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Does human organism consume water or is it only used as solvent?
Dune (novel) describes a body suit called Stillsuit:

a stillsuit is a "body-enclosing garment" of Fremen design which
  performs the "functions of heat dissipation and filtering bodily
  wastes", as well as retaining and reclaiming moisture

For this question, I am interested into reclaiming property of this suit. The book argues about the fact that the losses were virtually only due to exposed skin.
However, I am wondering if the human body is actually consuming (through biochemical reactions) any water or it is used entirely as a dissolvent or maybe as a catalyst), so that its loss entirely depends on the ability of reclaiming it externally.
Question: Does human organism consume water or is it only used as solvent?

Humans and all other animals actually are net producers of water ("metabolic water") by oxidizing sources of energy including fats, proteins, and carbohydrates - effectively the opposite of the chemical reactions that photosynthetic plants use to turn water and atmospheric CO$_2$ into biological materials and oxygen gas. There are also many metabolic reactions in humans that consume water (in particular hydrolysis reactions), but it is less than the amount produced.
However, water is indeed important as a solvent, and there are non-negligible losses through evaporation (especially when sweating) and an important role of water in the kidneys to assist in flushing waste.
If one was able to reclaim all evaporative losses and excretion losses, no additional water would be necessary. However, the energy requirements to do so go up exponentially the closer you get to 100% reclaimation.
The International Space Station has several water recovery systems to reduce the incredibly expensive cost of supplying enough water for humans on long missions in space. These systems include both urine purification and atmospheric reclamation but they do not approach 100% capture.

evaporation from the lungs and urine are both big source of loss, so the suits would do a lot. a suit has some advantages over the space station.

@John The main advantage would be insulation, in that if you keep someone in a humidified environment evaporation would be decreased, but that doesn't solve the problem of evaporation in the lungs unless breathing is also contained in the suit, and I can't think of any advantages a suit would have over a space station in terms of urine recovery. The advantage the space station has, on the other hand, is that it is large enough to carry the necessary equipment, has available power, etc.

"The main advantage would be insulation, in that if you keep someone in a humidified environment evaporation would be decreased" 'Insulation' generally refers to heat, not humidity. And keeping someone in a humid suit in a desert seems like a really bad idea, and would likely just cause them to sweat more. A better to reduce water loss would be if the suit can keep the person cool.

@Acccumulation The only way sweat cools you is if you allow it to evaporate, so if a Fremen suit is collecting all water it can't be allowing the wearer to cool via sweating anyways. Insulation need not refer only to thermal insulation.

@Acccumulation the suits are described as trapping and collecting exhaled water,urine, and a large percentage of sweat. It is basically a nearly sealed environment suit designed with complex special heat exchangers.

There are some animals that can reclaim enough metabolic water that they do not need any external sources to survive. The desert kangaroo rat does this, using a nephritic system so dense that the loops of Henle descend all the way into the bladder!

@forest as far as I remember, saying that these animals do not require an external source of water is not entirely correct: they simply find food-bound sources sufficient.

@EliKorvigo No, this animal actually uses only metabolic water.


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What does "operationally soluble" mean, re. Tax10 enzyme?
I am trying to work out whether the enzyme Tax10 is soluble or insoluble. I need to know if some buffers won't work with Tax10. I am trying to confirm Tax10 activity, having confirmed protein expression and having purified it.
Any help would be much appreciated! Thanks :)

Context:
Walker K, Long R, Croteau R. 2002. The final acylation step in taxol biosynthesis: cloning of the taxoid C13-side-chain N-benzoyltransferase from Taxus. Proc Natl Acad Sci USA 99(14):9166-9171.

The TAX10 gene overexpressed from pSBET yielded a ≈50-kDa protein (determined by SDS/PAGE), consistent with the size of the encoded enzyme, and this operationally soluble recombinant enzyme from preparative bacterial cultures was partially purified by anion exchange (DE-52) and ceramic hydroxyapatite chromatography.

(p.9169, below Figure 3)

I think all they mean is that the protein was found in the soluble fraction rather than in inclusions.

Fantastic. I thought that's what they meant. Thanks :)

source: Stack Exchange

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

sort: votes


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What (if any) is the shortest evolutionary process observed by humans?
So when I think of evolutionary processes, I think of it taking millions of years to happen. Like how humans evolved from monkeys or birds evolved from dinosaurs (I know that is super-duper simplified). Or how humans have parts that we don't need or use (the appendix, for example), but we don't have any records of a time when it was. But I wonder if there have been any evolutionary processes that happened on a human timescale or if we have evidence of something evolving in, say, thousands of years instead of millions? I think this would be interesting to learn about.

All species are evolving with every generation. Check out Remi.b's favorite site https://evolution.berkeley.edu/evolibrary/home.php for some basics on evolution.

@BryanKrause Remi.b's favorite site $\ddot \smile$. I often refer to this site following Corvus advice here

Haha that's nice, I hadn't seen that Q&A before. I'm more familiar with your use of the advice you got there than the original advice itself I suppose. :)

Definition of evolution
The whole problem boils down to the definition of the term "evolution". Typically, evolution is defined as a change in allele frequency over time. See wikipedia > allele if needed.
Answer with definition "evolution = change in allele frequency over time"
Using this definition, any event of death or birth is an evolutionary event. As such, in the human species, there are about 6 evolutionary events per second! This number will vary a lot among species / lineage of course.
Do you want to consider another definition?
If you are willing to use another definition, I am happy to investigate how common are events matching this definition. Please make sure to clearly define the term so as to leave out possibility for subjective appreciation. If you need inspiration for definitions, you might want to have a look at this post.
Sidenote: Evolutionary experiments
You might be interest in evolutionary experiments. An evolutionary experiment consists at putting individuals in a lab, let them breed under some circumstances and let them evolve. Of course, doing such experiment with elephants would be pointless as the generation time is so long. Common species that we use for such experiments include E.coli, S. cervisae (yeast) and D. melanogaster (fruit fly). Some of these experiments can be as short as a few days while others have been running for decades.
Somewhat related posts

How come most animals never seem to evolve over millenia?
Evolutionary chronology - if any, which species have evolved in the last 100 years
Why don't we keep evolving until we are super-human?

For a very introductive source of information in evolutionary biology, you can have a look at the website that @BryanKrause recommended: evo101

How are you defining "evolutionary event"?  You can do a lab experiment to generate antibiotic-resistant bacteria from antibiotic-sensitive parents strains in a few days or weeks, I think.
Humans drive the dodo to extinction over the course of a few centuries.
In Lake Victoria:  https://www.nytimes.com/1996/08/27/science/lake-victoria-s-lightning-fast-origin-of-species.html

Now an international team of researchers, using remote sensing to
  probe the sediments at the lake's bottom, have found evidence that
  what is now Lake Victoria was a dry, grassy plain just 12,000 years
  ago. For evolutionary biologists, the implications are enormous. The
  discovery means that the 300 unique fish species that have been
  documented in the lake must have evolved in the unthinkably short
  interval since the current lake began to form, a geological instant
  ago.

Another example:https://payseur.genetics.wisc.edu/IslandEvolution.htm

Gough Island, located in the South Atlantic about 3000 km southwest of
  South Africa, is home to the largest wild house mice in the world.
  These animals are about twice the mass of wild mice in the United
  Kingdom. Body size evolution has been rapid: mice were recently
  introduced to the island (in the 19th century) and a major size
  increase was observed over just a 40-year period. The drastic size
  change of Gough Island mice has been attributed to low temperature,
  extended longevity, reduced predation, and carnivorous eating habits.
  In a highly unusual behavior, these mice cooperatively feed on live
  and dead chicks of severely endangered albatrosses.

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


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Anaerobic Respiration vs Aerobic Respiration during physical activity
So I was wondering about the difference between aerobic and anaerobic respiration on the context of burning calories. While swimming we can choose to keep our head up and breathe, or keep our head below water for a stretch. Which will burn more calories for that time and why? And does anaerobic respiration cause fatigue of the brain due to insufficient oxygen?

Anaerobic respiration releases much less energy than aerobic respiration. Anaerobic respiration leads to a buildup of lactic acid in muscle tissue, which can feel like fatigue. Swimming is an aerobic exercise whether you head is at the stage of being under or over water. Exercises that count as anaerobic are those that require a lot of energy being produced by the cells in a short time (like sprinting).

@P.SN yeah but ultimately it is incomplete breakdown of glucose due to less oxygen availability... Shouldn't it affect the brain also?


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Does body fat percentage effect storage of fat soluble compounds?
Would a person with a higher body fat percentage store more of a fat soluble compound, or store for a longer time, than a person with a lower body fat percentage if they both consumed the same amount in the same time frame?

Does body fat percentage effect storage of fat soluble compounds?

Generally, yes.
Phenytoin, an anti-seizure drug, provides a good and well studied example.  The key issue here is that, for phenytoin, plasma half-life is proportional to the apparent volume of distribution of the drug.
(Apparent) volume of distribution is a pharmacokinetic property of a drug. It is the volume a drug would need to be dissolved in in order to achieve the concentration of the drug in plasma. For fat soluble compounds, this can be quite large, as the drug is primarily partitioned into fatty tissues, leaving a low concentration in plasma. Empirically, phenytoin's volume of distribution is higher for more obese patients, and (by the same reference), the half-life is proportionally longer.
As is often the case, though, it depends on the drug. For some lipid soluble drugs, an increased rate of metabolism by the liver in obesity compensates for the increased volume of distribution; for others, obesity doesn't have that much of an impact on volume of distribution in the first place.


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Why does decomposing matter emit a bad smell?
Often, when matter decomposes (such as a rotting carcass), a nasty smell is emitted.  After speaking to my teacher, it was likely due to the nitrogen compounds that leads to the bad smell.  Is this so?  Why then, do nitrogen compounds smell bad to us humans?

When bacteria and other microorganisms decompose matter, many gases are released alongside nitrogen, such as sulphur and methane. Our brains have evolved to perceive the smell of these gases as “bad” in connection to decomposing matter to protect us from eating them and being exposed to the harmful bacteria, just as we perceive certain plants as tasting bitter (the “bitter compounds” in plants are for its self defence) which could be toxic to us if we eat them.

@P.SN is it true though that brain's perceive at bad as due to smell? Also isn't bitter taste due to alkaloid poisons...So humans have evolved not to like alkali?

reframe the question, why did humans evolve to think the smell of rot is bad, AKA something to be avoided.

Since this question has no answer, I thought of taking a stab at it.

Why does decomposing matter emit a bad smell?

Due to cadaverine and putrescine. More information here: What produces the strong odor of decaying dead animals?

Why do they smell so bad? Why do we perceive those smell as bad?

Let's start from the basics. Stuffs smell because they release chemicals odorants. They are volatile and hydrophobic. Different odorants have different smell due to presence of specific functional groups. Thiols smell like garlic/rotten eggs, , nitro groups gives a sweet ethereal smell. More information here: How does the smell of a compound come about, and is it possible to define a smell?
Cadaverine and putrescine has two amine groups which gives off that rotten fish mixed with that characteristic decay smell. This compound now binds with receptor proteins present in cilia. This chemical stimulus binds initiates an electric signal in the neuron, which transmits the information to the olfactory nerve, which carries the signal to the olfactory bulb in the brain and the brain processes the signal. The olfactory bulb is part of the limbic system, which is also associated with emotions. A person recognizes the odor and give off the emotion  of "disgust" as a reflex action.

Recent studiesref also found that smell of death is somehow related with threat management mechanisms. The paper suggest that humans can identify threats via chemosignals. For instance, when people are exposed to fearful experience, they show a heightened startle reflex. This transmission of threat-arousing chemosignals is assumed to serve an adaptive function by orienting us to impending dangers. Cadaverine and putrescine are found to be chemosignals. The paper explains it more properly:

The decay of tissue can function as a "necromone" cue that signals an animal’s death to conspecifics. Alarm and avoidance behaviors (necrophobic behaviors) in response to these scents are widespread in the animal kingdom and thought to have evolved at least 420 million years ago. In fact, recent research shows that necrophobic behavior may have innate underpinnings through the activation of trace amine-associated receptors (TAARs), a group of specialized scent receptors in the olfactory epithelium. TAARs are known to detect specific chemicals that evoke behavioral responses, without the need for prior exposure to the scents. Certain TAARs respond to diamines (e.g., putrescine) by producing avoidant behaviors that likely serve to defend against immediate dangers . Thus, it is feasible that we have a chemosensory sensitivity to diamines like putrescine, given that their detection can aid survival.

ref: Wisman, A., & Shrira, I. (2015). The smell of death: evidence that putrescine elicits threat management mechanisms. Frontiers in psychology, 6, 1274. https://doi.org/10.3389/fpsyg.2015.01274

to clarify humans avoid the smell of rot, because rotting things pose a direct and indirect threat. poisonings, contamination, and places were predators and disease vectors will gather. eating rotting things will make you sick so you evolved to think they smell bad so you won't try it.


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Flow Cytometry Channels
I did a flow cytometry experiment for the first time. I had three conditions: (1) unstained healthy monocytes (2) healthy monocytes stained with green/red (488/570) from the Live/Dead thermofisher kit (3) dead monocytes stained with the same green/red dyes.
I did those condition to know what graphs to expects, and learn the FACs process and analysis. Would appreciate it if someone can answer the following questions:

So I have two dyes in my samples and a control. Which flow cytometry channel should I use in my plots (FL1, FL2, FL3, or FL4)?
How to know the percentage of live and dead cells in each condition?
Anyone knows a free analysis software?
How practical is R to do flow cytometry analysis?

I'll amend this answer as I get details from you.
What is your cytometer, and how are the optics set up? You typically have 1-5 lasers: UV (355nm), violet (405nm), blue (488nm), green/yellow (~561nm) and red (~633nm) lasers. Your FL number, FL1-4, typically refer to a particular PMT (photomultiplier tube) and filter combination. For example, a typical FACSCantoII has a 4-2-2 setup with 4 PMT on the blue laser, 2 on the violet laser and 2 on the red laser (if you bought the device that way, there are other configurations). These fluorescence channels are set up to detect a particular fluorophore or equivalent with a bandpass filter. The base filters on FACSCanto II red laser are 660/20 and 780/60. These filter light emitted by the stained cells at a particular range of wavelengths, and you read them as 600nm +/- 10nm and 780nm +/- 30nm, for example.
You can set your software up to be FL numbers or fluorophores, but what you need to know is what filter is FL1 and so forth? Typical cytometers like FACSAria, these are FL1 = FITC, FL2 = PE, FL3 = 7AAD, PerCP/Cy5.5, etc., FL4 = APC.
So you used a live/dead thermofisher kit, please provide us also the catalog numbers.
What we want to do is take the information about your dyes and about your cytometer and reconcile them to determine what channel they should fluoresce in. 488nm looks like FITC or FL1 and 570nm looks like PE or FL2, but these look like lasers, whereas you want to tell me the dye emission to match it to a channel, using the information about your device configuration!
As for software, there are a number of good, expensive options like FCS Express and FlowJo but they're costly. See if your core or what have you has these available for you to use on-site. Otherwise, the on-board cytometer software like FACSDiva may need to suffice, and often does. I've used some of the "free" ones but they're very clunky and/or terrible to use.
R has some usefulness for high-dimensional analysis, but you need to be able to use R fluently, and you can't draw manual gates. There do exist helpful packages with good documentation like X-cyt (broad institute), though. And for visualization like PCA and t-SNE, R has a lot of documentation for flow data. Also consider R loads everything into RAM so on a slower 2-4GB computer it might have lackluster performance.
To start with your analysis, I'll ask why did you use two dyes? The LIVE/DEAD product line are reactive with free amines which present inside and outside the cell. Dying cells have more permeable membranes and take up more dye. So when you analyze the cells, everything is positive, but the dead and dying cells are 1-2 logs higher intensity of staining compared to the live population.

So the first thing any flow experiment needs are controls. You have unstained controls, FMO controls and compensation controls. The unstained just gives you an idea your morphology by light scatter, but for low-dimensional experiements can act as an FMO. The FMO or fluorescence minus-one is a cell stained with everything in your antibody/dye panel except one marker, so that you can compare against the fully-stained sample and see where to draw your gate. Compensation controls help the cytometer correct for the fact that filters pick up emission from other fluorophores than the target. You also have a biological control, which is good, because for analysis you always want to see where a clear positive and negative population lay on your dotplots or histograms. Live cells help you see where the positive and negatives are but may have a weak positive signals, and unstained cells will have a negative population that is shifted down 1/2 log or so because they dont have any dye at all. The dead stained cells will show you a strong positive signal and potentially a weak negative signal. Use these to draw your gates.
So then compensate the data electronically with your software (follow the manual), and create a dotplot with FSC-A and SSC-A on the axes. Only experience will tell how your cells look on this plot, but for reference, a blood or leukocyte sample would like like this:

You want to draw a gate around your monocytes and then create a plot based on your monocyte gate (at least gate out debris). It's also useful for further experiments to stain with a monocyte marker so you can dump everything but your target cells, so use CD14, for example, which is specific to monocytes.
On the next dotplot, make the axes FSC-A and FSC-H. This is a doublet discimination step where laser area scaling done before a cytometer run helps a lot (see your core expert). The principle here is to gate out (get rid of) cells that are stuck together:

Then you would want to look for your target cells. If they're both live/dead dyes you're going to have the same signal on two different channels, so you can probably just pick one, like live/dead green.
You can do a histogram of FL1 based on the cells kept in the doublet plot. You should see two discrete peaks on a log or bi-exponential transformed intensity axis (width basis -10 is good to use, but FACSDiva does it automatically). Width basis is a co-factor that compresses the data around 0, so negative populations get smaller and you get better resolution among the positive populations.
You would draw a bifur gate between the positive and negative peak or a range gate around the positive, and select tell the software to generate statistics to get your percentages. And you can repeat for the FL2/red dye to get those percentages, too, but both markers are looking at the same thing.
Then, apply those gates to all your samples and adjust the gates based on what the data looks like.
Please try this presentation: https://www.slideshare.net/richardhastings589/kumc-introduction-to-flow-cytometry


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What are the safety precautions I should take if I want to experiment with C. elegans (at home)?
Caenorhabditis elegans (C. elegans) is a nematode (roundworm), and many nematodes do infect humans and cause diseases.
How much is C. elegans safe (or unsafe) in this respect?
C.elegans is a popular model organism, but is it safe to experiment with it at home? Or risk of infection shall outweigh desire and interest for home science?

Caenorhabditis elegans is completely safe, it is a soil worm not parasitics. you can google the name if you don't believe be.


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Can anyone identify this species of spider?
These spiders are all over everything on my padio in New Hampshire. Can anyone help me identify what they are?

How big are they?

They look like acari: https://en.wikipedia.org/wiki/Acari

They are approximately 1mm in total size leg to leg. I am suspecting that they are some sort of mite, but they don't seem to bite, or be in the tick family (at least not human blood suckers).

Pretty clearly mites, not spiders, but unfortunately I'm not a mite guy.

It depends upon the environment or surrounding

Based on your area and this pest control site I believe that the bugs in your picture are not spiders, they are clover mites. I have found that some clover mites are a darker brown color and also slightly larger. This image gives a better view of the features of a clover mite, including the longer pair of front legs and oval shaped body:  Clover mites don't pose a threat to people or animals as they live off of either plants or fungi, but smashing them can leave stains on furniture and clothing.


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Identify this mite from Rajasthan (India)

Can anyone tell me the classification of this bug? I found it in Rajasthan after it rained.

What’s the scale on the picture? It looks like some kind of mite, but those are generally < 1mm in size

red velvet mite of some kind. they get pretty big

Also, please update your question with approximate size of the organism and the habitat you found it in (for future reference). thanks.

Hi it definitely looks like a red velvet mite.  They often are called "rain bugs".  They are of a variety of species and sizes and can be quite large - up to 1 or 2 Cm. These links might help.
https://study.com/academy/lesson/red-velvet-mite-facts-life-cycle-diet.html
https://en.wikipedia.org/wiki/Trombidiidae
https://www.youtube.com/watch?v=OtHYSIRCZ1c

This is a Trombidium mite (class Arachnida).

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Effects of X-ray exposure on upcoming pregnancies
Recently we had a little fight with my girlfriend about the risks of genetic diseases for our potential baby. The thing is that she had her medical check recently and it included an X-ray examination of her chest. The doctor performing the scan warned her that she should not get pregnant for 3-6 months after the examination.
A note on the wall also read similar to this (in Chinese):

医生建议与X光射线接触的备孕期的女性朋友，最好在3个月后再进行怀孕，以降低胎儿畸形的风险。

Which translates roughly as:

To reduce the risk of fetal malformations, doctors suggest that women who have had X-ray expose are better to avoid getting pregnant withing three months.

(I guess, this advice might come from the fact that an egg develops for about 150 days before being released to the ovary?)
However, since the average radiation dose of the X-ray chest exam is reported to be around 0.1 mSv (which is about the dose of radiation you get by a couple of round-trip flights: from the US to Paris and back), I have doubts that this piece of advice has any solid scientific foundation to it. (Otherwise, I guess, airline companies should be legally bind to warn any female clients of dangers of transoceanic travel.)
Are there any studies that show effects of X-ray exams on future pregnancies? Can the risk of "fetal malformations" for any pregnancy starting shortly after an X-ray exam really be assessed?

Hmm. Why downvote?


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Can experiments in ELISA kits be monitored via both fluorometry and photometry?
In my bioanalytics course slides, the professor has written at one point that in a heterogenous immunoassay such as ELISA, we use fluorimetry to measure concentration of an analyte. In another slide it is mentioned that we use photometry to measure UV-vis absorption. I am confused... is it one or the other, or can we use both methods depending on whether the marker enzyme on the antibody is given a fluorescent or chromogenic substrate?

can we use both methods depending on whether the marker enzyme on the antibody is given a fluorescent or chromogenic substrate?

This is essentially correct.
You can have the same ELISA work on different methods of detection. The most common ELISA is colorimetric, and works by binding a secondary antibody conjugated to some enzyme to your primary antibody. Fluorescent ELISA platforms are less-widespread but only because the colorimetric ELISA is reputed and "gold standard."
Horseradish peroxidase (hrp) is a common conjugate system utilized in sandwich ELISAs, and by adding TMB solution to the reaction wells, the resulting reaction produces a diimine that turns the liquid in the well blue, and does so in proportion to the amount of analyte captured. You stop the reaction by adding an acid, which turns the well yellow, and you read the OD at 450nm (they also recommend you subtract the OD at 510nm to account for the light scattering of the microplate).

Figure 1. R&D Systems Quantikine assays, HRP-streptavidin detection. https://www.rndsystems.com/products/quantikine-hs-colorimetric-sandwich-elisas-high-sensitivity
On the other hand, we know that we can also conjugate the antibody with a fluorescent molecule if we wanted to, like FITC or PE. All we need to do is excite the molecule with an appropriate light source or laser to get a fluorescent emission, and read with an appropriate system to read those signals. The fluorescent intensity would then be proportional to the captured analyte, based on a standard curve just like any ELISA.
So the real answer is we can use one, the other, or both, just not at the same time.
Just be cognizant that different platforms can yield different results, so you have to validate your two platforms, and correlate the two to ensure reproducibility. Most labs just try to stick with one or the other, though.

I should add that this can be made flexible by using a streptavidin-fluorophore conjugate. Then the process is almost exactly the same, with each detection molecule binding to biotin.


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Please help me identify this jelly fish
I've seen these jellyfish in thailand and was wondering what species they were. All I know is that there are lot in the Chonburi area and they sting in not deadly but hurts.
Images for the jellyfish
Thanks for the help!

Those pictures don’t look like a complete jellyfish, which makes identification very hard. Also, there’s no sense of scale in the pictures - can you describe them in more detail since you were there to see them personally?

Well the bigger ones are around 15-25 cm tall (in water the ones I could see at least) and around 10-15 in diameter. I don't know if they are complete or not I could only see there are also one smaller which was around 10cm in height and 5 in diameter with a similar structure. Well they are hardly noticeable in water because the water is not too clean so I couldn't take picture in the water.  Also there are some people eating them on the shore. And their sting also leaves red lines like other jellyfish sting and usually hurts for around 15 minutes (asked others who were sting before)

It looks like a Rhizostomae, or crown jellyfish, but it's hard to tell. The  article here does mention that it's edible though and it's found in Thailand so I'm pretty happy with that guess.
More specifically, it looks similar to the jellyfish asked about here, which was eventually classified as a Lobonemoides, perhaps Lobonemoides robusta


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Sequence between PolyA signal and PolyA tail
Between the polyadenylation (PolyA) signal (AAUAAA in humans) and the start of the polyA tail, there is a short sequence of about 10~20 (G/U rich) bases, is there a special term for it?

Image credit: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3175714/

Does this region have any regulatory effect? When artificial mRNAs are made, the polyA tail is often just stuck to the end of the stop codon, omitting the polyA signal and this intervening sequence. The mRNA still works to produce protein, but could this sequence affect the amount of protein or duration of expression?

My guess is that the GU rich region helps to keep the pre mRNA in place before endonuclolytic cleavage occurs.

I am not aware of a particular term other than more generally referring to the sequence between the stop codon and the polyA tail as the 3'-UTR.


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How to quantify the strength of social bonding between the individuals of a colony? How to compare the strength of social bonding across the species?
Consider two different species of honey bees. If I have to compare the strength of social bonding between the two species i.e. in which species, social bonding between the individuals is stronger than another.
Is there any methodology to do the comparison of the strength of social bonding across the species?

I don't know about bees, but in identified animals such as monkeys or river dolphins, scientists can count how many times two individuals are seen together in the same group. You still can mark individual bees, but that seems a lot tougher to do.

@Rodrigo I suspect it's actually easier to do per individual, you just need to do a lot more individuals... :P

@arboviral Then you would count how many times each individual is seen alone or with others? Seems easier, but it depends on the definition of "social bonds".

@Rodrigo yes, I'm not sure how that would work - I mean, all bees regularly visit the hive, so in that sense they're always "with others". But the marking per se wouldn't really be a problem - in fact, it's probably easier than for a lot of other insects just because queen marking is so useful there are commercial products and established techniques for marking individual bees, like numerical labels that glue onto the thorax (https://www.mannlakeltd.com/queen-marking-numbers).

@arboviral Yes, the problem is to monitor some bees in hives with up to hundreds of thousands of individual bees.

Thank you, Rodrigo, arboviral. Observing one colony and interaction between individuals is difficult, but could be possible. What about comparing two different species? @Rodrigo, could you please send the link of the papers? (I will also search the work done in other taxa)

I have been thinking on this. Can we consider the effect of isolation of various group sizes - (1Individua, 2, 4,  ......., 100, ... individual) from colony and see the relative change in the aspects like behaviour, life span, social network?


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Are there any open phylogenetic projects that don't require coding to make a contribution
I am stay at home learner, not pursuing education formal education and currently doing a part time job. I've however completed masters in biotechnology and I'm studying to pursue PhD in molecular evolution eventually. I'm interested in knowing if there are any online open projects in phylogenetics and computational molecular evolution where I can contribute. Leave the projects involving coding. So are there such open projects that don't require coding? An example of contribution I can think of right now is submitting new phylogenetic trees. Please help, I can't find any information online.


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Is this a large bee? (species identification)
While hiking in some low hills near Taipei in the late afternoon in July an hour after it rained, I saw this large flying insect visiting flowers the way bees do.
I'm curious, is it a bee (if so, what kind), does it come from a hive or live on its own, and does it sting?
I'm estimating its body to be about 5 cm long. While not captured in photos, I'm pretty sure I remember it sticking its head into flowerers. It was moving flying from place to place fairly quickly and difficult to get any photos at all, this is the best I could do.
edit: Since further clarification of the size was asked for in comments, I'll add here also that the length of "about 5cm" that I mentioned wold be for nose to tail when stretched straight, (rather than in it's current somewhat curled position) and it could certainly be 4.5 cm. But I'm fairly sure it's closer to 5 cm (2 inches) than to 4 cm. I've added a few more images of the flower sans insect. I've cropped my friend on the left out of the images.

Five centimeters long?? As in, would cover the palm of your hand?

@Dubukay I've seen giant hornets in Japan about that long, so a 5 cm bee isn't impossible. But without knowing the size of that flower in OPs image we can't be certain of their estimate for the bee.

@user137 Yeah, I’m aware that it’s possible, but with those petunia-looking flowers that the bee is sitting on I figured it’d be worth checking

@Dubukay If the bee is 5 cm long, the flower must be at least 20 cm long. I also suspect OP's estimate is too large, but I'm no expert on Taiwanese flowers.

@Dubukay "Five centimeters long?? As in, would cover the palm of your hand?" As my palm is 9.5 cm wide (3 and 3/4 inches), no. 5cm is but 2 inches. When it straightens out, this insect is about 5 cm from nose to tail. I'll go to 4.5 cm, but I'm fairly sure it's closer to 5cm than to 4cm when measured end-to-end rather than in the somewhat curled position shown. Yes it sounds large, doesn't it! Thus the title; "Is this a large bee?"

@user137 I've added an edit to the question which reflects the comment above.

Note: My mistake. I did not notice the OP info that he is in china. There are giant honey bees in China, such as Apis dorsata Fabricius, however their size is only 17-20mm.
========
I suggest  Bombus dahlbomii. It can grow up to 40 mm long, 1.6 inch

Picture
Wiki

OP says they found the bee outside Taipei, but Bombus Dahlbomii is South American. The wikipedia link you give doesn't say if this bee is found outside South America.

Ops. My mistake. I cannot find a anything about a  40-50mm bees native to china. There are large enough wasp but the color and presence of hairs do not match.

Thanks, it certainly looks similar. Taiwan being an island active in shipping, there's certainly a possibility of movement from South America. Though I don't know how to read these 1, 2, 3 but if dahlbomii could be anywhere in South Neotropical Region then that would include here as well. Would this necessarily be a queen, and could it sting?

My bee's abdomen is dark/black and appears smooth, your bee's abdomen is bright orange and fuzzy. My bee's hind legs are orange and fuzzy, your bee's hind legs are black and smooth. Not knowing much about bees, I don't know if that is a big difference or not. There is also of course also the geography thing still...


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What are these four large snails doing?
Hiking in some hills near Taipei after a rain, I saw lots of large snails out and about. Here "large" means the shells are say 8 cm long, and the snail itself fully stretched out 10 to 15 cm perhaps.
At one point I saw a cluster of four snails stuck together in a confusing way. The one on the right was slowly climbing uphill, pulling the other three along.
What is going on here? I see some connections between some of the snails, but I can't really understand most of what I'm looking at here, nor why four snails would be stuck together sideways like this.

The middle two, at least, are having sex with their love dart.

@vkehayas ouch!

thumb up for snails love

These are probably giant African snails, Achatina fulica, an invasive species of land snails. The two snails in the middle are mating using love darts. The other two may be waiting for their turn.
See also: Wikipedia - Achatina fulica

Yikes again! A top 100 invasive species, spreads human disease, and a delicacy according to Wikipedia.

These snails, Achatina fulica, belong to a family of land snails called Achatinidae. They are invasive and while being agricultural pests, can also be vectors of pathogens. The two snails in the middle are actually mating through a reciprocal simultaneous exchange of gametes through the sexual organs that are clearly visible. These species of land snails do not use love darts as suggested by Dr. Evenor.

Please provide citations or other forms of evidence to support your answer.

As @theforestecologist indicates - for species ID answers we expect an image from a credible source that shows the IDd species and additional evidence is necessary, such as proof that the species indeed inhabits the region where it was spotted. etc.


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Is this a hawk, or an eagle?
I saw this large bird gliding fairly low over the trees while hiking in the late afternoon in some hills near Taipei recently. It seemed quite large compared to what I normally see here. It's quite difficult to gauge, but I'd guess the wing span was one meter or so.
It made that shrill, descending, single "peeeew" sound that I associate with birds of prey (probably mostly from old movies or TV commercials).
Is it at all possible to guess if this is a hawk or an eagle from these cell phone snapshots? These are cropped out of the full resolution originals. A half-size original for scale is also included.


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Epidermal layer and muscle wall of colon?
First of all,I wanted to ask that whether epidermis is present in colon ? And if yes than how is muscle wall present with respect to epidermis. Can anyone give me a pic that has both the epidermis and muscle wall of colon.

Is there a source that leads you to believe there is epidermis? Do you mean epidermis as in the outer layer of skin? Or are you thinking of epithelium?

Good question. The colon is lined by epithelial cells (as are all hollow organs). These particular epithelial cells are different from epidermal cells, which are another particular type of epithelial cells found in skin.
Epithelial cells are distinguished by the way they connect with each other using tight junctions to form a permeability layer between compartments.

In the colon, the purpose of the epithelial cells is to both to absorb water and to form a barrier between the luminal contents and the body.  They form the layer facing the lumen. The muscular layers of the colon, both the circular and the longitudinal, are further out from the lumen. You can see them in this histology slide:


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Greek grasshopper?
What is this fearsome insect seen on a Greek Ionian island?

During which point in the day did you observe the cricket?

That is in the family Tettigoniidae. It is a male. Species is Eupholidoptera chabrieri https://wikivisually.com/wiki/Eupholidoptera_chabrieri


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Is tyrosine hydrophobic or hydrophilic?
I’ve seen tyrosine classified as a hydrophobic amino acid due to its aromatic ring in some textbooks and as hydrophilic due to its hydroxyl group in other textbooks.
How does tyrosine actually function in a peptide under physiological conditions (aqueous polar medium and pH~7)?

I am sorry. That was just opinion... :)

https://biology.stackexchange.com/questions/71272/reading-an-amino-acid-physicochemical-properties-diagram/71275#71275

The answer to this question emerges from an examination of the structure of tyrosine — or, more strictly, the tyrosyl residue, which is how it exists in proteins, the concern of the question:

It has both hydrophobic and hydrophilic features and can exhibit both
  behaviours depending on the circumstances.

The ring is aromatic and hydrophobic, but the hydroxyl substituent is hydrophilic.
It is important not to try to fit things into rigid classifications that may not be appropriate for them. Indeed, one should ask how useful a particular classification is in any circumstance, and be aware of its limitations.
The classic illustration of the importance of these dual properties of tyrosine is in Perutz’s description of the differences between the oxy- and deoxy- structures of haemoglobin, where oxygenation of the haem cause the movement of tyrosine from the hydrophobic interior of the protein to the hydrophilic surface. This movement is associated with breaking of ionic bonds between the subunits in the overall change in quaternary structure:

(This is a modified version of Fig. 3 of the original, produced many years ago for teaching purposes. The wiggly line is a cartoon representation of the polypeptide chain of the α-subunit of haemoglobin between His-F8 and the C-terminal Arg residue. For clarity, the preceding region is not shown but its continuation indicated by an arrow head.)

Hi, @David. I was wondering why the arrows in the figure were so curly and convoluted? What's this meant to represent?

@Jam — The arrrow heads just indicate the continuation of the polypeptide chain. The wigglyness is just meant to indicate the omplexity of the structure, with the key point being the helices in which the tyrosine is embedded move. I was a believer in giving students diagrams that they could reasonably attempt to reproduce in a written examination question, rather than using elaborate computer representations where this was impossible. For this forum, the latter type of diagram would be better, I admit.

Tyrosine (Tyr or Y, 4-hydroxyphenilalanin) is usually reffered as polar amino acid because its hydroxyl groupe (polar is rather hydrophilic),  but there is a catch with the benzen ring and stacking pi-pi interactions.

So many authors just put this aa in the "middle". But the other parth of your question is much more complicated.

First of all you need to know that amino acids can behave as zwitterionts. Basicly this is state where is chared amino groupes and karboxyl groupes in amino acid equaly. This state descriped the isoelectric point which is value Ph where is amino acid occure as zwitter ion. The isoelectric point od Tyr is 5.66  Ph. So in 7 Ph it will be charged anyway.

Quick summary chemistry: Tyrosin is polar amino acid which is hydrophilic or hydrophobic up to conditions.

For biological use tyrosine is good adept for phosphorylation and others modifications of -OH group on C4 benzens ring. But basicly is up to circumstances how tyrisyl in peptideds will behave.

@David your answer is excellent (and I upvoted it), and you're right that the OP was interested in the behavior in peptides, but your aside here is wrong. Free tyrosine is of great interest in biology and medicine. It's a metabolic intermediate in a number of important pathways, include catecholamine synthesis.

The comment made by @DanHall is correct, so I have withdrawn my original comment. The point I wanted to make was that in considering amino acid residues in proteins, the zwitterionic nature of the free amino acid is irrelevant. Some of the free amino acids (tyrosine happens to be an example) have other roles in the cell, and in those the zwitterionic nature ensures their solubility in the aqueous milieu. However their side chain is key to their function.


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How would I represent this on a cladogram?
So, right now I am making a cladogram (More of a dendrogram) for a kingdom of fictional species, and I'm not exactly sure how to represent a certain relationship.
Let's say that the oldest class in the kingdom is Clade A. And, while it is a clade in itself, it also evolved into two other classes. The first class it evolved into was Clade B, but Clade A still persists. Then, later on, Clade A evolves into Clade C - but still persists.
If I was to represent this on a dendogram, how would it be done?

The short answer is that cladograms are not compatible with Linnean taxonomy.
The longer answer explain how and why. First, there aren't enough ranks in Linnean taxonomy to cover all the cladogram nodes. The "kingdom-phylum-class-order-family..." was originally based on similiarity and not on phylogenetic relationship. For example: the class Reptilia is no longer a clade, and the class Aves is a subclade of the order Sauroschia (of the "super"-order Dinosauria, which is a clade of Diapsida which includes modern reptiles and crocodiles). The birds (Aves) are evolution descendants of dinosaurs but they ranked by Linneous as class while dinosaurs, according to Linnean taxonomy were at most super-order.
So you need to choose: a pseudo-Linnean relationship tree or a cladogram phylogenetic tree (and then you should omit the ranks' names "class", "order" etc.
I'll try to sketch the tree you described:

 A
 |
 |-- B
 |-- C
 |
 .
 .
 .

Okay, I changed "Class" to "Clade".

A clade is a common ancestor and all of its descendants. So if "Clade A evolves into clade C" then clade C is a subclade of clade A. As long there are descendants of the common ancestor of clade A, clade A does not go extinct.

Note that clade A still includes clades B and C!


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How specific are Vitamin D promotors in the DNA?
As far as I understand there are genes that get regulated by the amount of Vitamin D that comes in contact with DNA. How specific are those promoters? Are there promotors that for example only get activated by calcifediol but not by calcitriol or cholecalciferol?

https://www.ncbi.nlm.nih.gov/m/pubmed/19944755/

https://www.ncbi.nlm.nih.gov/m/pubmed/21397016/

I’ll try and turn those into an answer later.


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Who creates first nitrogen compounds in the food supply chain
As I understand the food supply chain, organic compounds have to be created from a unlimited source (air, water...).
For instance, I figure that plants transform CO2 from air to organic carbon compounds, mainly carbohydrates, which are then the main source for most other life forms.
But I never heard about a plant turning atmospheric N2 to nitrogen compounds.
Where nitrogen compounds come from, and from which source ?

There are nitrogen fixing bacteria who turn N2 into NH3.  Some are free-living in soil, others live symbiotically with plants.
https://en.wikipedia.org/wiki/Nitrogen_fixation

Also some is fixed by inorganic processes, e.g. lightning converting nitrogen into various oxides.


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How are animal patterns encoded in the dna?
After seeing the patterns on the feathers of a argusianus argus pheasant (shown below), I am curious where is the information that encodes a pattern for a particular bird, and what form is this information in?
On the bird below, there is a pattern of gradient in a circle, wavy stripes, spots, a very soft caustic or honey combed pattern, among others.
I am interested in both the process of producing this pattern in a particular bird (which proteins do what), and also what coordinates this process (what in the dna controls these proteins).
For instance, some guesses: maybe some random seed is encoded in each organism, and that determines the initial conditions of some proteins, which through a cellular automata type mechanism the patterns are randomly but reproducible produced in each feather (I think this is similar to the reaction diffusion idea). Another possibility is that the information in the pattern is encoded somehow, pixel-wise (crazy!), in the JPEG style DCT basis, in the JPEG-2000 style wavelet basis, in the gabor basis, from some deep representation of some neural network, or something else.
Any insights and links would be appreciated.


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gene expression of tumor with different percentage of infiltrates
I'm performing differential gene expression analysis on rnaseq of  tumor samples that might have different amounts of immune infiltrate.
Tumors are extracted from patients that respond/not respond to immunotherapy
In my lists I found several immune response related genes significantly modulated but i suspect that this could be related to the different amount of immune infiltrate.
In order to highlight the genes that are induced by the tumors and not by the different amount of immune cells... it could be appropriate to normalize the raw reads counts (on which is based my analysis) on the basis of CD3 gene?

Consider that while a fair portion of your immune infiltrate will be T cells, that you can also have dendritic cells, macrophages, B cells, NK and NKT cells, and other cell types. I like to use this figure to demonstrate that fact, and also make note that the relative abundance of immune mRNA by cell type differs by indication (figure 1).

Source: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4852857/
Also consider that for T cell markers like CD4 or CD8, these are expressed by antigen-presenting cells, as well.

Thank you very much You are right . If i correctly understand it is not easy to separate the mRNA that came from the immune fraction from the mRNA that came from tumors also because some genes are expressed from apc as well.

the best that i might do is estimating the fraction of immune cells present in my samples (with cibersort) and evalute if the amount of immune cells is comparable between samples

@GuidoL I'm not 100% sure the method to delineate your gene signatures but a common issue I'd run into with mac/mono contamination, for example, is you'd see this huge p < 0.005 IL-8 expression, but the common cell that produces a lot of the IL-8 are macrophages. And IL-8 is also secreted by other cells, so you can't link the expression back to a single type of cell, either.


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Does Povidone-Iodine that penetrates through the skin stays in the body (cells, liver etc)?
Here it says on povidone-iodine:

"Route of Elimination: Povidone-Iodine is intended for topical application and is not eliminated"
"Clearance: Povidone-Iodine is intended for topical application and is not eliminated"
"Metabolism: Povidone-Iodine is not absorbed or metabolised"

Now Povidone-Iodine is a very widespread antiseptic used directly on open wounds and there are cases of people using it as a disinfectant before and after microneedling (ie: inducing micro-injuries with a dermaroller device over the skin) which ensures penetration of the substance through the skin and blood circulation and into the body.
What happens with it once it's inside the body - even if some is excreted what happens with the rest which isn't? does it forever lingers within the body (cells, liver etc)?

Your source (DrugBank via PubChem) is describing the typical pharmacokinetic information (ADME, absorption, distribution, metabolism, excretion) on Providine-Iodine, under the assumption it is not absorbed. It's true, a thing that is not absorbed has no volume of distribution, is not metabolized, and is not eliminated.
Though Providine-Iodine is not absorbed as is, Iodine is.
From the Lexicomp drug information for prescribers:

Absorption: Absorbed systemically as iodine; amount depends upon concentration, route of administration, characteristics of skin

Other pharmacokinetic properties are as for Iodine. It may be taken up by the thyroid. Clearance is primarily unchanged (as Iodine) by the kidney.
The absorption through the skin as iodine and elimination by the kidneys are the reasons for the prescribing precautions:

Use with caution in patients with burns (excess absorption)
Use with caution in patients with renal impairment (impaired excretion)
Use with caution in patients with thyroid disorders (taken up by the thyroid)

This case report of Iodine toxicity following prolonged povidone iodine administration is available on pubmed central. It's from the 80s, but it is still relevant and the comments section has a good overview:

The reports of iodine absorption from topical povidoneiodine
  solution suggest that absorption is enhanced when the
  compound is applied to denuded skin, mucosal surfaces with
  high absorptive capacity or extensive areas of intact skin. The
  evidence for iodine absorption includes documented serum
  iodine concentrations and thyroid function abnormalities.

I see, it wasn't understood from the text I've quoted that these claims were under the assumption that the Povidone-Iodine is not absorbed. I don't have access to the Lexicomp info so two questions: 1. I guess my original question concerns the PVP compound - what happens with the PVP that isn't excreted? (question continues in the following comment)

On the PVP page it says that: "THE RETENTION OF PVP IN THE BODY IS PROPORTIONAL TO ITS MOLECULAR SIZE, SINCE ONLY THAT OF LOW MOLECULAR WEIGHT CAN BE EXCRETED. THE RETICULOENDOTHELIAL SYSTEM RETAINS PVP WITH A MOLECULAR WEIGHT IN EXCESS OF 110,000" so does it mean it lingers forever in the cells of the body (possibly liver)? 2. I know that Iodine is metabolized but does this necessarily imply that the povidone-iodine molecule is?

@Amit none of my references are able to measure any absorption of the polyvinyl polymer, just the iodine (released by PVP). The question of excretion vs. retention in the reticuloendothelial system is one of metabolism and excretion, or excretion unchanged. Theoretically, if you were able to absorb  a high molecular weight polyvinyl polymer somehow, it wouldn't be excreted unchanged by the kidney (because it wouldn't be filtered by the glomerulus. It would have to be metabolized by the liver first, which would break it down into something that would be excreted by the kidney.

@Amit the point here is that it's the Iodine that people are/have been worried about (as far as the toxicity of PVP-Iodine is concerned). It's the iodine that is absorbed, and it's the iodine that is (potentially) toxic.

@Amit is there a particular reason you're interested in the idea that the polymer would accumulate and be retained forever in the liver?

I'm specifically interested in povidone-iodine use to disinfect the skin before and after microneedling (which I guess will have the side effect of allowing even high molecular weight PVP to enter through the skin) hence was wondering whether some may remain in the body (possibly disrupting normal functioning). I'm aware of the iodine toxicity risks :) BTW since I'm not a chemist is it likely that the commercial povidone-iodine solution is made such that it doesn't contain high molecular weight PVP or maybe it's not even possible since they'll be spontaneously created?

Let us continue this discussion in chat.


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Insect Identification Request - Is this a Satin Moth or something else?
Date:     July 2, 2018
Time:     11:00 AM
Location: Minneapolis MN
Size:     Approx. 1" from head to tail

I saw this moth at work today. I wasn't sure if it was just a Satin Moth, an albino (it seems to have some pigment), or something else. It fluttered over to the door and landed there to rest. A few minutes later it disappeared.
I would really appreciate some help identifying it. Please comment if I need to add additional information.


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Does the repellence of an insecticide affect its efficacy (measured in insect mortality)?
I am currently working on assessing the efficacy of a suspected insecticide on a particular species of insect. I happen to be looking into any repellence caused by the substance. I test for both effects at the same time by putting that insect in a no-choice bioassay. To be specific, my assay set-up consists of a petri dish, and the test article treated with the test substance is placed on one side of the petri dish. Insect species X is introduced into the petri dish, and every 24 hours, I get to count and remove the dead ones. All these are repeated for different concentrations of the test substance.
What I found is that mortality (proportion of insect X killed) initially increases with concentration, but then decreases after a particular concentration. I also found that repellence increases with the concentration of the test substance. So, what exactly is happening here? Is the repellence of the test substance having an effect on the mortality, such that repellence is causing a decrease in mortality?

Edit: I forgot to mention that I am not qualitatively measuring the repellence of the test substance. The petri dish, that is the assay, is divided into two halves via an imaginary line, and the test article is placed on one side of the assay. An index, which I call the 'repellence index', is used to measure repellence by dividing the difference of the no. of termites between the two sides of the assay, by the total no. of termites observed. Hope that clarifies my question more.

You have a good hypothesis: the decrease in mortality is mediated by an increase in repellence. It sounds like you have a measurement of increased repellence, and it's a plausible mechanism (if an insect isn't near an insecticide, it can't be killed by that insecticide). Now you should test it.
If you are measuring repellence using a different assay (e.g., a choice assay, where the insect can enter a chamber with the insecticide vs. one without), than you could use as the denominator insects that enter the chamber with the insecticide. Compare mortality of insects that enter the chamber with insecticide changes with increasing concentrations in this assay with the mortality in your no choice assay.

Edit: I forgot to mention that I am not qualitatively measuring the repellence of the test substance. The petri dish, that is the assay, is divided into two halves via an imaginary line, and the test article is placed on one side of the assay. An index, which I call the 'repellence index', is used to measure repellence by dividing the difference of the no. of termites between the two sides of the assay, by the total no. of termites observed. Hope that clarifies my question more.

@user43591 since you are quantitatively measuring the repellence, than you can quantitatively measure the mortality of exposed (vs. non-exposed) as suggested in my answer. There is, of course, more to it, but your next step would be to use the data you already have to look at mortality in the termites on the side with the test article only and see what the curve looks like there. Depending on the result, this should give more or less support to your hypothesis that the decrease in mortality above a certain concentration is due to repellence.

Whoa thanks man, never thought of that! Thank you very much!

@user43591 you're welcome! If I answered your question, feel free to mark it the answer using the checkmark to the left of it see someone answers


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What is the meaning of "gap" in G1 phase?
The full form of G1 phase is Gap one phase. G1 os also called first gap phase. Is there any specific meaning of " gap" here ?

The $G_1$ gap is the period between the last cell division and that start of DNA replication (synthesis). That's what "gap" means here. A period of time between two events. It's often described as time spent synthesizing proteins, but I prefer to think about it as the period before the signal to start synthesis lands. A cell can do any number of things in the meantime: synthesize proteins, grow, interact with other cells, move, differentiate, enter and exit $G_0$...

Albert's has a good chapter on the overview of the cell cycle and on the control system


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Some facts about the chameleophant please
Can you give me some facts (where it lives, their size etc.) about the chameleophant?
Can't find it on google...

I do not think you posted the question in good faith BTW, a simple google image search for "chameleophant" or a reverse search using the image will lead you to the website.

I'm voting to close this question as off-topic because this is not the place to post jokes, although I hesitantly admit I almost liked this post. Almost.

@AliceD I like your name

Kind of fits your image doesn't it ;-)

It does not exist. It is a photoshopped image. This is the original image which was used to create it:

It is listed on some websites with other photoshopped images, such as this one:
https://www.planetacurioso.com/2013/05/27/como-serian-los-animales-combinados-con-otros/

Okay thank you but why doesn't it exist?

@Squareoot Because evolution favors practical bodies. Look at the poor bugger, how would it shoot out its tongue at an insect if there was a trunk in the way? Duh...

+1 because you somehow managed to find the original pic. Clever. However, in the future, please flag this sort of questions and refrain from answering, as it encourages other users to post similar crap.


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Does meosis takes place in cell cycle?
Cell cycle is as follows- g1,s,g2,m( mitosis). Does this m stands for mitosis only or does this "m" stands for meosis also

Do you Know what the difference between mitosis and meiosis is?

The headline of your question seems to be incomplete. Is there a word missing?

Yes i know that

This is a question of convention really.
When people discuss the cell cycle, they usually refer to diploid cells (for diploid animals). So in your context, M stands for mitotic phase and does not directly apply to meiosis.
In meiosis, you could say that the cell also undergo a M-phase (actually two in a row, see footnote) but then the cell cycle becomes irrelevant as you get 4 haploid cells (gametes) that cannot duplicate by themselves anymore, effectively breaking the cycle.
Footnote
The M-phase in the cell cycle is a simplification of the process of cell division as this phase can be further sub-divided into a Prophase, Metaphase, Anaphase, Telophase (PMAT for the purists) followed by cytokinesis. In meiosis, you have a slightly different PMAT process during meiosis I (i.e. 1 cell -> 2 cells) followed by another PMAT (2 cells -> 4 cells). You can find additional information here.


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Can any animal ejaculate at will without physical contact?

Note: In this question, I'm asking about animals that have a penis that functions very similarly to humans. I've read some animals have dramatically different methods of copulation and physiologies, so for simplicity I'm only asking about males with reproductive systems very similar to mammals, birds, etc. However, if you feel a certain species deserves special note, please tell me about it.

Are there any animals that can ejaculate at will, while awake, without any form of physical contact with the sexual organs?
I read that a Muscovy drake everts his penis in about a third of a second and the accompanying video shows ejaculation once eversion is complete. This is so fast that I wondered how the male could aim accurately into a female's cloaca. I began wondering if the process was voluntary or involuntary, since a voluntary process seemingly would allow greater accuracy.
So, this led me to wonder are any animals capable of ejaculating at will without any form of physical stimulation to the penis or body?

Can humans ejaculate at will in your opinion? If not, you should clarify what you mean by "at will".

@Remi.b Ah! I had not thought of it that way. Thank you. I'll clarify.

There are literally oceans of animals who fertilize their eggs outside their body, I bet most of them don't require physical contact.

@swbarnes2 that's correct. Perhaps you should post it as an answer with some elaboration.


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Is this a soldier beetle? Bug identification
I'm curious to find out what kind of bug this is. Reverse Google image search suggested a type of soldier beetle, but I am not convinced.
The photo is taken in summer, in England
Thanks!

No, it is a longhorn beetle. Cerambicidae.

Welcome to Biology Stack Exchange! Generally, for species identification questions, you'll want to include the geographic area and time of day.

And also the date of photography and the season.

@KarlKjer You can probably make an answer out of your comment

It looks very much like Arhopalus rusticus, a species of long-horned beetle (Cerambycidae) that is found in England. https://en.wikipedia.org/wiki/Arhopalus_rusticus


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What color is the hemolymph of the Japanese giant hornet?
This is a random and very specific question that's been nagging me for quite some time. I've tried asking on other websites with no luck, and am hoping that somebody here can either give me an answer or redirect me to somebody/somewhere where I can get my answer. I guess it isn't required but I'd also prefer to know, if you can give me an answer, how you got your knowledge on it. Thank you in advanced!

We may never know. Every scientist brave enough to attempt an answer to this question has died from giant hornet attacks.

Well, if anybody lives in Japan then I kindly ask you to cut open a dead one if you find it...

Would it be different from other insects' hemolymph?

Yeah. Spider (an arachnid, but still a valid example)  hemolymph is blue because of copper, whereas some insects have hemolymph that is yellow or green.

I was able to figure this out for myself by watching videos of the hornets being eaten by other insects. The answer is that the hemolymph is a pale yellow color, like I've heard other wasps and some bees have as well.


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Does anyone know of any resources that detail an extensive number of receptor types, their effects, and signalling pathways?
In a similar manner to this Wikipedia page, although I am not too concerned about the localisation of the receptor, or any known ligands, as I can already access this knowledge easily.
https://en.m.wikipedia.org/wiki/Alpha-2_adrenergic_receptor

Hello @Roby Vicary, I think you forgot to link the wikipedia page in your question. To help you elaborate the question: Are you interested in any particular species? Could you give us an example for one or two receptors of the information you are seeking for if you arleady found some?

Hi, @Untitpol, thank you for the response, I have no serious regard for species at this time, the more extensive the better - although if I'm spoiled for choice, homo sapiens. I have added the Wikipedia link on alpha2 adrenergic receptors, the only thing lacking is the number of other receptor types to read up on.

IUPHAR database? As far as I know, this is among the most extensive database of receptors.

Thank you very much @cagliari2005 this is very close to what I am after, perhaps even better! Very thorough referencing, with useful "further information" sections

From the comment section:
The IUPHAR database is one of the most extensive database for receptors and ligands. It also contains a lot of additional information and direct references to the literature.


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What is the difference between a virus and virion
What is the difference between a virus and virion.  Correct me if i am wrong but i think that one can simply say that " virus outside a cell is called a virion" and that this stage is used to go from one cell to another

A quick google search of "virion" reveals the following: "the complete, infective form of a virus outside a host cell, with a core of RNA or DNA and a capsid."
This article is interesting too: http://www.virology.ws/2010/07/22/the-virus-and-the-virion/
Your definition is basically correct, but keep in mind that the viral particle itself never enters the host. It merely attaches to the host cell and inserts its genetic material.

@Astrolamb you're correct, except that whether the viral particle enters the host or not will depend on the virus.

Right, I'd forgotten about enveloped viruses. However, "the complete, infective form of a virus" which has an envelope includes said envelope, and since the envelope doesn't enter the cell, I argue that the capsid is not the entirety of the viral particle in that case. I suppose I'm arguing semantics at this point though :P


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Is the serum concentration of calcitriol different at different times in the day?
Given that calcitriol has a relatively short half-life in adults it would be possible that the serum concentration is at different times of the day different if it gets produced in different quantities at different times of the day.
Is this the case or is the level relatively constant over the day and doesn't follow a daily rhythm?

Calcitriol, or 1,25-dihydroxyvitamin D, is produced in the kidney by 25-hydroxyvitamin D-1α-hydroxylase from it's precursor, 25-hydroxyvitamin D.
Calcitriol has a plasma half life of about 6 hours. It is tightly regulated. This regulation involves a negative feedback loop on its own synthesis and via an inhibitory effect on PTH synthesis, and control by downstream effects (plasma phosphorus, calcium, FGF-23 and others).
25-OH-D, the precursor, has a plasma half life of about 2-3 weeks, and except in chronic deficiency or other pathologic states, is in plenty of supply for the appropriate production of calcitriol. Because of this, it is unlikely that, for example, daily changes in sun exposure or nutritional intake would propagate down to production of the active metabolite.

The image and a good review of Vitamin D can be found in this NEJM article
References ranges at my lab and in Lange's guide to diagnostic tests do not include any interpretation suggestions for plasma or serum 1, 25-dihydroxy vitamin D (calcitriol) at different times of day. Notably, though, this test is not often done clinically. It's primarily for the case where a patient has high calcium, low PTH, and no malignancy has been found.
Despite this (reference ranges do not distinguish between times of day), there may be a circadian rhythm within that range. Regulators and downstream effects of calcitriol do show a circadian rhythm, as is demonstrated in this classic 1972 study:

Is the tl;dr: We don't really know, both are plausible?

@Christian tl;dr: it isn't relevant for interpreting clinical values, but it is plausible (likely?) that there is some circadian variation.

@Christian I'd be surprised to not see some regular variation, along with those calcium, PTH, and phosphate levels.


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Epidemic threshold on a directed network
I am trying to understand the equations used in a paper

(https://www.nature.com/articles/srep00469.pdf)

Mainly I'm trying to understand how the epidemic thershold was calculated using the equation:
$$I^{t+\Delta t}_a = -\mu\Delta tI^{t}_a + I^{t}_a + \lambda(N^{t}_a - I^{t}_a)a\Delta t\int d{a}'\frac{I^{t}_a}{N}+\lambda(N^{t}_a - I^{t}_a)\int d{a}'\frac{I^{t}_a{a}'\Delta t}{N} $$
From the supplementary information (https://media.nature.com/original/nature-assets/srep/2012/120625/srep00469/extref/srep00469-s1.pdf (eq.17)), I get that $$I^{t}_{a} - \text{number of infected individuals in the class a, at time t}$$
$$N^{t}_a - \text{total number of individuals with activity a, at time t}$$
$$\lambda - \text{transition probability, } \mu - \text{recovery probability}$$
I understand that first two terms $-\mu\Delta tI^{t}_{a}$ and $I^{t}_{a}$ represent the number of recovered individuals, and number of infected individuals of class $a$ at time $t$ respectively. Rest of the equation is a mystery however.
In the supplementary information eq.18, we get:
$$\int daI^{t+\Delta t}_a = I^{t + \Delta t} = I^{t} - \mu\Delta tI^{t} + \lambda \langle a \rangle I^{t}\Delta t + \lambda \theta^{t}\Delta t$$
where $\theta^{t} = \int d{a}'I^{t}_{{a}'}{a}'$, I don't understand why we get rid of N in the $4^{th}$ term and how we obtain a moment of a distribution from the $2^{nd}$ term to get this. We then get:
$$\theta^{t+\Delta t} = \theta^{t} - \mu\theta^{t}\Delta t + \lambda \langle a^{2} \rangle I^{t}\Delta t + \lambda \langle a \rangle \theta^{t}\Delta t$$
Which again makes no sense to me, I feel like there is a lot of steps missing here. From here onward it's just dark magic for me, no clue what's going on.
Then this is written as differential forms:
$$\partial_tI = -\mu I + \lambda \langle a \rangle I + \lambda\theta$$
$$\partial_t\theta = -\mu\theta + \lambda \langle a^{2} \rangle I + \lambda \langle a \rangle \theta$$
From that somehow the Jacobian is calcuated as
$$J = \begin{pmatrix}
-\mu + \lambda \langle a \rangle &  \lambda \\
\lambda \langle a^{2} \rangle & -\mu + \lambda \langle a \rangle
\end{pmatrix}$$
Eigenvalues:
$$\Lambda_{(1,2)} = \lambda \langle a \rangle - \mu \pm \lambda \sqrt{\langle a^{2} \rangle}$$
Threshold:
$$\frac{\lambda}{\mu} > \frac{1}{\langle a \rangle + \sqrt{\langle a^{2} \rangle}} + \mathcal{O}(\frac{1}{N})$$
I would appreciate if someone could explain this to me, I have been trying for few weeks now, and it just makes less sense more I look at it.
Now that's the threshold on an undirected network, if I were to calculate the threshold on a directed network how would I do that? Would it be something like this:
$$d_{t}I = -\mu Ia + \lambda(N_{a}-I_{a})a\sum_{{a}'}I_{{a'}}\frac{m}{N} + (N_{a} - I{a})\lambda \sum_{{a'}}{a}'I_{{a}'}\frac{m}{N}$$


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How can enzymes be immobilised on glass?
I’m studying a hypothetical model for urease activity, which involves fluorescence measurement, hence the need for an optical window to which the enzyme urease is immobilised.
From my previous knowledge, immobilisation of enzymes on a solid surface is done through the covalent bonding of the enzyme (outside its active site) with a functional group on the solid surface capable of covalent bonding.
My question is, isn’t glass supposed to be inert? How can enzymes be covalently immobilised on glass? And if they can’t be, are there other materials that could be used instead of glass for an optical window?

Glass can be functionalized by organosilanization so that biomolecules can be covalently attached via some cross-linker. As an example, one might aminosilanize the glass and then cross-link their enzyme of interest with glutaraldehyde.
For what it’s worth, urease activity can be measured in solution.


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Why would a horse-fly quickly dip into water?
For several years I have noticed a large horse-fly, flying very quickly down to the surface of my pond (in Sweden), touch the surface, and fly off. Sometimes it dips down a few times, taking some quick turns above the surface in between. Once, I caught it, and could see that it was a male of some Tabanus species.
(Since they are so quick, I haven't been able to tell if they are all male, but considering the size I believe they are all Tabanus sp.)
Now I want to know why they are doing it. It seems too quick for drinking water, and they shouldn't be feeding there. Could it be some sort of mating or territorial behaviour? I have only ever seen them one at a time, though. In sunny weather it seems to happen at least a few times per hour, all through the day.

Possibly to cool down if they get too hot? I seem to remember reading about this kind of behaviour in dragonflies; but am unable to locate the source.

@RHA interesting, i hadn't considered that at all! in that case it should go together with warm and sunny weather. another thing to keep track of...


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What is the name of this beautiful insect?
I spotted this magnificient looking insect last night in my house in Singapore. It was around 1.5 inches long and had a silverish golden back with long legs and antennae.

 ^ Click for full-size, higher-quality image

 ^ Click for full-size, higher-quality image

Pretty! You should add your location, that makes identification easier. (All i can say is that it's a heteropteran of some sort)

The presence of more than three veins in the forewing membrane (just barely visible in the top photo when magnified) and terrestrial habits narrows this to infraorder Pentatomorpha; the four-segmented antennae eliminate the superfamily Pentatomoidea; not knowing the local fauna forbids further progress from me.

This is indeed a true bug (Hemipteran) in the infraorder Pentatomomorpha.
As Arthur Frost said in his comment, exact identification is difficult for those of us on the other side of the world.
However, a fortuitous series of internet rabbit holes may have led me to a very similar looking specimen.
Homoeocerus striicornis and Homoeocerus angulatus appear to be quite similar in appearance to your insect, and so I would not be surprised if your insect was at least in this genus (see here for more pictures) within the "leaf-footed bugs" family (Coreidae).

I'd say Homoeocerus angulatus is more likely only because the sightings maps on inaturalist show this species being found in Singapore.

I can't say that any incredibly reputable or peer-reviewed resources in English online provide definitive support for this identification, but this is at least a step in the right (a?) direction.


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How are Mono and Diglycerides metabolized without the Free Fatty Acids of Triglycerides?
Having difficulty figuring out what the body does with ingested mono and diglycerides if the usual process of TAG metabolism includes the FFA released from the TAG returning to the MAG to recreate a TAG in the enterocyte, whereas with MAG and DAG consumption, those FFA don't exist. There are many studies (Nagao, 2000, Takatoshi, 2002 and others) confirming that DAG oil consumption leads to weight loss, which is seemingly obvious as the fat cannot be stored without the FFA getting repackaged into TAGs for storage in the adipose tissue. I have not found any studies on what actually happens to the MAGs in lieu of its normal course. I would much appreciate if someone could direct me to literature discussing this process or help me better understand it. Many thanks! Anyone?

Inside the intestinal lumen, di- and triacylglycerol are hydrolysed to free fatty acid and monoglyceride by lipase.
These diffuse through the plasma membrane of enterocyte where they will   used to resynthetize triacylglycerol, and ultimately the lipoprotein chylomicron for transport into the general circulation.
Contrary to what your question seems to imply, the glycerol to which the free fatty acid are affixed is not necessarily coming from the food: glycerol is routinely produced by glycolysis. (This notably also happens in the adypocytes). There is no requirement that food contain a ratio three fatty acid to one glycerol to be fully absorbed - if the weight loss property of DAG are true, it may be through  a different mechanism.

My question was not where the glycerols come from as there are present in MAGs and DAGs as well. The question was that without the extra FFAs which exist in TAGs, the MAGs which are entering the enterocyte do not have the usual accompanying FFAs to re-synthesize into TAGs.

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Which infectious disease would increase global life expectancy the most if eradicated
In the 1700s it was estimated, by Daniel Bernoulli, that wiping out smallpox would increase global life expectancy by over three years. If we could wipe out one infectious disease today, which would produce the largest increase in global life expectancy and by how much would life expectancy change?


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Why does applying pressure to a venipuncture site prevent haematoma?
From what understand, when drawing blood, a phlebotomist puts pressure on the venipuncture site while withdrawing the needle to prevent a haematoma.
I'd like clarification;

How does this prevent a haematoma?
And why is it not necessary until withdrawal?
I assume it's not necessary, and counterproductive to apply pressure prior to withdrawal, besides complications or unusual procedures etc?

My best guess at a rough idea if what's happening is simply pressure restricts flow out of the vein, so slowing blood leaking into surrounding tissue, helping clotting? Or maybe it increases vein inner wall cell damage, releasing agents triggering faster clotting?
Thanks

I wonder this as well - always thought the purpose is to pressure-close the capillary ends to prevent a sudden rush at the moment the needle is withdrawn.

Prevention of hematoma (as we say in the colonies) is by causing hemostasis within the vessel (here, a vein). Careful pressure during withdrawal, followed by firm pressure after withdrawal until primary hemostasis is achieved reduces the rate of hematoma formation.
Thorough mechanistic studies being absent, we can still confidently make some statements about what is likely happening, based on our knowledge of physics and hematology.

Why is it not necessary until withdrawal?

Good venipuncture technique results in a single puncture of a vein that is no larger than the needle. With a single puncture, during the blood draw, all blood exiting the vessel enters the needle and the collection tube. This is why pressure is not necessary until withdrawal of the needle.  In fact, pressure at this point may cause the needle to damage the vessel at another site, allowing blood to exit into the tissue.

How does pressure prevent a hematoma?

On withdrawal, external pressure to a punctured vessel that is greater than the internal pressure of that vessel will stop the flow of blood, preventing blood from entering the tissue.  At a standard venipuncture site, e.g., the antecubital vein, it takes approximately 2-10 minutes for primary hemostasis (in the absence of aspirin, or otherwise poisoned or disordered platelets). If you prevent flow out of the vessel during this period, you'll prevent formation of a hematoma. There are other mechanisms at work here that help, e.g., vasospasm, so you may still avoid a hematoma without pressure, but the rate of hematoma formation is higher when this isn't done

Does it increase vein inner wall cell damage, releasing agents triggering faster clotting?

Possibly, but the primary mechanism is simple physics. Increase the pressure until a plug is formed, and you prevent blood from exiting the vessel into the tissues.


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Why are these ants moving as a pack?
Recently I took this shot of a 'pack' of ants moving towards some destination, and I was wondering, is this normal? Aren't ant scouts lone wolfs, and when a viable source of food is found near the ant colony, the worker ants form a trail to facilitate transport? If so(I'm poorly versed with biology as such, being an electrical engineering student), what purpose could this formation serve, my opinion being bent on supposed predator protection. This is not the only one I've noticed, but it is new to me, and a quick google search without any technical terms to feed it, yielded nothing substantial. This is the monsoon season here in India, if it is of any consequence to this peculiar behaviour.
I'd love to found out more about this(tag edits would be helpful), thank you :D

As you are engineering inclined, I would suggest you look at the Ant colonization optimization algorithm. This optimization algorithm is based for the most part on "real-life" ant behaviors and uses as a premise the pheromone-based communication of ants.

This looks interesting! @cagliari2005

This is a really wonderful phenomenon. Ants disperse far and wide, but when one of them finds food, it brings it back to the nest, and in doing so leaves a pheromone trail. The next scout follows this trail, and finds the food, and then leaves a second pheromone trail over the first one. As this continues, the trail gets stronger and recruits new ants to haul off the bounty. You can have fun with this. Take your finger and rub across the trail to erase it. Or place a piece of tape over it. This will confuse the ants for a while, until they make a new pheromone trail. If you have some time, break up a potato chip, or some other bait, and put it on the cement. Watch the first scout find it, and then leave a trail behind. Soon there will be many.

Sir if I'm understanding this correctly, this is the beginning of a food trail with an initial number of ants joining it, and more would do the same eventually. I did consider this, but what was odd was that, for one, the ants were in no hurry to scuttle back, i.e. they were walking at an extremely leisurely pace, waiting for the group to reassemble, and then moving, and secondly, the fact that they were moving in a single direction barring a few ants which look like they are straying off course, but not going in the exact opposite direction as would the case with a pheromone trail be.

They are not in a hurry. You are correct that in a food trail, you would eventually see ants going in both directions. They may be moving away from the nest in a single line, and then dispersing later to search for food.


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Insect identification Colorado
We found this bug in our house today. So far have not been able to identify it after past hour online. Its pincers look way larger than most normal beetles I can find. Can someone help us finger out more about this critter? Thank you

Perhaps the closest I can find is a stag beetle? Although we are in the city and not heavily forested

It looks a lot like dorcus curvidens, but according to the wikipedia page, it's found in Japan. But I would lean heavily towards a dorcus species.

That is a cottonwood stage beetle. Lucanidae, Lucanus mazama https://bugguide.net/node/view/666700/bgimage


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Does cell compartments and cells shell have the same meaning?
I encountered these two words today. Do they mean the same thing? Does a cell shell and cell compartments refer to a cell that has been emptied of its DNA?


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Are Triceratops and Eotriceratops similar enough to be considered as the same genus?
Everybody knows Triceratops, the horned dinosaur from Late Cretaceous North America, who lived 68-66 MYA.
In 2007, Eotriceratops xerinsularis was named and described (Wikipedia). It lived in (what is now) Canada about 68 MYA. It is a little bigger than Triceratops but in many aspect very similar, e.g. they both have long horns and solid frill, and postcranial skeleton. Gregory S. Paul, in his Princton Field Guide to Dinosaurs 2016, suggested putting Eotriceratops xerinsularis in the same genus as Triceratops, renaming it to Triceratops xerinsularis. I find this suggestion appealing, but I know Paul's taxonomy is unorthodox and not mainstream (e.g. I do not agree with the thesis that Torosaurus is merely a full adult Triceratops).
So the question is: can Eotriceratops xerinsularis be put in the same genus as Triceratops and is this suggestion is plausiable enough?

Taxonomists have wide leeway over assigning higher taxa. The publication process in which Eotriceratops was described as a new genus made it a new genus. However, given a different set of reviewers, they may have rejected the new generic description, and suggested that the author put it into Triceratops. The process is somewhat arbitrary, and there are some random elements to higher taxon assignment. But it is the system we use. If somebody were to write a paper to synonomize Eotriceratops with Triceratops, and that paper were accepted, then Eotriceratops would cease to be a valid name. Its all about publication precedence. Gregory  Paul may have good reason for his suggestion, but it must be published before a change is made.

Not sure if relevant to this exact species but a VERY good talk about how & why we have so many different potentially worng) dinosaur species: https://www.ted.com/talks/jack_horner_shape_shifting_dinosaurs

Can you add references?

Eotriceratops was a larger species of triceratops so they both were similar in name but different in size
Well eotriceratops was a larger ceratopsid but both of them had different predators for example the triceratops horridus was hunted by the T-Rex but for the eotriceratops I don't what predators it had

Welcome. We expect answers to be clear and complete, without personal opinions. Importantly we ask answers to be supported by citations, preferably journal papers.


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What's the current conclusion about humans being omnivores vs herbivores?
What's the current conclusion about humans being omnivores vs herbivores?
And particularly, how is this relative to time? That is, is possible herbivoreness a "strictly" modern phase in human evolution? Or has it even occured yet?

The only people who claim that humans are herbivores rather than omnivores are basing that claim on ideology rather than science, since it is an observed fact that the vast majority of humans do eat meat when it is available.

do you have links to articles that claim that "herbivoreness a "strictly" modern phase" or any reference where you got this question?

@aaaaa I'm using it as a heuristic guess, since to distribute a diverse vegan meal to other than self-sufficient countries one needs some tech behind it, since stuff has to be transported around. Obviously herbivoreness might also be a location-dependent thing. In cold and short sunlight areas meat may have been one of the only foods available during e.g. winter months.

the guess should be based on something, and that is a lot of things to consider. I would suggest you start search on scholar.google.com for paper that studied some of that

Humans are omnivores as they can eat and digest meat. Early humans were hunters and gatherers and meat was a part of the menu from time immemorial. I don't know the exact technic term but some of our teeth were designed to handle meat (canines?). Sure, people can willfully limit their diet to plants only but from the biological point of view humans are omnivores.

some links to scientific literature would be good

I suggest you read this excellent review by Luca, Perry and DiRienzo:
Evolutionary Adaptations to Dietary Changes, Annu Rev Nutr. (2010) 30: 291–314.
I quote:

The evolutionary history of hominins has been characterized by significant dietary changes, which include the introduction of meat eating, cooking, and the changes associated with plant and animal domestication.
(...)
Meat is a critical food resource for modern human hunter-gatherers, along with plant foods (...) The earliest evidence for meat-eating in hominins dates to ~2.5 Mya.

There seems to be a scientific consensus about the fact that the human digestive system has evolved to consume both animal and vegetal foods.


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Can we send signals to nerve?
I want to know two things.

Can we send a signal to a nerve using external source like electricity?
Can we differentiate signals sent from receptors like pain receptors, pressure receptors etc.

Yes, almost no matter what you mean.
The trivial answer is yes, if we record from them. But I'm guessing that's not what you mean.
Please clarify your question.
You may benefit from browsing related questions such as this one:
https://biology.stackexchange.com/questions/52842

Yes. One of many examples would be transcranial magnetic stimulation (TMS).
Often, yes. I work with Drosophila (fruit flies), and we can differentiate between the electrical activity of sensory neurons, even those that innervate the same structure (e.g. sensillum) based on the amplitudes in the recorded electrophysiological signal. Neurons usually fire within a certain narrow range in terms of amplitude and that's one of many ways to differentiate between different neurons, or determine how many different neurons are found in the region where you are poking your recording electrode. Of course, if two neurons fire at the same amplitude, you would not be able to tell them apart using this electrophysiological method.


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Is there a biological determinant for right- or left-handedness?
When I was very young, I was sent by parents to examination where I was told both my hands are dominant in the same way. My parents preferred to make my life easier and chose to focus on my right hand development.
However, all my life I find myself naturally using my left hand - with a knife, to lift things, etc. Yesterday something happened that really twisted my perspective - I was playing bowling and I really sucked at it. And then, the moment I started playing with my left hand, I got perfect strikes.
I use my delicate motor abilities a lot with my right hand (drawing for instance), and now I wonder - how can I tell if I used the correct hand all my life?

This question ends with a question about the poster's personal life history. There is a biological question in the title, but it is never mentioned in the question itself. After five years, surely it is time to dump this question as completely off-topic.


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How long does it take for Vitamin D3 to have physiological effect
As far as I understand Vitamin D3 has no direct physiological effect but has to be first converted. If a person if given a mega-dosis. (50000-200000 IU) of Vitamin D3, how long does it take till the body produces a physiological response?
Is it a matter of hour? Is it a matter of days?

This sounds like an upstream question... i.e., you want to know this in order to know something about what happens if someone takes a large dose of vitamin D3. Can you flesh out your question?

@DanHall I changed the question to be a level higher upstream.

I not sure we still don't have an X-Y problem here. Is this actually the thing you're trying to figure out? Or some thing that you are trying to find out in order to answer a different question. I'm making an attempt to answer, but give me a minute, since a quick search has shown one of my assumptions (that nobody would study that large a dose) to be false.

Well, it turns out I don't know the answer to your question, and I'm not comfortable offering an authoritative answer just by reading some new literature. In a different context, a patient with Vitamin D deficiency, it will take 3+ weeks before calcitriol levels normalize in response to oral Vitamin D3. That (normalized levels of calcitriol) is the physiologic response to oral Vitamin D3. The response to mega doses would likely be different, but I don't know what it would be. There's some work out there, but you'd have to draw some conclusions yourself.


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Are these fruit flies really coming back to life after being frozen?
I've found this video on Reddit where they pretend these are frozen fruit flies coming back to life... I didn't find any publication related to this specific experiment. Is this just a fake video?

! froze grasshoppers in a jar for a few weeks ( home freezer 10 F +/-) .When slowly warmed to room temperature , they began moving.

Short answer
Short-term freezing kills fruit flies. Long-term cryo-preservation of D. melanogaster is also not possible.
Background
Per a publication of Koštál et al. (2016), long term preservation of insects is only possible for embryos, or larvae in diapause. Indeed, freezing is an effective way to kill adult fruit flies (source: Phys.org)
However, D. melanogaster adults show very weak capacity to enter reproductive diapause, and larvae possess absolutely no capacity for diapause Koštál et al., 2016).
Reference
Koštál et al., Scientific Reports (2026); 6: 32346

When I worked in agrocery store I was in charge of taking down the salad bar. Regularly, fruit flies would land on stick to the cold/frozen metal. When the salad bar was turned off, they would fly away.


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Will the interaction of two proteins vary across different tissues?
Suppose protein A and B is both abundant in tissue X an tissue Y. Will A and B interact in X but not interact in Y?
I guess A and B could be biomarkers of a certain disease, and in the pathological tissues their amount remains relatively unchanged but no longer interact, thus losing their functionality and causing the disease.
One possible condition would be that A and B don't interact directly but require a third protein C to act as the scaffold to form the complex A-C-B. So when C is expressed in tissue X but not in Y, we would observe this phenomenon.
Are there other mechanisms or examples?

Your example of an interaction mediated by a scaffold protein is certainly one way of controlling protein interactions. This doesn't just happen in different tissues either, it is also used to fine-control the interaction of certain proteins within one cell, the most notable example for this are the kinases in the MAP pathway (see for example this paper).
Another possibility I can see is that A and B can interact, but only if (at least) one of them is modified, e.g. by phosphorylation - so the actual interaction happens with A-p and B. In a case like this it's not unlikely that the protein that modifies A is only expressed (or active) in certain tissues, which then mean A(-p) and B can only interact in these tissues.