pp. 240-242.

Caption - "Chlorophyl cells (algae)" - doesn't make sense.  From my limited knowledge of these things, it looks like a diatom, which seem to be a very commonplace subject for microscopes.  But one article I read implied that a trained biologist had been very impressed by this photo - maybe the writer had the wrong end of the stick.  Not sure what sort of diatom it is, if it is one.

Supposedly, the head of a tetanus bacterium, showing the spore, which, according to my brief Internet research, is possibly about 5 micrometres wide - so the quoted magnification of 23,000 sounds about true, if it really is a tetanus bacterium.

Supposedly, a typhoid bacterium, which, according to my brief Internet research, is possibly about 1 micrometre wide by 3 long.

Included because it's not labelled and I'm not sure what it is.  Diatoms?  No reference for where this one originally came from.  This copy from https://www.rife.de/images/calibrate1.jpg.

"Magnification" isn't a particularly useful measure; you can magnify anything as far as you want as long as you don't care about resolution.

Top picture is probably a dinoflagellate, possibly Gymnodinium family. Last are almost certainly diatoms of some sort, maybe Actinocyclus. Browse the beauty here

@BryanKrause That's true - and the "typhoid bacterium" does seem to be magnified considerably further than it has the resolution for.  Not sure how to express "resolution" numerically, though, so I just left it at "magnification", meaning "magnification possible without the image being reduced to a smudge".  (Which, in the case of the "typhoid bacterium", might be about half what it has there - but making the image smaller might have made the caption illegible).

Having had a quick read of the report, I have a few comments - first off, this seems to be a second-hand report of something that hasn't actually been observed by the authors.
Second, the light microscopy resolution limit is limited by
$$wavelength/2$$
As defined by Abbe's law, where x,y is the plane of focus, $λ$ is wavelength and NA is the numerical aperture of the lens.
$$Abbe Resolution_x,_y = λ/2NA$$
Practically this means that the shorter the wavelength, the smaller the resolution can be. For visible light the shortest is around 380 nm, so the limit would be 190 nm or 0.19 micrometers. This is about the size of the smallest bacteria and a few viruses reach this size. However, because of the limitations in how we make optical media (lens glass etc) the practical limit is quite a bit higher. Electrons have very short wavelengths (around 4 picometres), so much greater magnifications can be achieved, which is why EM is used for imaging viruses. Based on these physical laws, I would be very surprised if Rife achieved the magnifications he thought he achieved. Indeed, many of his claims of discoveries based on his magnifications (e.g. that cancer is caused by tiny E. coli-like cells that take up to 5 morphologies) are utter nonsense - of course he was the only one capable of seeing these, with his high-power microscope and he wouldn't let anyone else handle or use these...
So, I do have doubts about the magnifications expressed. In the journal Rife's magnifications are based on "diameters" rather than an actual dimensionless magnification (ratio of actual size to apparent size). Diameters was a commonly used method of working out object sizes, but I don't know how to convert between the two. I would say, seeing as there are actual fundamental physical limits to the resolution, that what is being seen here are what is known as empty magnification - increase in size without increase in resolution. The same sort of effect you get with a digital camera when it doesn't have an optical zoom, but instead relies on making the pixels bigger in the field of view. In this case it will simply be bigger projection than the limits of resolution.
Now, on to the actual question. What are these things? Taking on face value that images 1-3 are what the captions say they are on pages 222-224 of OP's linked publication, then we have some candidates.
OPs first image is almost certainly a dinoflagellate, these are a polyphyletic group of single-celled algae that, like diatoms, have beautiful structured cases. They also have flagellae, which enable movement. Which dinoflagellate this is, I don't know, they are diverse and not at all my field. I suspect something in the Gymnodiniaceae.  Dinoflagellates are about 30 micrometers in size, so easily within the limits of a light microscope, and you can see this in the ability to resolve the chloroplasts inside the organism. This image has no better resolution than would be produced by a decent conventional light microscope, only much bigger - camera trickery!
Image 2 could well be the spore end of Clostridium tetani, as the caption suggests. The spore is round and surrounded by a thick walled structure, but to my knowledge should have the rest of the bacterial body coming off to one side - looking rather like a spoon, with the body being the handle and the bowl of the spoon being the spore. I would expect to see the body of the bacterium sticking off to the side here, so I don't know for sure that it is what it is claimed to be, but we could be looking down on one along the longitudinal axis. There is some sponge-like "structure" visible in the middle of the "spore", but to me this looks like what you sometimes get in the middle of air bubbles on the slide.
Image 3 could be a member of the Salmonella group of organisms that cause typhoid, as these are slightly sausage shaped rod bacteria, however, I have seen many a stain blob that looks just like this using a low power objective. Note that Salmonella has flagellae too, and despite the large size and supposed massive magnification, we still can't see them. Hence, magnification and resolution probably not what is noted. So, whether this is actually Salmonella, is hard to say, but it could be.
Image 4 is from a different source - Rife.de, who seem to be an website for promoting Rife and his "cancer treatment". These look a lot like diatoms to me, but there is nothing to suggest that these were taken by Rife, and they look suspiciously like modern photographs using a modern microscope with something like Normarski optics or perhaps dark-field illumination, given that all the rest of Rife's images look much less clear.

Thanks very much for looking at this in so much detail!
According to https://www.britannica.com/technology/magnification "diameters" is the same as "x", so, if so, that's easy at least!

I'm not sure where Rife.de get their images from, other than the caption "Rife Research Group Of Canada" (which isn't them).  They seem to attempt to be a site seriously discussing the topic (there's a forum attached, and a lot of other archive materials), but they do seem to take the "it's basically real" position.  Full set: https://www.rife.de/observations-with-the-rife-microscope.html .

In #3 the flagellae seem reasonably visible at the right, if not well focused.  The internal detail is reasonably impressive - I'm not ready to hail it as a wonder, but it was at least a well-done job of staining and photography.


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Heart rate sensor electrodes to be used for blink detection (simple EOG)
I have a cheap ECG/HRV/heart rate sensor module for Arduino, bought from Aliexpress. It has 3 electrodes: RA, LA, RL, which I guess mean right arm, left arm, right leg. The module outputs one single time series data, like one referenced electrode of an EEG.
I would like to use this cheap module to record blinks (one coarse channel is enough for this), with its electrodes placed around one eye. But I am stuck with this problem:
What I have found so far on the internet about EOG electrode placement says that the ground electrode should be placed somewhere on the forehead or near the ear/neck. But which of these 3 electrodes should be deemed as ground? What arrangement of the 3 electrodes would you advise? (What are the equivalents of these 3 electrodes in a commercial EOG sensor?)
I appreciate any helpful comment. Thanks in advance!

Can you share any documentation for your sensor, manuals or instructions? Why doesn't that manual answer your questions?

I agree with @MaximilianPress -- It depends on how the device is wired, whether there is a fixed ground electrode etc.

As it is the case of almost all Aliexpress-marketed no-brand Arduino modules, there is zero documentation, except how to wire it up with Arduino. And no matter how much I googled, all applications only involve HRV/ECG sensor wiring of the module, even though is could be capable of acting as an EOG sensor I think.

Despite initial difficulties, after inspecting the module really closely, I could successfully identify the (only) microchip on it, which is an Analog Devices IC, with all necessary functionality embedded in one piece. Name is AD8232:
https://www.analog.com/media/en/technical-documentation/data-sheets/ad8232.pdf
It seems that pin 4 and 5 are connected with a resistor. Pin 5 goes to "RL" pin of the module board. Pin 3 goes to "RA", which at the same time IC docs refer to as IN-, and pin 2 goes to "LA" which the docs refer to as IN+. So I suppose the mystery is solved, but I can not try and check the setup in action in near future
(So far no matter in what configuration I wired up the module with my eyes, it could not work, but emitted a rhythmic noise. That is why I asked the question originally. But I found out that the source was the problematic power supply, not the electrode arrangements I tried. Now I need to get a proper power supply to try the module then.)


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Glycemic Index and two-hour blood glucose response curve (AUC)? Where are the AUC charts?
I understand the "Glycemic Index" (GI) of foods is calculated using the area under a 2-hour glucose/blood response curve (AUC) after a 24 hour fast and consuming carbohydrates. Therefore a higher GI indicates there is more glucose available in the blood stream during this 2 hours.
It seems the GI is a general indicator and glucose/blood levels over 2 hours and has little information on when the spike of carbohydrate to glucose conversion occurs or when carbohydrates are first converted to glucose. Is this a true statement?
I searched for the AUC charts online but found little information. I suspect the AUC charts would show when the glucose/blood levels first increase and how they are effected over time. Does anyone know where to find these charts for foods?
Also, is the correct forum to be asking this in? Unsure if Beta Medical Sciences StackExchance is appropriate.

You could search something like:
https://scholar.google.com/scholar?hl=en&q=glycemic+index+AUC+glucose
and your results will include papers that calculate glycemic index for some food based on glucose measurements. For example this one:
Robert, S. D., Ismail, A. A. S., Winn, T., & Wolever, T. (2008). Glycemic index of common Malaysian fruits. Asia Pacific Journal of Clinical Nutrition, 17(1).
has this figure:

You can expect that the conversion of carbohydrates to glucose begins immediately after eating, so it's mostly the rate that varies by food, producing different curves.

This paper is available from https://pubmed.ncbi.nlm.nih.gov/18364324/

I added another question on performing the GI calculation using integral calculus here: https://biology.stackexchange.com/questions/110854/calculating-the-glycemic-index-using-an-auc-glucose-blood-curve


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How do we know how long speciation occured?
Just as we use radiometric dating to age rocks, what is the method used to age how long ago speciation occurred in genetics?

https://en.wikipedia.org/wiki/Molecular_clock

Does this answer your question? Phylogenetics and the Tree of Life


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What prevents the diffusion of proton gradient in Gram (+) bacteria
The proton gradient in bacteria is important to power FTPase and flagella. How do Gram (+) bacteria maintain a proton gradient without a periplasm (Gram (-)) or intermembrane space (mitochondria). Why don't the protons diffuse away from the Gram (+) bacteria when they are exported?

Welcome to the site. Please take a [tour] and visit the [help] for more information on what we do here. Please note the page on homework. Ideally your question should demonstrate an attempt to find the answer yourself, and, no - "I google searched and didn't find anything" isn't an attempt. The answers to this should be easily found in your microbiology textbook!

Does this answer your question? How do Gram + bacteria use a proton gradient for F-type ATPase?


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How to judge the distance of nodes in biological evolution tree
I would like to know the method of judging the distance between two nodes in the phylogenetic tree. For example, in the diagram below, is node 299 closer to node 151, or closer to node 201?

Welcome to SE Biology. Please finish reading the [Tour] to find out how this site works, and the Help on asking questions. Generally we like posters to research questions before posting and explain why they were unable to find an answer. Did you?

It depends somewhat what you mean by "closer", but phylogenetic distances are usually judged by "branch length". By this logic, just eyeballing it, node299 is almost certainly closer to node151 than node201.
This means roughly "how far you have to travel up and down the tree to connect 2 nodes". From node299, it looks like you have to actually go back down the tree to pass through node151 to get to node201, so node151 is really in the middle here. Note that branches represent evolutionary time, so that the branch length distance between two descendants of the same ancestor can be expected to be around twice the evolutionary time experienced by each descendant relative to ancestor.
The arrangement of the tree in the left to right axis is arbitrary, for example for any subgroup you can flip it 180º and there is no change in the actual topology of the tree.
This is harder to see in a circular layout like this, but in a standard cladogram it is more obvious:

As one example, you can take the "Dinosauria" clade and flip it so that the chicken is closer to the the crocodile, and there is no difference.
In this specific case, you are noting the "root" of the tree as one of your nodes (node151). The placement of the root is generally the most uncertain/poorly estimated part of the tree, so making arguments based on it is non-ideal, but from the point of view of computation, the answer is unambiguous.

Thanks a lot for your answer. But I have another problem. I want to know why the distance between two nodes evolved from the same ancestor is farther than the distance between the two nodes and the ancestor node.
Is this situation caused by the introduction of genes from other species during the evolution of these two nodes?

@rona not sure that i understand. The distance (ancestor to descendant 1) or (ancestor to descendant 2) is always going to be shorter than the distance (ancestor to descendant 1) + (ancestor to descendant 2), if we're talking about the same ancestor. Negative branch lengths are technically possible but so rare they're not worth considering. Each of those lineages has experienced evolutionary time. Updated answer in bold to be explicit.


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Calculating the Glycemic Index using an AUC Glucose/Blood curve?
Does anyone know the mathematics to calculate the Glycemic Index using a AUC Glucose/Blood curve?  Is there an article documenting the process?  I understand that algebra and integral calculus is involved.
For instance, here is an AUC Glucose/Blood graph of foods against a Glucose reference:

I know the definition of the Glycemic Index is the relative rise in blood glucose level two hours after consuming food.  It is the area under a 2 hours glucose/blood response curve, following a 12 hour fast and 50 g ingestion of a carbohydrate.
I know Glucose has a Glycemic Index of 100 and I'm unsure how this relates to the integral of (area under) the Glucose curve in the above graph.  Also, the Glycemic Index appears to be unit-less, which is further confusing.
I try a rough calculation as follows and the results appear off.  I draw a rectangle where the glucose curve is pictured here between 0-60 min, it comes out to 10 mmol/L - 6 mmol/L = 4 mmol/L y-axis, 60 min - 0 min = 60 min x-axis.  The resulting area of the GI is 4 mmol/L * 60 min = 220 mmol/L * min and when the GI for Glucose should be 100.
Appreciate guidance here.

Glycemic index is the ratio of blood glucose AUC for some carbohydrate source to a reference source, usually either glucose or white bread.
It's unitless because it's a ratio of numbers with the same units:
(concentration/time) / (concentration/time)
Glucose is defined as having a glycemic index of 100. This is an entirely arbitrary choice. It could have been 1, it could have been 42. 100 is convenient, because it will tend to make most foods have numbers in an easy range, basically the same reason that proportions are often expressed as percentages ("20%" rather than ".20").
To calculate area under  the curve from a set of discrete measurements like in the graph above, typically one would use the trapezoid rule though any other integration approximation would give similar results.
An example from the methods section in one paper:

The incremental area under the blood glucose response curves (IAUCG) to test and reference foods were calculated geometrically using the trapezoid rule, ignoring the area below the fasting baseline

So, for the above curve, the first step would be to subtract the fasting baseline which appears to be around 5.8 mmol/L, then use the trapezoid rule to get the AUC in units of mmol/L * time for glucose and each fruit, and express the glycemic index for each as 100 * fruit/glucose.

For above graph using the glucose curve with two sides, Baseline: 10 mmol/L - 6 mmol/L = 4 mmol/L.  Trap Rules: 30 min -0 min * .5(0 mmol/L + 4 mmol/L) = 60 min * mmol/L,  120 min - 30 min * .5(0 mmol/L + 4 mmol/L) = 180 min * mmol/L,  60 min * mmol/L + 180 min * mmol/L = 250 min * mmol / L, then GI for glucose is 100 * (250 min * mmol / L) fruit / (250 min * mmol / L) glucose = 100.  Does this calculation appear correct?

Another question, if the Glycemic Index of a fruit is 50, the fruit/glucose ratio is 1/2.  Does this imply the fruit has less glucose over time than the reference glucose?  Or perhaps the integral of the fruit extends past the 2 hour window?

If you go to the paper they report the AUC for glucose to be 259+/-15 mmol x min/L from the actual data, so yes it seems like your 250 is a pretty good estimate from the figure but I'm not going to bother auditing your math in this format.

Glycemic index is a measure of how much a food affects blood glucose. That's it. If you want to know how much total energy a food contributes, better to look at calories. Glycemic index doesn't measure anything else about metabolism, just blood glucose.

@Nick Importantly, blood glucose is under homeostatic control, so it's not as if every molecule of glucose in the diet causes a proportional change to blood glucose. GI is just a simple measure based on something easily measurable by a lab (blood/plasma glucose), it's not an attempt to create a full metabolic model.

Thanks. I’m still confused how same 50 grams of carbohydrates can yield different AUC curve areas, unless like you say the the carbs may be equal but they effect glucose/blood levels differently. As glucose is energy I would expect the area the curves to be the same for the same carb content, unless the curve extended beyond 2 hours.

@Nick Yeah, it's just not that simple.

do you know of any other resources I can read to reconcile this question?  Specifically, why glucose level area does not correlate to carbohydrate intake of the food?  Are different food carbohydrates either being converted to something else other then glucose, or the glucose / blood level remains high beyond the 2 hour measurement window, which would lead to a lower glycemic index and area under 2-hour curve?  Thanks

in another post regarding glucose, someone stated "glucose levels will change depending on the type of carbohydrate, and some form of carbohydrates are even impossible for the body to digest and are either digested by bacteria in the gut or simply excreted in the feces."  So this may suggest the perhaps only some mass of carbohydrates may be converted into glucose, which would suggest the low AUC integral and Glycemic index for some foods.  Does that sound right?


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Human Body's rate of conversion of carbs, protein and fat into energy?
I understanding there are some complicated processes, but I'm interested in generally how fast the body converts certain chemicals into energy and the period of time this conversion occurs.  I'm specifically interested in carbohydrates, protein and fat (perhaps distinguishing saturated from unsaturated).
I have the following notes where glucose is energy, do they appear correct?

Carbohydrates convert to glucose over a 2 hour period after a meal.  The peak glucose/blood levels are 30 - 45 minutes after a meal.  Conversion starts about 15 minutes after a meal.  1 g of carbohydrate / 1 g of glucose conversion.
Protein converts to glucose over 3 - 5 hours after a meal with a 70% conversion of protein into glucose.  I also read that protein converts to glucose at a rate of 3 - 12 g protein / hour.  1.3 g protein / 1 g of glucose conversion.
Fat converts to glucose over 4 - 6 hours after a meal.  Only about 5-6% of the fat triglycerides are converted into glucose.  I also read that 2.5 g of fat / 1 g of glucose conversion, which seems to differ then the 5-6% number.

This question seems to be based on the false assumption that proteins and fats are necessarily converted to glucose. It is possible for certain amino acids in protein to be converted to glucose by gluconeogenesis, but not others. However they may also be used for protein biosynthesis, metabolized oxidatively as different intermediates or even converted to fat. As regards fat itself, only the glycerol moiety can be converted to glucose, but whether this happens or the glycerol is metabolized differently depends on the nutritional state of the individual.

It is quite complicated, the speed of conversion of carbohydrates, protein and fat in to energy is definitely not linear and dependent on what the body is doing.
You should be close to right in carbohydrates. Since digestion starts in the mouth with the release of amylases to chop down starch and since the absorption of glucose is quite fast in the early stages of digestion in the intestines, your numbers should not be far off if you consider a non-branch form of starch. That will change depending on the type of carbohydrate, and some form of carbohydrates are even impossible for the body to digest and are either digested by bacteria in the gut or simply excreted in the feces.
Regarding protein, this is where your assumptions start to be off. The primary purpose of protein is not for energy production, but to supplement the cells with aminoacids to build other proteins. So, although it is possible to convert protein into glucose, it is not done in digestive system. Also, each aminoacid is converted into a precursor that will generate some energy eventually, not glucose. And depending on the aminoacid, the amount of energy differs, which makes it more complicated to give an estimation.
As for fat, they cannot be converted into glucose by the human body. As you mentioned, this is the slowest macromolecule to be absorbed by the body but it is also the most energy dense. Although 1 g glucose generates about 3 cal, 1 g of fat generates around 9 cal (protein is around the same as glucose).
Regarding on how fast macromolecules can be converted into actually energy, some cyclists can burn up to 120 g glucose per hour during a race.

The poster mentioned triglycerides in relation to fat, rather than fatty acids. The glycerol portion of triglycerides can be converted to glucose in the liver. I imagine that is where the 5–6% figure comes from.

@David yes, the 5-6% of the triglyceride conversion to glucose figure is confusing.  I read that body fat, which I understand is made of of triglycerides, is only 85% usable energy per unit weight.  Much different than the former number.  Any idea if these numbers are correct?

@Vilut you mention that fat cannot be converted into glucose by the human body.  You mention that 1 g of fat generations ~9 kcal of energy.  Therefore ingestion of fat resulting in energy availability to the body.  Its now my understanding that fats are converted into fatty acids and glycerol. These fatty acid chains are converted into energy via a process called beta-oxidation (electron transfer), which generates acetyl-CoA entering the citric acid cycle, yielding ATP.  Is this correct?  How long does the process take vs others like carbs?

@Nick, yes, fatty acids are converted into Acetyl-CoA through beta-oxidation, which then enters the citric acid cycle to result in ATP that the cells can use.
As for the length of the processes, I don't know. What I know is that, in athletes, glucose is used primarily in big and speedy efforts (100 m), while fatty acids are primarily used in long efforts (marathon and ultra marathon). Which means that glucose can be used to produce ATP fairly quickly relatively to fatty acids. Of course, other factors should be taken into account for more precise values.