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What does FETCO2(end-tidal fraction CO2 concentration) represent?
What is end-tidal fractional CO2 concentration? I have searched online and found little actually explaining what this measurement is. Thanks again.

I'm not sure if you're asking about the procedure or the underlying concepts of CO2 concentration or how a capnometer works.  But in brief, it is measured at the end of an exhaled breath, which is least 'contaminated' by inhaled but unused air from the conduction zone (trachea, etc.).  The measurement is done by looking at the blockage of light from an infrared light to a sensor by the CO2 - exactly the same mechanism by which global warming works.  And the way it's reported is, in this case, as a fraction from 0 to 1.  It could be reported as a percentage by multiplying by 100, or as a partial pressure by multiplying by the total atmospheric pressure (often 760 torr at sea level).


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What are the interaction energies/chemical potential values for the cytoplasm - protein interactions within the cytoplasm?
I'm trying to simulate phase separation in a biological based system using a Cahn Hilliard model. I have 3 components, they are 2 theoretical enzymes and the cytoplasm. I have found plenty of sources describing the interaction energies/chemical potential/free energy for protein-protein interactions, however, I cannot seem to find any of these values for cytoplasm interaction with proteins. Any help would be appreciated. Please let me know if I am not being specific enough. Thank you!

source: Stack Exchange

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Is this a wasp nest?
Under a tree in an area often sunny, but not sunny enough for grass to grow, and also often humid, but not sufficiently so for moss to propagate, the two plants have left just enough of an ecological niche for a member of the animal kingdom.

Do you recognize this nest? Are these ants? Are they wasps? Should I be wary (of carpenter ants, of a particularly angry type of wasps)?

Where was this picture taken, and when? What type of soil is it? Have you seen anything unusual around? There are many, many different kinds of ants, ground wasps, and other species that dig holes in the ground. Some are aggressive, others not. Until you see something going into the hole or coming out of it, I wouldn't worry about it.

In addition to MattDMo's comment, holes are often re-used, so the critter that made a hole may not be the current resident. If you're looking at a substantial nest of any social hymenoptera you're going to see the occupants coming and going regularly. Less so among solitary species (which are also not typically aggressive).

A neat trick I've seen is to push a little dirt over the hole and wait to see what pushes it clear again, that'd give you an answer. If you can set-up a camera to take time-lapse snaps of the hole, that would be even better than sitting staring at it for hours.

@JiminyCricket. I might not suggest that for a yellowjacket nest, but in that case you're likely to see guards as well as foragers coming and going.

@BryanKrause - It's fine to test, just be ready to run far away and fast. How aggressive a wasp is (towards a disturbance of a nest) is proportional to the size of the nest. If it's a small nest, a wasp might only repair the hole. If it were a large nest, there would very likely be visible activity all day long. So the risk is low.

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Nanodrop is suggesting that a PCR reaction worked but no bands show up when I run the PCR products on an agarose gel
I ran a PCR to extract and amplify a gene I need from a plasmid.
The nanodrop measurements show an increase in the amount of DNA present after the PCR reaction, and the A260/280 is ~1.8, so I think it is measuring DNA and not contaminant.
When I run the product on a gel however, there is no band present, not even any non-specific bands.
I have tried increasing the percentage of the gel to make sure the DNA isn't running off, and increasing the amount of DNA I load onto the gel. Neither worked and there is still no band.
Does this suggest that the PCR didn't work and that I should re-try the PCR? Or should I try to re-run the gel and change something else?

did you run a positive control using the same DNA template and reagents other than the primers? 2) what happens if you take the amplicon sample and re-PCR it? (Danger: you will want to confirm that the product is right by some means if you do this) 3) what happens if you run the reaction in a RTPCR machine and watch the curve? 4) what is your PCR protocol?

Trust your gel and trust your controls.
The Nano-drop can't tell you whether you have a PCR product or not. ND measures UV-vis absorption of organic compounds with coordinated double bonds in your sample, not whole single-stranded or double-stranded DNA. It only gives you a DNA concentration because you're telling it your sample contains DNA rather than some other absorptive substance. A nucleotide has about the same absorption spectrum whether it's incorporated into a PCR product, a primer, or just free floating dNTPs. You added a bunch of primers and dNTPs to your PCR reaction, and that's why you have a higher concentration on the Nano-drop. The nanodrop concentration in the reaction mix shouldn't really change based on whether it worked or not.


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Clarification on Gene Copy Number Calculation: Amplicon vs. Genome Size
I need clarification regarding gene copy number calculation. I used the amount of DNA extracted (90 ng/ml) to calculate the copy number of Pseudomonas sp. The amplicon size was 164 bp. I'm using the below formula for my calculations.
https://www.idtdna.com/pages/education/decoded/article/calculations-converting-from-nanograms-to-copy-number
which uses the length of dsDNA amplicon.
I addition, I found a webpage where they calculated the copy number using the whole genome as a template.
https://www.technologynetworks.com/tn/tools/copynumbercalculator --> In definition session there is an example.
Clarification 1: Is it correct to use the genome size instead of the amplicon size? Should I also use the genome size for my calculations?
Clarification 2: When I used the DNA amount and the amplicon size in the formula, the gene copy numbers were extremely high—eleven orders of magnitude higher than the reference, whereas many articles state that it should be closer to eight orders of magnitude. Is this number acceptable?

Clarification 1: Is it correct to use the genome size instead of the amplicon size? Should I also use the genome size for my calculations?

The ng concentration of DNA in your sample includes all of the DNA, not just your amplicon, so it depends on which sample type you're converting from. Are you measuring a genomic DNA extraction from bacterial cells or a purified PCR product? Either can technically be used for making a standard curve, but amplicons can be a little problematic. It's more common to use either the whole genome, or a plasmid with the target sequence cloned into it. Here's a guide on that. I sometimes purchase synthetic templates from IDT for my standards, but I always include about 30-40 flanking bases on either side of the target, so I have to include those bases in my copy number calculations.

Clarification 2: When I used the DNA amount and the amplicon size in the formula, the gene copy numbers were extremely high—eleven orders of magnitude higher than the reference, whereas many articles state that it should be closer to eight orders of magnitude. Is this number acceptable?

You're converting from weight to copy number. If you only use the amplicon sequence, you're assuming that 100% of the DNA sample consists of full-length copies of your amplicon (as in a purified PCR product). If it's genomic DNA, then you're actually converting to genome copies, of which only a tiny fraction contains your amplicon sequence. A Pseudomonas genome is at least 4 orders of magnitude larger than your amplicon, so around 99.99% of a gDNA sample is NOT your amplicon sequence (depending on whether or not there are multiple copies on the genome). That alone accounts for the differences your getting between the two calculation methods.

Thank you so much for the detailed explanation and clarifications! Your point about the distinction between amplicon and genomic DNA makes a lot of sense, and I now see why my copy number calculations were off. I was indeed converting from genomic DNA, so the massive difference in scale between the genome and my amplicon explains the inflated numbers. I’ll look into adjusting my calculations accordingly, as you suggested. Thanks again for your help!


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

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

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


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Primer dilution verification
I just received a primer (details are displayed in the picture). Since this is my first time doing this, I want to do it correctly. My goal is to make a 10µM primer.
So, If I get it right and based on the paper I received, should I have to add 665μl Sterile distilled water (Inside the primer tube) and then aliquot 90μl Sterile distilled water with 10μl of primer tube mix?

Yes, this is correct. Note that it is not important that the water has been sterilized, it needs to be nuclease free.
Also, for long term storage TE buffer might be a better choice. This will not result in inhibition of your PCR by the EDTA component of the buffer, since the amount of it in the final reaction is neglectable.

Thank you very much for the response as well as for the tip!!!!

@KGee If this answer helped, make sure to accept the answer by clicking the checkmark


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Qpcr Copy number formula
I recently started to get involved with quantitative PCR. I have some data and I want to calculate the copy number of them. In the output Excel file, I have the following cells (I am running Quandstudio v.1.5.2).
Well| Well Position|Omit|Sample Name|Target Name|Task Reporter|Quencher|CT|Ct Mean|Ct SD|Quantity|Quantity|Mean|Quantity|SD|Y-Intercept|R(superscript 2)|Slope|Efficiency

I found the following formulas
copy number = 10^(ct - intercept)/(slope)
copy number = 2^-ΔΔCt

I have two questions.
a) Are these formulas accurate?
b) Is there any other suggested formula that I can apply to my data?
If there is any helpful article that has calculation formulas, it is more than welcome!

Welcome to the Biology Stack, this site values questions that show some attempt to research the answer for them selves. So - what can you tell us about the two formulae - What situations would you apply them in? Why are they different?

The second formula (2^-ΔΔCt) you are presenting does not calculate a number of copies of your target. It is instead used in relative quantitation, where you want to know the relative expression of your gene of interest normalized to a reference gene, and compare it between samples of different treatments.
From your question, it seems that you want to perform absolute quantitation instead, more precisely, you want to know about the exact number of copies of your target in different samples.
For this, you need to run your samples alongside a standard curve consisting of several dilutions of a known quantity of your target. You have to know the number of copies of the target which are present in each dilution step by following the method described here: https://toptipbio.com/dna-copy-number-qpcr/
After running your plate and provided the efficiency of your primers is ~ 100 % and is similar between your standard curve and samples (which you should have tested before), you now know the relationship between number of copies of the target and Ct value. The Ct value you have in each sample can thus be extrapolated to a number of copies.
Edit (because I did not go all the way) :
Then you can plot the Ct values against the log of the concentration of your standard. You extract the formula of this curve, and you replace x by the Ct value of your sample in order to know y = concentration of target in your sample.
Otherwise I found this here : sciencedirect.com/science/article/pii/S0301472X02008068
"Most real-time PCR instruments have software that can automatically compute the amount of template of an unknown sample from a standard curve. However, it can be done manually by putting the observed Ct value for an unknown sample into the formula: (observed Ct − y intercept)/slope." intercept and slope being the ones of the calibration curve.

Thank you very much for the prompt, analytical, and clear answer. You reply without being ironic, trying to evaluate my skills, or asking me testing questions. I think,  I understand the logic and the connection between the curve and the copy numbers. And regarding the first formula? Can this be used for direct copy number calculation? I am asking cause I want to understand how to connect the rest of the excel columns with copy numbers and ct?

I have never seen the first formula before. I do not know what type of samples you have run, what it is your columns contain. But what I know for sure is that you need to have a calibration curve in order to know the relationship between Ct and number of copies.

... I just found here : https://www.sciencedirect.com/science/article/pii/S0301472X02008068
"Most real-time PCR instruments have software that can automatically compute the amount of template of an unknown sample from a standard curve. However, it can be done manually by putting the observed Ct value for an unknown sample into the formula: (observed Ct − y intercept)/slope." intercept and slope being the ones of the calibration curve.

Thank you once again for the reply as well as for the paper!!!!! Now I can practice myself on qPCR data!!!


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What is the true response of human photoreceptors to different wavelengths? Why is there so much disagreement in the literature?
I can find several qualitatively different diagrams of the responsiveness of human cones and rods to different wavelengths of light.
A page referencing Bowmaker and Dartnall, 1980 has the following diagram (which indeed matches that from their paper):

Very similar plots (with the same truncation for M and L cones, and the same slight rise in sensitivity at shorter wavelengths) can be found here.
For a graph with an even sharper nonmonotonicity of the L cone at blue wavelengths, see here.
On the other hand, some diagrams show much more mountain-shaped response curves, like those derived from Stockman & Sharpe at this page (which produce for instance Wikipedia's graph):

Similar qualitative graphs can be seen in this figure, this one, or this one.
My vague impression is that the second category of graphs tends to come from more recent or reputable sources, but I'm very unsure about this, and in general I'm confused why there seems to be so much disagreement here. Are there good survey articles that discuss this discrepancy and the reasons for it?

The first one seems to indicate strong response into the ultraviolet - the discrepancy could be that the first is in-vitro, the second is with the lens in-place which blocks the ultraviolet. Can you clarify the conditions of measurement?

@ARogueAnt. It sounds like Bowmaker and Dartnall removed the lens: "The eye was dissected under dim red light (Kodak safelight no. 2). An equatorial section of the globe was made, and the anterior half lifted away. The vitreous body was then removed from the posterior half without disturbing the retina, and the remaining eye cup placed in ice-cold mammalian Ringer solution of pH 7 1." And I believe Stockman & Sharpe used live subjects, so that would seem to explain it.

That fits at least with the UV response. I'm not sure about the scaling though, I'll bow out.

It sounds like a issue with the precision of the graph. high precision graphs are not smooth curves

Welcome to Biology.SE. In the absence of units, some sort of internal standard, or any other way of meaningfully comparing these curves I would say it is impossible to make valid comparisons. Do any of these publications claim there are disagreements? If so, can you please provide a quotation and reference — if not, I think the "discrepancy" is probably illusory.

@tylersome I’m not sure of the exact units of absorbance used here, but so long as there is a consistent ordinal scale it’s still possible to meaningfully compare the two curves - for instance, the top curve shows a higher value for the L cone at 400nm than at 650nm, while the reverse is true in the bottom plot. This property is invariant under any monotonic scale for the y-axis or per-cone normalization. (Of course they could be measuring different things entirely, and not just using different scales for the same unit, which I would count as a satisfactory answer to the question.)


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What "most closely related to" means in phylogenetic trees?
Here is a sample phylogenetic tree from a textbook publisher:

We often ask questions like "Which organism is most closely related to the pig, the hedgehog or the cow?" I don't like these particular questions, and maybe that's because I misunderstand what "most closely related" means in phylogeny.
I have been told and have read that the most closest relatives share the most recent common ancestor.  For my question, we would have to say the cow is the closest relative of the pig.  My gut feeling says we cannot say that is truly the case unless we have sufficient DNA evidence.  For example, what if we compare the pig and hedgehog genomes and find, say, 80% match.  We might then compare the pig and cow genomes and find, say, a 78% match.  Would this not mean that the hedgehog is more closely related to the pig than the cow is to the pig, despite the heuristics we have been handing students about reading phylogenetic trees?
Here is an extreme example to make my case:  Is the oldest species of archaea more closely related to humans or to the species of bacteria which most recently preceded the archaea?  If we use the "most recent common ancestor" answer, we must say the archaea is more closely related to the human, but I would find its temporal proximity (and thus likely % of shared DNA) to the bacterium to be a much more convincing argument for relatedness.
Question:  How should we interpret and approach these sorts of questions, or are they bad questions due to their lack of context?

Can you draw out a simplified example where the pattern you propose would occur? Perhaps using just one gene with a short sequence as an example, or imagining genes as something that are collected over time in a lineage the way someone collects rocks. That is, start with a common ancestor of hedgehogs, pigs, and cows, which then goes through changes to result in the hedgehog lineage on one side and the pig and cow on the other, which then branch again to separate pig and cow lineages.

The phylogenetic trees are constructed based on a model that links observations with an ancestral relationship. So I think you need to specify which evolutionary sequence you're considering (as Bryan Krause says above), and which types of observations you're interested in correlating to it. Your question focuses on genetic sequences as the main observations. The whole "Woesean revolution" that established the three domains was based on overturning an older phyologeny based on sequence data. That our lineage includes endosymbiosed bacteria is a different fact of evolution.

@BryanKrause I do not entirely understand your request.  Are you and Ryan saying that a phylogenetic tree is based on only one observation at a time, like only one gene?   Regardless, I'm not exactly sure what it practically means to say "the cow is the closest relative of the pig" in any phylogenetic tree.  What traits, observations, or characteristics are we referring to when we make such a statement?

I'm saying that this is how things actually diverge, one step at a time. So, if you know what the "family tree" looks like (from your picture), I'm challenging you to produce something that looks like your hypothetical numerical relationship. Of course not exactly "78%" or "80%", but I'm suggesting that you run through a hypothetical stepwise process, starting from the common ancestor, and see what you need to do to get that result where you would "calculate" a closer relationship between species not shown as closer according to the tree.

You can do this with a totally made up and hypothetical case; you could start with a gene like AAABBBCCCDDD if you wanted and then change, add, or remove letters one step at a time, or you could use traits/attributes as long as you modify them stepwise. Re-create something like the process that would create these relatives as long as you follow that branching pattern.

Of course it's totally up to you if you actually want to do this exercise or not, but if you do and spend some time on it I think it'll help you understand the answers and better yet understand the whole process a lot better.

@Bryan Krause:  I tried your exercise, and I run into the same problem.  Let's say, for the sake of argument, that the hedgehog has gene AAABBBCCCDDD, but the branch leading to pig, whale, and cow has gene AAABBBCCDDDD, then the pig has AAABBBCDDDDD while the other branch toward cow and whale gets AAABBBCBDDDD.  The cow then gets AAABBBDBDDDD and the whale gets AAABBBBBDDDD.  The pig and hedgehog have 2 letter differences, and the pig and cow also have 2 letter differences.

@Bryan Krause: 2nd scenario: Let's say that the hedgehog has gene AAABBBCCCDDD, but the branch leading to pig, whale, and cow has gene AAABBDCCDDDD, then the pig has AAABBDCDDDDD while the other branch toward cow and whale gets AAABBDCBDDDD.  The cow then gets AAABBDDBDDDD and the whale gets AAABBDBBDDDD.  The pig and hedgehog have 3 letter differences, and the pig and cow have 2 letter differences.  This implies the pig is closer related to the cow.

@Bryan Krause:  Final scenario:  Let's say that the hedgehog has gene AAABBBCCCDDD, but the branch leading to pig, whale, and cow has gene AAABBBCCDDDD, then the pig has AAABBBCDDDDD while the other branch toward cow and whale gets AADBBBCBDDDD.  The cow then gets AADBBBDBDDDD and the whale gets AADBBBBBDDDD.  The pig and hedgehog have 2 letter differences, and the pig and cow have 3 letter differences.  This implies that the pig is closer related to the hedgehog.
Summary:  I'm not sure how this exercise helped, as I can generate any possibility.

Let us continue this discussion in chat.

Phylogenies are an attempt to answer precisely the question of what things are most similar, where "similar" can mean one of a number of things. In statistical terms, a phylogeny is a hierarchical clustering of available organisms based on some similarity criterion. This attempts to make use of second-order information to make guesses about closest relatives based on more than just pairwise similarity; pairwise similarity can give you incorrect answers due to convergent evolution / homoplasy.
A phylogeny based on mitochondrial DNA only will differ from a phylogeny based on full proteome sequences, will differ from a phylogeny based on morphological characters, and so on and so forth. These are all different measures of similarity with advantages and disadvantages. We can further pass these data through one or more models of how the data in question might evolve through the tree. These might include the maximum parsimony model based on Jukes-Cantor distance, maximum likelihood based on the F84 model, or something else.
I believe that the specific measurement that you would be most interested in is the branch length. Branches in phylogenetic cladograms are calibrated to show evolutionary distances according to the evolutionary model fit to the available data.
If you are interested in the nearest relative, you may therefore simply measure the length of the branches differentiating any two tips of the tree. Whatever path is shortest from a tip (organism) $A$ to any other tip will be the nearest relative of tip $A$.
This provides an unambiguous method of identifying a closest relative in a tree. Of course, it does not account for organisms that may be missing from the tree that you consider!
For a clearer guide on reading phylogenetic cladograms, I would suggest this resource.

The common scientific figure of speech is "The closest living relative", because the species are like a puzzling family tree, a phylogenetic tree. We can also theorize about a well documented fossil as "the closest known relative".
We can also use close relatives in a plural and general sense:
The closest living relatives of hyenas are mongooses and civets.
The red panda is most closely related to skunks and raccoons.
Armadillos are most closely related to sloths and anteaters.
It's an interesting and practical way to reason about the tree of life. It is best measured with genetic similarity.
Some species have mysterious ancestry, sea cows, red pandas, hyenas, and so it's useful and interesting to know what family of species they belong to.
The notion of relatedness can be referred to as genetic distance. To research biology trees on the web it's usually best to search images i.e. "amphibian phylogeny"
This notion indicates the evolutionary relationship and genetic similarity between organisms, highlighting their proximity on the evolutionary tree.


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PCR and large-scale PCR
I have performed PCR with 50 μL, which showed a clear band in the gel electrophoresis. I then performed large-scale PCR with 3650 μL, which showed an unclear band in the gel electrophoresis. What can be reason for this? Could it be plasmid loss even though there is a band, just a very unclear one? It should be mentioned that the single PCR was performed in the summer, and the large-scale was performed now

It could be poor mixing of the reagents, poor thermocycling of the larger volume, or a host of other issues.  More details on how both experiments were conducted would be useful. Is the 3.6 mL reaction in a single tube? How are you cycling a volume that large (separate water baths)? Did you increase the length of your steps to account for slower temperature change of the larger volume?

@acvill thank you. I made the large-scale in a falcon tube and then moved the mixture to PCR tubes each containing 50 μL, so the PCR conditions should be the same as the single PCR amplification

Still the question is: Did you mix really well?

Do you have photos of your gels?

I made the large-scale in a falcon tube and then moved the mixture to PCR tubes each containing 50 μL, so the PCR conditions should be the same as the single PCR amplification

If all reagent concentrations and cycling conditions are the same, I suspect that you did not sufficiently mix your large-volume reaction prior to dispensing as 50 μL aliquots.

It should be mentioned that the single PCR was performed in the summer, and the large-scale was performed now

If you were using the same polymerase and primer stocks for the small- and large-volume reactions, were the stocks properly stored in the interim? Recombinant DNA polymerases in glycerol buffers have shelf lives of months to years depending on the supplier specifications and storage conditions, though you should expect some decreased activity after several months.


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qPCR - different results total RNA vs mRNA
I have performed qPCR on a tissue, where I have extracted total RNA and also purified mRNA. I ran the qPCR samples together, and have therefore been exposed to the same conditions except the purification step from total RNA -> mRNA. In my results, a gene is down-regulated in the total RNA, but it is not in the mRNA. What could be the reason for that?

What is the mean magnitude of cycle number difference between the treatment and control in each case? I would favor the total RNA results since mRNA enrichment has different biases for different transcripts.

@acvill the mean magnitude difference of the RQ values for the total RNA is 6.63, and for the mRNA -0.8957 - I have subtracted the treatment from the Control

There are a few possibilities.

For whatever reason, your transcript of interest is poorly captured by your mRNA enrichment such that, in both the control and the treatment, mRNA enrichment selects against your mRNA. This would be evident if the CT value for the mRNA control is much higher than the total RNA control, assuming that the mass of total RNA you used in your mRNA enrichment is the same as the mass of total RNA used in each qPCR replicate.
If your primers / probes are nonspecific, your total RNA qPCR results could be the result of downregulation of some off-target noncoding RNA. If your mRNA enrichment protocol is non-destructive (i.e. relies on positive selection of mRNA and not degradation of non-mRNA), you could test the specificity of your primers / probes by performing qPCR on your non-mRNA fraction. Though, interpretation of these results could be confounded if point #1 is also true.


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Does recombination occur in both chromatid of a chromosome with homologous chromosome? Or only 1 chromatid participate in crossing over?
A chromosome has two chromatids. In meiosis weather both chromatid participate in crossing over or just only 1 chromatid does?

So, I am asking whether 1 turquoise and 1 purple chromatid participate in crossing over or both chromatid of turquoise and purple chromatid participate on 1 to 1 basis?

The diagram you provide is just a schematic, showing a simple version to clarify what is happening in a crossover. It seems that at least once crossover has to occur in each bivalent for normal chromosome segregation to take place. This is called obligate crossover. Multiple crossovers do take place, but in eukaryotes this is usually limited to be four crossovers or less for each chromosome pair.

I think like that , different alleles coding for different traits are present on different positions on two chromatids
So both can participate in the recombination  only when chromatids of torquoise and purple have contrasting characters present on each chromatid
Conclusion :- both chromatids of a chromosome will participate in recombination but at different time

Different time means in different cell cycle? So in same cell cycle can both chromatid recombine?

Different time means in one cycle as there are no only one  trait to recombine in one cycle , for eg. If two genes coding for blonde hair and tall height separately but present on a same chromatid then they will recombine with the chromatid having respective alleles on non - homologous chromosomes at different time , as one chromatid can not perform two recombination at a same time , it was my opinion!


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Generally, order and other higher taxonomic categories are identified based on the aggregates of characters. Please explain this
In a book it is written: Generally,
order and other higher taxonomic categories are identified based on the aggregates of characters.
What does it means? Every group is made only after observing aggregate of characteristics then why it is said so? This statement can be seen in a standard high school book (NCERT class 11th chapter 1) in India.

Welcome to the Biology Stack Exchange. Please take the [tour] and visit the [help] for more information on this site and how it works. What do you think it means? This sounds pretty straightforward to me and we have a homework requirement here.

To rephrase bob1's comment: what do you think it means? or, why doesn't it make sense to you? I agree that the text you show is badly written, but hopefully you can still puzzle out a meaning with some effort, it is not technically complex.

Hi bob1 the statement is straight forward but I have question about aggregate word. Any group form considers many characters. Then why it is written for higher order groups only.


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Can a person survive without platlets in the bloodstream?
Can a person survive without platlets or thrombocytes in the bloodstream, if I guarentee that the person is isolated and won't injure?
Any help will be appreciated. Thank you!

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

No. Platelets not only function to prevent overflow of blood from the body by making clots. A considerable increase or decrease in the platelets in the blood can cause thrombocytopenia. Thrombocytopenia is a disease with nose bleeding, red spots on skin, vomits of blood, pink-coloured urine and headaches as common symptoms. Also, even if an isolated environment is provided you cannot prevent slight injuries like acidity and dust particles in the air.


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Do mutations that cause the loss of a complex trait occur more often than mutations causing gain of a complex traits?
The Wiki entry on the evolution of biological complexity states that "[m]utations causing loss of a complex trait occur more often than mutations causing gain of a complex trait". There is no inline  citation supporting this claim, nor could I find anything of the sort in the bibliography. So I was wondering whether this is thought to be the case and what key work has been done concerning this claim i.e. major papers either for or against the thesis.

Many mutations are needed for complex gain of function. Only a tiny mutation is needed for loss. Only one change is needed to break a long chain of synthesis. For example, the chain needed for melanin sythesis - see albinism http://www.albinism.org/information-bulletin-what-is-albinism/

@PolypipeWrangler While the principle you mention is a good general guide, there are exceptions. For example, a single mutation in a regulatory region can change the location and/or timing of expression of a protein and produce complex changes. See the often dramatic results of mutations in insect Hox genes.

While I don't have a citation at hand, I don't think that one is needed. The principle follows directly from the notion of mutation in a complex system.  Put simply, once you've got a functional complex trait in play, there are many ways to break it and much fewer that can further improve it.
This fact is often mis-interpreted by creationists to claim the evolution of complex traits is impossible. With a population under selective pressure, it doesn't matter if more mutations are negative than positive, because the positive traits produce many more descendants.
To take a current example, the SARS-CoV-2 virus has an important complex trait in the form of the spike protein that enables it to invade human cells. An infected person produces a vast number of copies of the virus, many of which have mutations that destroy the functionality of the spike protein. So those mutations disappear immediately, while the non-mutated or neutrally-mutated copies infect as usual and the rare improvement in efficacy brings us developments like the Delta strain.

+1 I think it is worth qualifying what is meant by more often. In a particular individual the loss of trait is certainly more likely than the gain. On the other hand, the direction of evolution as a whole demonstrates acquisition rather than the loss of traits: complex organisms evolved from simple ones, contrary to the creationist argument.

@RogerVadim "Direction of evolution" and "creationist argument" should have some scientific definitions attached if they're to be posted here, I think. This question seem to be simply about the mutation event (based on the context of the referenced wiki quote).

@Armand I am saying that "more often" is both correct and wrong, depending on what one is talking about.


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Which landmark paper first described the differentiation of T-cells?
T-cells are distinguished from B cells in part by their locus of differentiation/maturation (thymus). This is textbook knowledge, but I was wondering which particular person or people were responsible for making this discovery. I'd appreciate any links to their original papers/works. Thanks a lot!

This paper appears to be a history of the discovery of B/T differentiation and the role of the thymus. I believe that you should find a number of important references therein.
It describes specifically a series of publications in the 1950s and 1960s that may be relevant (section "Identification of T and B cells"), such as this one by Gowans.


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Deionized water - can it be beneficial for metabolic acidosis?
I ran into an interesting question today that examined the science around alkaline water and its advertised 'generalized health benefits' assumed to be (but incorrectly) stemming from a rise in blood pH. Logic behind the misassumption itself stemming from a rise in urine pH.
What I'm trying to figure out, is would deionized water (slightly acidic water) actually improve short term metabolic blood acidosis and ironically raise pH levels? Proposed ideas are 1) an acidic water stimulated elevation in bicarbonate secretion (kidneys and exocrine pancreas ) and  reabsorption (to circulation), 2) elevated mineral resorption or 'leaching' from cells. These don't sound all that great in themselves, but regarding a short-term net effect on pH (either on urine or a hypothetical blood ph), could not deionized water have a net alkaline effect due to bicarbonate regulation and cellular reabsorption of minerals being inherently 'slower' than the near instantaneous acid-base reaction?
Alkaline metabolic products of an acidic source that may be included in water (ie lemon) do not count as justifications to an answer. Only looking at water.
If anyone has any relevant studies, feel free to share them, I can't seem to find anything outside of fish.

I'm no expert in blood pH regulation, but it seems highly unlikely that you can treat acidosis by attempting to lower the pH further.  The normal treatment of (acute) acidosis is to give alkaline fluids, usually a bicarbonate solution.  Also, I wouldn't trust any information from the alkaline water peddlers -- it looks like a typical scam.  See for example http://www.quackwatch.org/01QuackeryRelatedTopics/DSH/coral2.html

Absolutely, as a scientist of metabolism I'm fully aware of the quackery in alkaline water. But, my question really is based in the idea: if bicarbonate water increases urine pH, this logically indicates an elongated systemic shift to lower blood pH. Perhaps, by causing a quick decrease in urine pH, an elongated shift towards increasing blood pH wouldn't be out of the question? (As you can guess I'm no expert in blood pH regulation either)

I don't think increased urine pH generally indicates a decrease in blood pH. It seems more likely that urine pH goes up when drinking alkaline fluids precisely because regulatory systems act to keep blood pH constant. Also, this is not a closed system, due to respiration CO2 exchange; and urine pH does not affect blood pH -- it's the other way around. Just some points to think about!

You're absolutely right in this regard, but I do feel there would be a window of a lower blood pH, as compared to baseline, following elevated excretion of alkaline minerals/chemicals/metabolites ect. And just by logic, an opposite effect in which increasing acidity of urinary pH may consequently cause systemic overcompensation leading to a more alkaline blood pH. All theory though, I can't find any definitive proof of this concept anywhere in any manner ("blood pH compensation causing or following a change in urinary pH")

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Do bacteria duplicate the copied virus DNA to put into a Cas9 protein when fighting the virus off again?
When bacteria insert a part of invading virus DNA into its own genetic sequence, on the 2nd invasion does it duplicate that copied DNA again from wherever the bacteria placed it and put it into a Cas9 protein to search for the invading virus.

Virus invades bacteria.

Bacteria copies portion of virus DNA into its own genetic makeup. (Gains immunity)

Virus attacks attack a further point in time down the line.

So does the bacteria then copy that portion of bacteria that it had copied in the past to put into the Cas9 protein? Or does it temporarily remove the virus DNA to go fight off the virus again, to later reinsert the virus DNA back into its own genome?

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

So does the bacteria then copy that portion of bacteria that it had copied in the past to put into the Cas9 protein?

The DNA is not copied, but rather transcribed. The captured piece of viral DNA (called a spacer) is transcribed into a guide RNA that is incorporated into the Cas9 protein to make an active Cas9 complex.


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why can you avoid onions making you cry either by protecting you eyes or your breath?
i was wandering why onion makes me cry when i'm cutting them, so i tried three different things :

first i tried cutting onions with swimming glasses, and it worked (i didn't cry)

then i tried cutting onions without breathing, and it worked too.

it doesn't makes sens to me ! it seems like the second experiment contradicts the first (and vice versa) : my eyes are not protected and yet i don't cry !

and finally, i tried with my nose obstructed, but breathing from my mouth, and it also worked

but i think that is just a variation on the second experimentation, which add an important precision : blocking breathing is not exactly the action that avoid tears, it's not breathing through the nose
i tried to read and understand this paper, but it's way above my capabilities
in the answers to this question, Why does cutting onions cause tears?, it's specified that the lachrymal gland can also be activated in the nose, but it doesn't explain why blocking one of the two way is enough ?

Holding one's breath while chopping onions won't prevent irritation; maybe not breathing results in less gas movement in general, but cutting the onion will cause air movement and eventually the lachrymatory factor will reach the eyes, so breath holding doesn't confer any protection against onions. As to your last question, what way are you referring to?

Does breathing increase the air flow (and onion fumes)  past the eyes?

@anongoodnurse well, try it, i works perfectly ;) it does prevent irritation. And not only for the first few seconds, but one whole minute each time. And i was speaking of the two ways that lachrymal gland can be activated : through the eyes and through the nose. Protecting eyes, or protecting breath.

about the air flow, my third test already covered this question : when i was blocking only my nose, i was breathing, so the air flow was "normal", but i didn't get any tears

I will try it next time I chop an onion, thanks! I'm old, but I can still learn some new tricks. But will you believe me if I report that it didn't help? Or if I tell you that the scientific literature doesn't support your experience? And it has been studied, both for reasons of curiosity and economics (to develop a "tearless" onion.)

well ;) i would have no reason not to believe you, and i would be glad to know ! but that wouldn't change the fact that it works for me :) and for some of my friends that where curious with me :) Actually one of my friends already observed this phenomenon, and as a biologist herself she has an hypothesis : if the lachrymal gland receives a contradictory message : irritating gaz from the eyes but not from the nose, or the opposite, the reaction doesn't start. It might differ among peoples ? i don't know how to verify this hypothesis anyway :/


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Difference between "biotroph" and "parasitic"
In the studying process for my exam I learned about ways of life of pathogenes in plants. There, it was mentioned, they can live nekrotrophic, hemibiotrophic or biotrophic.
As far as I understand, a biotrophic way of living includes being completly dependent on your host. Therefore, those pathogenes do not kill their host.
That sounds like a parasitic way of life. However, I neither found a source that proved me that this is the same nor did I found a source that specifically explained the difference.
I would be very grateful, if some one can explain this to me!
Thank you in advance!

I think the Wiktionary definition of biotrophic is enlightening (emphasis mine):

Describing a parasite or symbiont that needs its host in order to stay alive.

So, all non-necrotrophic obligate parasites are biotrophic, but not all biotrophic organisms are parasites.
Fungi of the lineage Glomeromycota (also called arbuscular mycorrhizal fungi) may be considered biotrophic plant symbionts. Association of these fungi with roots improves plant acquisition of nutrients from soil and, in exchange, allows the fungi to obtain photosynthesis-derived carbon sources from the plant.1 Textbook sources corroborate that such fungi are biotrophic.2

These fungi have a low, or negligible, saprophytic ability and can apparently produce viable propagules only upon the biotrophic colonization of a susceptible host root.

References

Corradi N, Bonfante P. The arbuscular mycorrhizal symbiosis: origin and evolution of a beneficial plant infection. PLoS Pathog. 2012;8(4):e1002600.
Azcón-Aguilar C, Bago B, Barea JM. Saprophytic Growth of Arbuscular Mycorrhizal Fungi. In: Varma A, Hock B. (eds) Mycorrhiza. Springer, Berlin, Heidelberg. 1999.


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Walking or running makes me consume 200 to 550 kcal/h, that's true, but always 68 to 72 kcal per kilometer whatever the effort done. Why?
My connected watch tells me that when :

I'm walking I'm consuming 200 - 250 kcal per hour,
running: from 500 to 550.

and this is ok.
But it also tells me, that how many kilometers are my trips, I'm consuming 70 kcal (68 to 72) for each kilometer, whatever I am going cool slowly (at 4.5 km/h) or running 10 kilometers (at 9 km/h).
It's not what I would have guessed.
In my mind, my body should spend more calories during a distance where it is doing more exercise than when it doesn't.
It's possible that I'm doing a logic mistake, but I'm missing something here, and I'm intrigued.

Connected devices aren't perfect, no matter how "smart" they're advertised to be. To actually determine the amount of energy you're using requires an awful lot of specialized equipment.

In addition to Matt's comment, are you considering resting metabolism? All the "background" stuff: keeping your brain on, your digestive system going, running your kidneys, synthesizing replacement proteins in all your tissues. If you include that in your calories per distance, there's going to be more background per distance when you move slower. If you sit still, your calories per distance are going to become infinite.


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How could a cell only have chromosomes from father or from mother?
How could arrangement one even be possible? How could a cell only have chromosomes from father or from mother?

[Image modified from "The laws of inheritance: Figure 5," by OpenStax College, Concepts of Biology, CC BY 4.0]

Hi! I suggest you read the guide on how to ask a good question: https://biology.stackexchange.com/help/how-to-ask
For example, you might add an explanation on why you think the example is not reasonable, and we may be able to help you.

That graphic is just confusing you.
The cell doesn't keep track of all the chromosomes from Mother versus all the chromosomes from Father so it can sort them out later.  That I know of!  [I don't think imprinting counts because its effect varies between genes]  But the paternal and maternal chromosomes are still separate before meiosis - there hasn't been any meiotic crossing over during fertilization or mitosis!
So by chance, in this diagram, two chromosomes from one parent went one way, and two chromosomes from the other parent went the other.  For 2 chromsomes the odds are 50-50.  For 3 chromosomes the odds would be 1/8+1/8 = 1/4.  For 23 chromosomes the odds would be 1/4000000.
However, the figure isn't finished misleading you!  During prophase I, there is also chromosomal crossover which exchanges segments between the two chromosomes.  So even in that very rare case when a child inherits one parent's form of all chromosomes ... it is still mixed in with stretches of the other parent's DNA.
I like OpenStax, but they are still in an early stage.  Their graphics are weak and many errors can be found.  But as long as you keep up this attitude of challenging your sources and asking questions, you can thrive using resources like this.


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Stem Cell Replication
Reading from the internet, I've come across quotes that said stem cells have the potential to replicate indefinitely. However, there are other sources that say cells that are specialised will have their telomeres shortened each time the cell undergoes cell division until it renders them unable to reproduce.
I would like to ask if stem cells that replicate in terms of self-renewal will have their telomeres shortened as well to a point where they can only renew themselves a set number of times before they cannot undergo cell division anymore.
Thank you.
[P.S. I'm no biology student, just a curious person seeking answers, hence do forgive me if this is supposedly a basic question. I've tried looking online for answers but it seems quite difficult to get a satisfactory or targeted answer.]

Telomere shortening is intrinsic to the process of replicating linear DNA (termed the end-replication problem). Adult stem cells that rapidly proliferate express the enzyme telomerase which is capable of lengthening shortened telomeres, thus allowing theoretically indefinite replication.
Further reading: Telomeres of Human Chromosomes

On which signal do stem cells replicate? is the presence of telomerase (from external sources) the only signal?

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Does my brain have limited learning capacity or memory?
Lately in my free time I like to read books, articles etc etc.. What I have discovered, or maybe it is an illusion(lack of concentration or something), is that I usually forget most of the material that I read about, and have lost my ability to remember names of objects, planets or whatever I read about. Does that mean that I am over-reading or that my brain has limited memory/learning capacity? I should also mention that I have an IT job, which you know requires high concentration throughout the day.

This sounds more like a health advice. Please edit your question to clearly outline the scientific premise and add details and examples if needed.

this is a much better fit for the https://psychology.stackexchange.com/

I disagree with @John comment, neuroscience of the memory is one of the areas of biology.

technically all of psychology falls under biology, but we have a stack devoted to that one subject that will be better able to answer.

The Bekenstein bound limits the amount of information that can be stored in any finite amount of space, so a fortiori your brain does have a limit. Of course, the limit imposed by this bound is vastly higher than the practical limit (if it weren't, our brains would become black holes).

Short answer is yes, the brain has a limited capacity. It's a large but limited physical system with numerous but countable connection, it follows that it must have a limited capacity.
Learning wise, we usually say we learned something when we can recall it at will. I'm not sure I agree with that definition, but if this were the case, learning would be intimately related with memory capacity, so the answer would also have to be yes.
All this without taking into account energy consumption and metabolism which would impose also further limitations, e.g. I bet you that if you switch the activities around and start reading in the morning and try to work at night your work would suffer but your retention capability would improve (just a guess). Now, is all this relevant? I can't say, we (humans) might be working already at full capacity, in this case it would be relevant, or we could be very far away from this theoretical limit and all this is moot.
If that was really your question then you're done.
However, you seem to be preoccupied with a mismatch between the expectations of your own retrieval abilities after a particular "type" of activity and what you can actually remember.
I would be remiss in I didn't say that I agree with WYSIWYG's comment, I'm sure this is not the place for health advise. So with that in mind my 2c:
your expectations can be misaligned, that's always a possibility; your retrieval abilities can be impaired, which means that you learned fine but cannot recover it; or may favorite: you might just be tired! IANTTOAD


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Contradiction to evolution
It is said that evolution occurs according to requirement ..if it is true then women who really needs safety should be strong and men who don't should not be strong...isn't it contradictory?

Why don't men need safety? Evolutionary men were supposed to protect the woman while they are weak (pregnancy, caring for small children).

It is not.
The result of an evolutive adaptation depends on different kinds of selective pressures. So, the solution can be more complex that you may expect and there can be more than one solution to the same problem as well.
To stick with the example you made. One possible solution could be to have stronger females (note that this is true for many species of insects for example) another solution could be to have cooperation among the two genders and have for example stronger males that protect the females.
Also, you have to take a broader look at the effect of one particular trait because its evolution doesn't need to answer only a single problem but to fit in a context. For example to have a bigger and stronger body can be a problem if you don't have enough food to sustain it, so that particular solution, that looks obvious at first, can lead to a suboptimal result in a determinate context and can be counter-selected in the long run.
Moreover, especially in the case of social animals, the social context affect the evolution as well. For example, you may have a society in which strong woman are less likely to have children because of some social rule rather than because of some strictly-environmental reason. If we as a society, again just an example, decide that only girls taller than 190cm shall reproduce, then after a few generations you will have selected that trait.
Finally, remember that evolution doesn't propose the only "good" new traits, it proposes "random" ones, you never know in advance whether they will be useful in future or not.


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Skull of which animal ist it?
Hi someone found this skull in ancient city of iran I'm just curious to find out which animal belongs this skull?

Welcome - if you think that I have given the correct answer, use the check (tick) mark next to my answer to indicate that.

This will be one of the two-toed ungulate mammals (Artiodactyls), I think one of the smaller ones, probably in the family Bovidae, which includes the antelopes and goats as well as cows and sheep.
Furthermore, because the laws of frequency tell us that it is rare to come across a rare species, therefore this is most likely to be a common species. So, what species are common in Iran, that have two horns curved gently towards the back of the skull?
Goat (Capra hircus) or sheep (Ovis aries) are the most likely animals, though I lean towards goats in this case because of the shape and position of the horns.

Having had many goats (of several breeds) and having to guard my rear around some of them, that was the first thing I thought of when I saw that partial skull.


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Is there a recently published Flora of Japan in English?
I am currently getting into the study of the flora of east asia. For China, Taiwan and Korea I could quickly find modern treatises, see 1-3 below. But not for Japan, to my surprise: Even after quite some searching all I could find is a 111 year old text, see 4.

Question: Is there a more recent English language publication on the Flora of Japan?

Hong, D.Y. & Blackmore S. (Ed.) (2015). Plants of China. A
companion to the Flora of China.  Cambridge University Press, New
York

Chang-Fu, H. & Chung-Fu S. (2019). Introduction to  the
flora of Taiwan, 1: geography, geology, climate,  and soils.
Department of Botany, National Taiwan  University, Taipei

Lee, Y.-N. (2006). New Flora of Korea.  Kyo-Hak publishing,
Seoul

Takeda, H. (1913). The Vegetation of Japan.
The New Phytologist, 12(2): 37-58


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Good source for current taxonomic keys
I’ve recently taken back up my interest in entomology and taxonomy. I used to be a biologist, but have long since moved to another field to make my way. I realize that all of my taxonomic keys are likely way out of date as they are mainly from the 1970s and earlier. So I’m looking for keys mainly dealing with the order Neuroptera in insects. Does anyone know where you can obtain current info?

There's the International Committee on Zoological Nomenclature, which has ZooBank, a collection of publications on nomenclature etc.  Keys would strongly depend on where you are in the world. Have you checked out the external links on Wikipedia for Neuroptera? Looks like some candidates there.

Thanks bob1, those two leads are what I needed.


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Haploview command line: how to get tagSNP
I am trying to use Haploview command line software to compute haplotypes and extract tagSNP for those. When I use the standalone version on my local computer I tick the 'Show tags in blocks' option so that when I export my haplotypes I get the tagSNP to be marked with '!'.
I am trying to do the same thing with the command line version but can't find how to achieve that. My command is as follow (submitted to Linux running server):
java -XX:+UseParallelGC -XX:ParallelGCThreads=1 -jar haploview.jar -nogui \
                    -pedfile $pedfile \
                    -info $info \
                    -out $out  \
                    -maxDistance 100 \
                    -skipcheck \
                    -missingCutoff 0.5 \
                    -blockoutput GAB \
                    -dprime \
                    -log ${out}.log \
                    -memory 124000 \
                    -aggressiveTagging \
                    -aggressiveNumMarkers 3 \
                    -taglodcutoff 3 \
                    -tagrsqcounts \
                    -tagrsqcutoff 0.8 ;

I manually set arguments to the same value when using the standalone version so the only thing differing seems to be the 'Show tags in blocks' option.
Could you explain me how to get the tags to be marked in the *.GABRIELblocks files or how to do it myself using other output files ?
Thanks a bunch !


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Suggestions for an experiment?

I would appreciate suggestions for my year-long AP Biology project. Such a project would consists of a standard experiment, to be done over the period of a year, so it would have >to be fairly substantial.
I'm interested in anything cell/DNA/molebio related with a mathematical connection. I >would prefer something other than mere statistical analysis, maybe something like >differential equations.
I have access to standard undergraduate lab equipment; assume that I'm able to procure all necessary materials and that I'm capable of performing the experiment. Thank you for the help.

As per the suggestion of shigeta below, I leafed through the links, and found gene circuits interesting. So, what exactly is a gene circuit, how are they modeled, and what are they used for?

systems biology.. do a cell bio experiment and develop a mathematical model for the system. you can validate the model using the experiments..

You really need to narrow this down. We don't know your competences, the materials you have available, the fields of the various labs you may have access to, there is no way of answering this question without a much more specific scope.

Yes, I probably should have been more specific about that; it'll be edited. I'll look into systems biology.

Still going to need a little more on the equipment side.  I consider tissue culture standard undergrad work because that's what I did a lot of the time in undergrad.  I also have been doing Westerns since high school.  You mention cells, do you have a way to culture them, you mention DNA, do you have gel rigs and the means to isolate DNA, and molebio is so broad it's not really limiting.

Yes, I will have access to everything you mentioned.

I'm still not certain that this is a good question for SE, because I'm not sure it can be answered, but I would look into a forward genetics experiment.  You can do predictive and analytical modeling, and push the forward genetics over a whole year easily.

I suggest you ask the gene circuit question as a separate question. And you can get specific with it, too – as in "how would I construct an experiment with such and so requirements/resources to do such and so regarding gene circuits"

This is a bit hard - most possible answers you still aren't going to like, but I'll give you three suggestions.
It sounds like you want to take something with a mathematical model and try to modulate it with molecular biology.
It seems unlikely that I can really give you a specific project, but there are four sources  I will recommend you look at.
I think I'd suggest the further limiting assumptions:

you want to work with E coli - its the easiest and most readily available organism to work with.
you want to work with a system that is self contained within a single plasmid - so it relies only upon 2 genes to act, 3 at the outside or you will have issues getting it all to work.
you want a mathematical system that already has a well fit model that  you will peturb.  building a new model might be a bit of a big first off project.  (but who am I to tell you what to do - these are just suggestions).

The First suggestion I have is Jeff Hasty at UCSD.  He has focused a lot on oscillating gene circuits.  He has simple systems that might be reproducible with a small lab, most recent work that combines a GFP oscillator with LUX is pretty cool. Both oscillators and LUX are independently good systems to work with. .  I've been a science fair judge and I can tell you, just reproducing one of his systems would be an impressive lot of work
Another body of work to look at is Adam Arkin. He has looked at lots of circuitry component candidates.  Articles such as "The hunt for the biological transistor" might get you thinking.  This is a broader body of work, and so it might take a while to get an idea from it.
Third, if this is boring to you and you want to look more broadly, you can look through the iGEM competitions.  These are projects with oscillators and bio synthesis systems which sometimes have mathematical models associated with them.  The big advantage here is that you might be able to start or join an iGEM team and then some or all the plasmids will be made already - mol bio gets very expensive if someone doesn't gift you some materials.


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What should be evaluated in food decomposition experiment?
Briefing
Some days ago I noted that 3 cookies left on my desk since 3 months ago are still "fresh", and by that I mean... not spongy like some cookies that get soft after some time outside.
However this particular brand of cookies do get spongy, I'm not sure why don't these do!
I also noted that there is a cockroaches/flies infestation in a home nearby, so these are getting in my house, but none of those insects dare to eat the cookies.
So, I decided to make an experiment inspired in the well known experiment of Watermelon vs McDonalds Burger where a watermelon decomposes extremely quick, and the burger does not. This article even mentions one that hasn't decomposed after two decades!
I understand that watermelon decomposes so fast mainly because of the sugar/water that it contains, but that is another story, let me tell you what I want to do.
Problem
In this experiment the only notable variables taken into account were: Visual appearance (picture), and time.
For my cookies I want to do a similar experiment, but I want to know which variables should I consider, so far I only have these in mind, but I want to know what else can be considered for food products:

Date of packaging
"Best before" date label
Visual appearance (daily pics)
Time gone by before going spongy
Humidity of room (3 daily measures across the day)
Temperature of room (3 daily measures across the day)

And the samples will be:

Being in a closed room (eg. my room)
Being in an open room (eg. dinning room)
Exposing to insects directly (eg. roaches, ants, flies)
Adding a drop of "morning saliva" (mainly for the bacteria)

Question is
In general, what do I need for food experiments? I think these are OK, but maybe I'm overdoing it on some, and maybe I need to consider some other parameters.
My experiment's objective is to see if it decomposes, why does it take X time to do so, or why doesn't it decompose at all, if it is safe to eat, or if it shenanigans like McBurgers.

You could weigh the cookies in a time course to see how quickly the cookies are degraded. Also, you could take some samples and make cultures in Petri dishes to see if there are differences in the microbiota associated with each one. In this line, maybe you'd want to sterilize the samples by some means, just to ensure they have the same microbial conditions. You could also measure the porosity of the samples by pacing them in water and measure how much water it can absorb, or something like that. I assume you do not have an HPLC engine, but you could also make extracts and see how the spectra varies over time.


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Epistasis Across Chromosomes and Individuals 'Homozygous for Interactions'
Apologies for any failures in nomenclature. I'm a mathematician who is making a foray into genetics for a masters thesis. Specifically, I'm generating artificial diploid genetic sequence data and phenotype data based on known epistatic interactions.
Primary Question
I am familiar with the concept that having multiple copies of a single allele (e.g. one from each parent) can actually increase expression and thereby change the quantitative phenotype (at least in some cases?). Can this also happen with epistatic effects? For example, consider the case that locus 1 ($L_1$) and locus 2 ($L_2$) exhibit some positive interaction ($\beta$) on the trait ($Y$).
$$E[Y]=\mu+\beta(L_1L_2)$$
If both chromosomes contain the allele in question at both loci, then does this individual exhibit more of a trait increase than if he only had one chromosome with the epistatic alleles?
Secondary question
Can alleles interact epistatically even when they are present on different chromosomes? e.g. assume allele A at locus 1 interacts with allele B at locus 2. Individual has A at locus 1 and b at locus 2 on chromosome 1. He also has a at locus 1 and B at locus 2 on chromosome 2. Do A and B from the different chromosomes interact? My intuition is yes but I want verification.
Many thanks!!!

Question 1: The phenomena you describe in which it matters whether you have one or two copies of an allele (e.g., the AA phenotype being different than the Aa phenotype) are known as dominance effects. Dominance effects can interact with epistatic effects (in which the phenotypic effect of one locus depends on the genotype at the another locus).
One good example is the interaction between the Agouti locus and the Mc1R locus in the oldfield mouse (Peromyscus polionotus) in determining coat color. Dark-color homozygotes for the Agouti locus have dark coats irrespective of the allele at the Mc1R locus, whereas color in Agouti heterozygotes or light color homozygotes depends on genotype at the Mc1R locus. The figure below, from Steiner et al (2007), illustrates:

Question 2: Epistatically interacting loci need not be on the same chromosome. The loci discussed above provide a perfectly good example. Mc1R is on chromosome 1, where as Agouti is on chromosome 7, yet they interact epistatically.

Ah! I can't believe I completely forgot that there were different types of dominance. Specifically in Question 1, this would be either codominance or intermediate dominance, is that correct?

I'm not sure I understand what you are asking. If we have alleles A and a, we can have dominance (Aa and AA have the same phenotype), codominance (Aa has both the aa and AA phenotypes), or incomplete dominance (Aa has a phenotype intermediate between aa and AA).


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Left Ventricle vs. Right Ventricle size in different Animals
Why are the right ventricles in chicken hearts significantly smaller than the left ventricles, whereas in cows the two ventricles are of roughly equal size.

The question is interesting +1. Can you please add a reference and/or a figure showing that they differ? If you happen to know whether these traits are shared among all birds and all mammals respectively, that'd be great to state it.

I don't know where you got your information, but it's not correct. The bovine (cow) heart is very much like the human heart in that the right ventricle is significantly smaller than the left. It's important to note that the difference is in muscle mass, not volume of blood each ventricle holds. More muscle is needed to pump blood through the body than through the lungs.


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Are wasps attracted to a sting
A little backstory, I was trying to get something that was in a little wooded bit at the back of my garden and stepped on a swarm of wasps was stung 3 times and got out of there but I brought 8 wasps inside and was wondering if they know if you've been stung and are attracted to it and also out of curiosity what would happen to a wasp if it was stung by another wasp

Tackling the second part of the question first: If a wasp is stung by another wasp, that's usually super bad for the wasp in question. Wasps are pretty good about not stinging one another, but occasionally wasps from other communities come in and cause a ruckus, or even predate on other communities of wasp specifically. If a wasp gets stung by one of these, it's about to die horribly, then get eaten.
On the other hand, if it's stung by 'friendly fire', it'll just die horribly. The venoms wasp stingers carry, while merely irritating and only occasionally fatal due to allergies on our scale, are generally pretty lethal to insects, arachnids, and other tiny critters; also, having a huge hole in your exoskeleton doesn't help.
As for the attraction question, the answer is a solid and absolute 'Eh, probably not.'.
Wasps, like a lot of insects, communicate on pheromones and dancing, but on the whole their 'deal' when not hunting is to repel, not kill. They don't care if what they sting gets killed or not; so long as it gets out of their zone of control. While they do issue alarm pheromones and other calls to action, these are not associated with stings in particular, which mostly deliver poison and sharp force trauma, not orders to the swarm.
You'll probably want to clean out the stings in any case, but it's unlikely that your new house guests want anything so much as just going home. Usher them out the door, and they'll be happy as clams.

I thought Wasps don't eat other insects, they do feed them to their larvae.

@RHA That seems like a petty distinction. Are wasp larvae not wasps?

Well, they have a different diet. Wasps eat sweet stuff (either excreted by the larvae or from your soft drink).

@RHA I think that varies by species. Wasps are freaks like that.

Well, all species of Vespoidae work like that. These are the colonybuilding, stinging creatures that most people call wasps. There are off course many solitary wasps, but these hardly ever sting people.

@RHA True enough. But if we're not rigorous in what constitutes a wasp, then why are we here?

I was stung this afternoon. I drove home, washed the site with vinegar and was icing it, when out of nowhere a wasp came in through the open window and began to buzz around the part of my arm where I was icing. It landed, walked around for a few seconds, as if it was investigating. It was the oddest thing!

Hi. This is not an answer, but rather a comment about something that happened to you. Please delete this as an answer and move it to be a comment instead.


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Hardy weinberg equilibrium and Wright Fisher model
Is the hardy weinberg equilibrium derived by using a model similar to the Wright Fisher model, just without assuming genetic drift and finite pop size? Both seem to use the same assumptions except Wright Fisher takes into account finite pop size and genetic drift. What is the model used to derive Hardy-Weinberg equilibrium called?

Welcome to Biology.SE
When you talk about the 'Wright-Fisher model' I suppose you are referring to the 'Wright-Fisher model of genetic drift (WF)'  involving the use of a binomial distribution.
You are correct that the two models make very similar assumptions. However those assumptions are generally speaking found in a large set of different models just because they often simplify the math. I think it is quite wise to consider these two models as very much independent.
Shared assumptions
Both the WF and the Hardy-Weinberg model (HW) assume

non-overlapping generation
panmictic population
absence of selection, migration and mutation
random mating
no sex-ratio bias

Of course, violation of some of these assumptions are relatively easy to model but such complication is often not taught in intro classes to population genetics.
Wright-Fisher model derivation
Let $2N$ be the total number of haplotypes, where $N$ is the population size. I here just assumed a diploid population but derivation for a haploid population is just as easy. Let $k$ be the number of occurrences of allele A, so that the frequency of the allele A is $p=\frac{k}{2N}$. Assuming sexual reproduction only, the number of occurrences of the allele A in the next generation is
$$k' = {2N \choose k} p^k (1-p)^{2N-k}$$
Quick side note: Effective population size
The variance of this distribution is $var(k') = 2N p (1-p)$. The variance of the allele frequency in the next generation is therefore $var(p') = var(\frac{k'}{2N}) = \frac{1}{4N^2} var(k') = \frac{2N p (1-p)}{4N^2} = \frac{p(1-p)}{2N}$.
Replacing $N$ by $N_e$ and solving for $N_e$ yields
$$N_e = \frac{p(1-p)}{2 var(p')},$$
which is the definition of the effective population size $N_e$.
Wright-Fisher model assumptions
The WF does not per say assume a finite population size, it is just that when the population size is infinite, the model loses all of its appeal!
Hardy-Weinberg model derivation
See here for a more complete discussion
The derivation of Hardy-Weinberg genotype frequencies is simple enough to not rely on any pre-existing model. Let's consider the simple version of the HW model, the one with a bi-allelic locus. The two alleles A and B exist at frequency $p$ and $1-p$ respectively. Imagine you have to draw an allele from this population. The probability to draw a given allele is equal to its frequency. Now draw a second allele. Assuming the population is large enough or assuming that selfing is allowed, the probability of drawing a given allele is still the same at the second draw than at the first draw.
As such the probability of drawing the allele A twice is simply $p p = p^2$. Similarly the probability of drawing the allele B twice is simply $(1-p)(1-p)=(1-p)^2$. The probability of first drawing the A allele and then the B allele is $p(1-p)$ and the probability of first drawing the B allele and then the A allele is $(1-p)p$. If we don't make the discrimination between AB and BA genotypes and just call them all AB, then the frequency of the AB genotypes is $2p(1-p)$. Of course $p^2 + 2p(1-p) + (1-p)^2 = 1$.
Hardy-Weinberg model assumptions
It is common to say that HW assume infinite population size. This is correct if you make from HW the interpretation that the genotype frequencies are exactly at $p^2$, $2p(1-p)$ and $(1-p)^2$ and that no evolutionary change will occur. But if you interpret HW as indicating the expected genotype frequencies from which deviation exist, then you do no make the assumption of infinite population size. Under this second interpretation, one can test deviation from HW expectations with a binomial test (or most often, when the population size is large enough with a $\chi^2$ goodness-of-fit test).
Related post

Solving Hardy Weinberg problems is very related and offers a good tutorial.


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Are there dichotomous keys for identifying medical conditions?
I know dichotomous keys are often used to identify flora and fauna.
I was wondering if they are also used in medicine for identifying diseases -- are they? If not, why not?

For histopathology they use them all the time to describe cells and tissues, very much as they are used to describe biological entities.  Characteristics like size, cytoplasm to nucleus ratio, grouping, staining characteristics, immunohistochemistry and now molecular attributes are all used to categorize a cell of interest.  For cancer, the identity of the malignant cell is crucial to diagnosis and subsequent effective treatment - based on successful treatments used in the past for people with that type of cancer.
Here is a histopathology dichotomous key I found at Noelways.com

There are several doctors that post on this site, so hopefully one of them can give a better answer. Anyways, several years ago I took a certification program as an emergency medical responder (basically the lowest level of EMT in my area). Various dichotomous keys are used to assess patients. These were not diagnostic but rather used for determining correct patient management. For example, here is a key for airway management. Obviously, these would be committed to memory.

I think the equivalent concept in medicine is the differential diagnosis.

Welcome to the site. We are looking for longer, informative answers. See the guide: http://biology.stackexchange.com/help/how-to-answer

I grant that longer answers are more useful, but it's all I had, not being a doctor. Should we have waited three months instead, for the more helpful and complete answer? I actually don't see anything on your help link that refers to length of answer. In fact, I would argue that my answer falls under "Have the same problem?", which says "Help us find a solution by researching the problem, then contribute the results of your research and anything additional you’ve tried as a partial answer. That way, even if we can’t figure it out, the next person has more to go on." (We can take this to Meta.)

Sadly, no. In plants, you know exactly the number of sepals, the number of petals, the shape of leaves, the type of pollination and other variables used in 'travelling' through the key.
Equivalently, a dichotomous key in medicine would require that a patient with a certain disease display all of the signs and symptoms so-and-so (eg. belly pain, vomiting) and none of the signs and symptoms this-and-that (eg fever and cough) for any given disease. Very very sadly, this is not the case.
As an example, appendicitis: in the typical clinical picture, a patient presents with dull pain around the navel for a few hours with loss of appetite, before progressing to sharp right lower quadrant pain with a low fever and nausea. Simple? No. This presentation appears in about 30% of patients with proven appendicitis, the rest may or may not have had pain around the navel, may or may not have lost their appetite, may or may not run a fever that may or may not be suitably low-grade, they may or may not have been nauseous, they may or may not have vomited, they may or may not have accompanying malaise, some even show up without the basis for diagnosis (sharp right lower quadrant pain)...
To make things even more complicated, there's a significant number of patients who DO present with the classical signs of appendicitis (including the obvious appy symptom of sharp lower right quadrant pain) or dangerously similar, but don't have it. What do they have? Your guess is as good as mine, the differential diagnosis is loooooong, and includes things ranging from "OR RIGHT NOW BUT IN A DIFFERENT SPECIALTY!!!!" to "Don't you dare take that patient to surgery, it could kill them!"
And that's just a 'simple' appy. There's a reason they call it the art of medicine.

Interesting perspective. But in my mind, anyway, it's a number of dichotomous keys that overlap. This comes together in the differential. It all happens on almost a subconscious level after many years of experience, and becomes "a gut reaction" (which is really not intuition at all), that which you call art. But to say there are no dichotomous keys in medicine is an oversimplification for sure.


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A hypothetical nerve damage question
If a 100 pound bucket is dropped on someone's hand, what will this do to the nerves, will they get crushed, will they die? And how will this affect that person's ability to feel or move their hand?

From what height?

About 3 feet off the ground


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What is the mechanism behind the association of a sensation with a stimulus?
I'll explain the question with an example.
Consider Gustation: glucose tastes sweet, bitter gourd tastes bitter and salt tastes salty. Now, sweet obviously feels good but suppose there is an alien species whose biochemistry is different from us,  they don't use glucose as a fuel. Now glucose maybe toxic to them so they experience a bad taste whenever they ingest glucose. In this case, the sensation is different!
Another Example would be Photoreception. How is it decided that light having wavelength of 700–635 nm would be considered red and not blue? I know that your answer would be "This is because light of this wavelength stimulates the red cone and not the blue one." Then my question would be why stimulating the red cone gives us the sensation of red colour and not of blue colour?
Similarly, Why does air of temperature higher than our body gives us a sensation of "Hot" and not of "Cold"?
I know that having different sensations for different stimuli affects our reproductive fitness. Those which can detect changes in the environment are more likely to survive than those which don't. Those which developed "sweet sensation" for glucose can gain more energy than those who don't. But it doesn't explain the relationship between the experience of a stimulus and the stimulus.
It seems like our own body has invented experience and sensation and these phenomena don't have any physical significance.

"...these phenomena don't have any physical significance." That's a bit confusing, if you consider survival a "physical significance".

@anongoodnurse What I mean by "Physical significance" is that they are just illusion and don't actually exist. How anything "looks like", "smells like" or "tastes like" are just things completely made up concepts by the brain.


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Do action potentials cause the neuron to heat up as well as its environment?
I have read that we might be yawning to cool our brains down, so then a thought occurred to me. If we need to cool down our brain, then our brain but heat up for some reason. The only reason I could see would be the action potential causing some sort of temperature increase. My query is how exactly would a neuron heat up, if it does do so in the first place?

While it is possible that action potentials themselves result in waste heat, there are other processes within the neuron likely to contribute much more to energy lost as heat. The action potential itself uses energy that's been stored in chemical and electrical gradients that are the result of numerous sodium-potassium pumps which require the energy in ATP. There would be some loss of energy in the operation of these pumps.
But far more heat is likely generated by the mitochondria within the neurons. These are the structures that convert most of the energy in the breakdown products of carbohydrates and fats into the ATP the Na-K pumps require. Generous estimates put the efficiency of this production at roughly 50%. That means about half the energy from the food-stuffs used to create the ATP is lost as heat.

How much heat can a neuron waste? Is it enough to effect its function?

"Waste heat" simply means energy that escapes during a transfer of energy from one form to another. We call the roughly 50% of the energy in carbohydrates that can't be converted into ATP waste heat because it doesn't end up in the desired form of ATP. But that "waste heat" is what mammal's bodies uses to maintain a high body temperature enabling us to be more active than, say, reptiles in colder environments. The body has many mechanisms to dispel heat if it begins to get too hot, think sweating for example. Blood helps carry heat from the brain to where sweat can occur.


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How are antibodies extracted from donor blood?
When blood is donated, the antibodies within it are extracted, but how exactly do they do it? How do they take out the antibodies within the blood, what process do they go through?

Do you have a source that the antibodies are removed?

Just look at it, if they didn't remove the donor's antibodies only people with the same blood types could donate. If the antibodies weren't taken out for example type O wouldn't be a universal donor. O has A and B antibodies so it wouldn't be compatible with any other types. In order for it to be the universal donor(which it is) the antibodies of the donor blood must be removed. It's also common knowledge, but here is the logical explanation for Chris.

This is the reason why O- (universal donor) is so much sought after. And why blood for some blood groups is easier available (A + for example) than for others. Oh, and belittling other users is always a bad idea since you want something. There is no obligation to write an answer, though.

I am really sorry Chris if you thought I was belittling you. I didn't see my answer having an offensive tone, sorry if it did. I was just trying to answer your question so if others stumble upon this and have the same question the answer would be present.

I don't believe they do remove the antibodies but rather they match and screen the donor antigen and antibody profiles to those of the recipient. The process is very briefly outlined on the Red Cross website;

Most blood is spun in centrifuges to separate the transfusable components – red cells, platelets, and plasma

The primary components like plasma, can be further manufactured into components such as cryoprecipitate

Red cells are then leuko-reduced

Single donor platelets are leukoreduced and bacterially tested.

The article in wikipedia explains the screening for blood transfusions;

Patients should ideally receive their own blood or type-specific blood products to minimize the chance of a transfusion reaction. Risks can be further reduced by cross-matching blood, but this may be skipped when blood is required for an emergency. Cross-matching involves mixing a sample of the recipient's serum with a sample of the donor's red blood cells and checking if the mixture agglutinates, or forms clumps. If agglutination is not obvious by direct vision, blood bank technicians usually check for agglutination with a microscope. If agglutination occurs, that particular donor's blood cannot be transfused to that particular recipient.

Thanks Michael_A, if you have time to answer a follow up question here it is. Are all the antibodies and antigens in the centrifuged blood removed or do some necessary antibodies get transferred to the patient.

@genius Antibodies are not removed by centrifugation - they stay in solution. When you spin so high, that antibodies precipitate, all the cellular components of the blood will not survive this.

I believe the antibodies are predominantly in the plasma component. Cross-matching donor and recipient blood tests for the presence of problematic antigen-antibody interactions.


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Which magnoliophyta groups are NOT pollinated by bees and why?
Considering the bees as the family Apidae which families of flowering plants are definitely not pollinated by them and what could be the reasons?
-Could you say that the relationship is preserved at the family level?
(Please suppose that both groups live in the same geographic context)

This is an interesting question, but it also sounds like a homework question (and a good one). What research have you done to try to answer it? Can you give us a few examples of why plants might not rely on bees for pollination?

Not a homework question. Actually is part of my PhD research.  I'm looking for putative ecological relations on taxonomic groups that co-occurre in the same place and nearby regions (less than 10km distance). I looked for the families of flowering plants that are always present every time a member of the family Apidae has been found.

The result is a long list of many families. I was wondering if there there is a family that it is very known that is not pollinated by bees (Apidae). That's why I did that question.

This is the list:

Amaryllidaceae
Iridaceae
Hypoxidaceae
Asparagaceae
Orchidaceae
Pontederiaceae
Commelinaceae
Smilacaceae
Melanthiaceae
Liliaceae
Eriocaulaceae
Poaceae
Cyperaceae
Juncaceae
Bromeliaceae
Arecaceae
Hydrocharitaceae
Juncaginaceae

Potamogetonaceae
Alismataceae
Dioscoreaceae
Musaceae
Lythraceae
Onagraceae
Myrtaceae
Melastomataceae
Cannabaceae
Rhamnaceae
Rosaceae
Moraceae
Urticaceae
Magnoliaceae
Zygophyllaceae
Krameriaceae
Begoniaceae
Cucurbitaceae
Resedaceae
Brassicaceae
Caricaceae
Cleomaceae
Piperaceae
Saururaceae
Aristolochiaceae
Simaroubaceae
Rutaceae

Anacardiaceae
Sapindaceae
Burseraceae
Meliaceae
Opiliaceae
Loranthaceae
Santalaceae
Schoepfiaceae
Hydrangeaceae
Cornaceae
Loasaceae
Berberidaceae
Papaveraceae
Ranunculaceae
Menispermaceae
Lauraceae
Convolvulaceae
Solanaceae
Hydroleaceae
Asteraceae
Campanulaceae
Polygalaceae

Fabaceae
Salicaceae
Hypericaceae
Linaceae
Passifloraceae
Euphorbiaceae
Malpighiaceae
Violaceae
Erythroxylaceae
Putranjivaceae
Picrodendraceae
Podostemaceae
Boraginaceae
Rubiaceae
Asclepiadaceae
Gentianaceae
Apocynaceae
Cistaceae
Malvaceae
Bixaceae
Talinaceae
Chenopodiaceae
Polygonaceae
Caryophyllaceae
Plumbaginaceae
Amaranthaceae
Nyctaginaceae
Cactaceae
Phytolaccaceae
Portulacaceae

Sorry! I think I should reformulate my question.. :(

Flowering plants evolved before bees, so clearly in the ~100 million years, they must have been pollinated by other methods. Some plants still retain this ancestral characteristic.
This paper shows a species Magnolia tamaulipana (Magnoliaceae) which is pollinated by beetles.

Thank you for your answer and the source! But, in this case, could you call the feature: "Not pollinated by apids (Apidae)" is an ancestral characteristic?


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Can anyone tell what kind of berry/currant this is?

I found this currant-like plant in Helsinki, Finland. It seems very similar to red currant but it has hairs on its fruits, and the fruits are pear-shaped. Can anyone please identify this plant? Many thanks!

Did you find it growing wild or did it seem cultivated?

@picapica It seemed to be growing wild, next to a street!

I am pretty sure this is a species of Ribes (Grossulariaceae, vernacular Finnish: herukat), and that it is not native to Finland.
I would guess that it might be a variety of R. rubrum L., but it also might be a species unrecorded in Finland so far. You might consider sending the photo to someone at Helsinki Botanical Garden, or at the Natural History Museum. (If you got a twitter account, you might just sent the link to this page to @Raino_Lampinen and ask on his opinion.)

Cool, thanks a lot! I should try out the Twitter :) I'll update it here when I get the answer!


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Databases medicine and therapy - animal & human studies, technology readiness level
I am looking for some universal databases that would offer information about drugs and therapies currently in development.
The area of interest is mostly cell and gene therapy. I am looking for anything from preclinical research to clinical trials. I am also searching for data related to technology readiness level of those drugs/therapies.
Any help will be deeply appreciated.

There are plenty of clinical trials databases out there. Without more specifics on what you particularly want, we won't be able to help.

Forgive me. Here is exactly what I would like to find: cell and gene therapy technology readiness level, scientific data including all animal and human studies.

Sites like clinicaltrials.gov might be of some use. By specifics -you just want to find about all of them, because there are likely to be hundreds and all in different stages. The data is in the form of publications, which may or may not have been made public.

Try searching clinicaltrials.gov with the terms "gene therapy" and "cell therapy". If that isn't adequate, feel free to bring what you don't like here.


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What is this giant mosquito-like insect?
I found this bug in my kitchen in this morning, in a suburb of Houston Texas, about 30 miles Northwest of downtown. It was on the wall, and when I went in for a closer look, it quickly flew away - up towards the light, then crash landed behind the refrigerator where I hit it with bug spray.
It looks sort of like a mosquito, but much much larger.
Everything I find online about "giant mosquitoes" points to the Crane fly or "mosquito hawk" - which I've seen plenty of (very common here). I'm no expert, but this doesn't look like a cranefly.
I also read that giant mosquitoes are known to hatch after hurricanes, and there was just a huge one <200 miles from me. But those accounts speak of smaller insects (albeit, still very large for a mosquito).
For example, this article about "gallinippers" in North Carolina, speaks of mosquitoes only the size of a penny.
I did not think to put a coin in the shot for reference, but based on the size of the paper towel underneath it, it must be at least the size of a quarter.
Is this even related to a mosquito? What could it be?

Related: https://biology.stackexchange.com/questions/115030/what-is-this-huge-mosquito-looking-insect

The better entymologists among us may need to correct me, but I believe you are looking at a robber fly, especially based on the characteristic long, tapering abdomen, as well as the proboscis that reminded you of a mosquito and the large size.
I see a couple people posting images from Texas that look a bit like yours (especially the all-black body) on Google images but none of these mention a genus/species for me to dig further on. Bromley, S. W. (1934). The robber flies of Texas (Diptera, Asilidae). Annals of the Entomological Society of America, 27(1), 74-113. may be useful but is a bit too deep for me to dig into for you.

iNaturalist has over 9000 user-submitted photos of robber flies (family Asilidae) from Texas alone, breaking down into 9 sub-families, (I don't know how many genera) and further into 96 species. Here is the breakdown into 9 subfamilies ... I can't tell which one it belongs to: https://inaturalist.ca/taxa/47982-Asilidae/browse_photos?grouping=taxon_id&place_id=18

Bromley 1934 is also available here; the advantage to this copy is it's free of charge, but printing (if desired) is one-page-at-a-time.  Other disadvantages include the age of the work (it is almost certain that more species are presently known from Texas), the need for specialist vocabulary, and the paucity of illustrations.


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Can elephants be allergic to peanuts?
Can elephants be allergic to peanuts? If yes, what is the reaction? Does the trunk swell up? I tried googling the issue but the only thing I found was a children's book about Eppie the Elephant. I realize elephants are not particularly fond of peanuts.