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Quantitative Trait Locus process?
I do not seem to understand the concept of Quantitative Trait Loci(QTL's), can anyone explain it to me in detail? Reading the wikipedia article helped somewhat, but I do not understand it well.
What I understand:
-quantitative traits = a number(quantity) of phenotypes(traits) that vary
-To "make" a QTL, one must "map" the phenotypical traits to the genes that they are believed to propagate.
-This is done by AFLP-PCR, or Amplified fragment length polymorphism, according to wikipedia at least. This process cuts the genomic DNA into pieces and then amplifies the target region with primers via PCR. Then it is visualized using some type of gel technique?
-I am not sure how this gel data then allows the mapping of phenotypes to genes. I know gel electrophoresis can help to identify the length of a gene or region of a gene if using a ladder to compare.

I would disagree with your definition of "quantitative traits" and instead describe it as traits that are quantiative instead of qualitative. Eg, height is a quantitative trait whereas presence or absence of hairs is a qualitative trait

When we say that something is a genetic marker we mean that we can establish its linkage to a chromosome AND that we have some way of discerning, or detecting, how the marker has segregated after meiotic recombination (this definition is only valid for diploid species that undergo sexual reproduction).
So, for example, in the fruit fly, Drosphila melanogaster, the white gene is linked to the X chromosome. Wild-type flies have red eyes, a mutation in the white gene yields flies with white eyes.  You can use genetic crosses (matings) to (a) show that the white gene is linked to only one of the four fly chromosomes, and (b) if you have other genetic markers on that chromosome you might be able to construct a genetic map showing the order and distance of the linked genes.
You can also use a DNA fragment from a chromosome as a genetic marker--if you have an assay that lets you track the fragment after meiotic recombination.  A Southern blot, using a labeled probe is one way to accomplish this (e.g. a Restriction Fragment Length Polymorphism or RFLP).  PCR that lets you detect a RFLP or a SNP serves the same function, and is much quicker than a Southern Blot (and requires less DNA starting material).
A QTL is just one of these "molecular" genetic markers that shows linkage to the trait you are assaying. So, for example, if you had RFLPs or SNPs sprinkled all along the human chromosomes, and if you had a way to detect the segregation of all those markers after meiotic recombination, then you could use DNA from a family with lots of kids of varying heights, where one parent was tall, and the other parent was short, to see if any of your genetic markers were segregating, or linked to the phenotype of height in the children (this example assumes that height in humans is a quantitative trait).

If I may paraphrase you a bit, so the concept of a genetic marker is valid only for organisms that can do crossing over, or meiosis, since crossing over events allow for exchange of genetic material, and the closer a gene for a trait lies on a chromosome, the tighter the linkage will be. This means then that when looking for a genetic marker, we are looking at linkage? And also, therefore QTL's are simply a type of genetic marker, an gene in the chromosome to be studied for linkage to a chromosome? And then this is done by adding a probe that would fluoresce when examined?

Haploid organisms, like bacteria, and their viruses also have genes and DNA, and therefore have genetic markers. It is just that they don't have meiosis. You can still construct genetic maps, I was just trying to be precise. I think your understanding is correct. There are only two things to emphasize. The QTL is probably not the gene you are interested in, it is probably not even a gene, it is a proxy for the gene, because it is a hopefully tightly linked marker; you would still have to do further work to find the gene. Also you may want to ask how a Southern blot works.

Thank you, i think I know how a southern blot works, but do you have any suggestions for a image that would sum up the concept of QTL? I feel like learn better from images in general. Also as an aside, cant bacteria do some type of homologous recombination, i remember reading about it but maybe it was just my imagination.

@RoSiv Yes they can, for example a phage genome can be integrated in the bacterial genome through recombination. This is done through recombination att-loci (att for attachment). Of course this is only one example. http://en.wikipedia.org/wiki/Site-specific_recombination


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How is the "fine mapping of pelvic regulatory region" done in this paper?
Could anyone please explain to be in very basic terms how Fig 2, and the associated text(located above the figure) is done? The jargon is too much for me to understand and I really need a simplified, step by step, version of the process to aid my understanding.
Here is a copy and paste of the text, the figure, and the figure description in that order from the paper:
"Fine mapping of pelvic regulatory region. To further localize the position of the cis-acting changes, we looked for the smallest chromosome region co-segregating with bilateral absence of pelvic structures in a cross between pelvic-complete [Japanese marine (JAMA) and pelvic-reduced (PAXB) fish (13)]. High-resolution mapping identified a 124-kb minimal interval, containing only the Pitx1 and Histone 2A (H2AFY) genes, which showed perfect concordance between PAXB alleles and absence of the pelvis (fig. S1A).
Recombination in natural populations can also be used to narrow the size of regions controlling polymorphic traits in sticklebacks (18). We therefore tested whether markers in the Pitx1 region were associated with the presence or absence of pelvic structures in lakes with dimorphic stickleback forms: benthic and limnetic sticklebacks from Paxton Lake, British Columbia (PAXB/PAXL), and pelvic-complete and pelvic-reduced sticklebacks from Wallace Lake, Alaska (WALR/WALC) (fig. S2) (13, 14). Microsatellite markers located in an intergenic region approximately 30 kb upstream of Pitx1 showed highly significant allele frequency differences in fish with contrasting pelvic phenoytpes (P < 10−35) (Fig. S1B and table S2). In contrast, markers around thePitx1 and H2AFY coding regions showed little or no differentiation above background levels. These results suggest that an approximately 23-kb intergenic region upstream of Pitx1 controls pelvic development. This region is conserved among zebrafish and other teleosts (Fig. 2A), suggesting that it may contain ancestrally conserved regulatory enhancers."
http://scienceintheclassroom.org/sites/default/files/stickleback_2.jpg

"Fig. 2.  (A) VISTA/mLAGAN (http://genome.lbl.gov/vista/) alignment ofPitx1 candidate region from pelvic-complete stickleback (SALR), medaka, and zebrafish. Red peaks indicate >40% sequence identity in 20-bp sliding windows; grey bars at topindicate repetitive sequences; and circles indicate microsatellite markers used in association mapping in fig. S1. (B) Reporter gene expression in transgenic animals. (C) Pel-2.5-kbSALR from a marine population drives tissue-specific EGFP (green) expression in the developing pelvic bud ofSwarup stage-32 larvae (36). (F) Detail of (C). (D and G)Altered Pel-Δ2.5-kbPAXB sequence from pelvic-reduced PAXB stickleback fails to drive pelvic EGFP expression. (E and H) A smaller fragment from marine fish, Pel-501-bpSALR, also drives EGFP expression in the developing pelvic bud of multiple stage-30 larvae. This region is completely missing in PAXB."
Source :http://scienceintheclassroom.org/research-papers/what-pelvis-can-teach-us-about-evolution/university
Paper:Adaptive Evolution of Pelvic Reduction in Sticklebacks by Recurrent Deletion of a Pitx1 Enhancer.  Chan et al.

This is conceptually similar to our discussion about QTLs, except that I believe that in this example the authors had already narrowed down (which means crudely mapped, as opposed to finely mapped) the actual genetic region by some previous experiments.
Based on that prior work they may have already deduced that they were seeking a single gene (or a Mendelian factor). Note that this is different than a QTL. QTLs are used when the phenotype of interest is polygenic, and cannot be mapped to just one single Mendelian locus.
The other important thing to realize is that the genetic map (derived from meiotic recombination between genetic markers), is an abstract concept, and on its own cannot be aligned to the physical map. The physical map is built by either creating a DNA library and making a restriction map of the clones to form contigs, or more likely by sequencing all of the clones in a library--or just using an NGS shotgun approach.
It is the RFLPs (the small DNA sequences that can be used as genetic markers)  that tie, or pin, or link the physical map of DNA to the genetic map. Once this alignment has been achieved in the region of interest you just need to establish the left and right boundaries of your region of interest. That should yield one, or more, candidate genes. Rough mapping, or gross mapping, might narrow the genetic interval to a segment containing dozens, or scores of genes, while fine-mapping lets you zoom in to perhaps just a handful of genes.
So the authors do a cross between a wild-type and a mutant, and then figure out some way to homozygose the recombinant chromosomes (I am assuming that the phenotype is recessive). Then they do two things. For each recombinant chromosome the score the phenotype (in this case that involves an anatomical structure for the pelvis). Then they also isolate genomic DNA from those scored animals and use their RFLPs to establish the molecular markers that map genetically the closest to the segregating phenotype.
With both a genetic and a physical map in hand they can establish the left and right boundaries.

That helps a bit, but I guess I am still confused on how QTL's come into play in this experiment. I guess I do not have a concrete idea about what exactly a QTL  is. I wish there was simple picture summary for the concept. Thank you though.

I'll try to help clarify the picture, but given that I have not read the paper, I am not too clear on the context.
A. IT compares the DNA of the stickleback (the SALR), medaka, and zebrafish. If there is a red peak, there is relatively high sequence identity (or similarity), indicating similarity (in evolutionary ancestry in this context?). Gray is repeating sequence, perhaps due to duplication or some kind of evolutionary history. For microsatellite markers, I believe that the paper is referring to the use of microsatellites (small tandem nucleotide repeats) as markers to compare the three.
B. Reporter genes are expressed and help the researcher identify something (by giving information, such as fluorescence etc.) (eGFP indicates green fluorescent protein e= enhanced)
C-H. These are just pictures of the fishes. Note the fluorescence (green). It indicates some expression (of the gene of interest). The absence or presence of the fluorescence indicates something, based on what the eGFP was attached to.
Hope this helped! But you need to do the analysis yourself, or at least I can't :P

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Synteny, genetics?
Could anyone explain the concept of Synteny relating to genetics? A picture would help. I tried read the wikipedia source along with another PDF
http://gep.wustl.edu/repository/course_materials_WU/annotation/About_Synteny_Analysis.pdf
And I feel it only somewhat helped. From what I gather synteny is about the order of genes, relative to their homologous genes? Or their location in general?

Same relative location i.e order in different chromosomes. Also have a look at homologous synteny blocks

Syntenic blocks contain the same genes of order between chromosomes of different species.

The figure above shows (left to right) syntenic block shared between human chromosome 17 and corresponding chromosomes in three other mammals (horse, pig and chimpanzee). And as expected, the more distinct the species (such as pig and horse) the more disarranged the order of genes are.
Ref: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3758187/

What do you mean by "the same genes of order"?   Did you mean something like "the same genes, in the same order,"?

yes same genes, same order.

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How do sporozoites travel into the human host when the mosquito is sucking blood?
I mean how are the sporozoites able to swim in the reverse direction of blood flow through the proboscis of the mosquito into the human body?

Nice question!  Basically, the mosquito does not only suck; it also injects some saliva into the host with its saliva glands.  From National Geographic:

The mosquito starts salivating as soon as it probes the [host]’s skin, releasing substances that prevent blood vessels from constricting, stop blood from clotting, and prevent inflammation. Sometimes, Choumet could see the saliva as small bubbles that hung around the tips of the mouthparts. And even after the mosquito stops feeding, pockets of saliva linger in the lower layers of the skin.

And from cdc.gov:

After 10-18 days, the parasites are found (as "sporozoites") in the mosquito's salivary glands. When the Anopheles mosquito takes a blood meal on another human, the sporozoites are injected with the mosquito's saliva and start another human infection when they parasitize the liver cells.

The probiscus is actually equipped to inject saliva as well as to suck blood.  And once the saliva has entered the victim, it can spread to the whole body since the blood is constantly moving.  From mosquitnoband.com:

Mosquitoes also have special hematophagous arthropod saliva in their proboscis. Hematophagous arthropod saliva is a scientific way of saying “spit from a blood-sucking creature with an exoskeleton.” This specific type of saliva has chemicals and proteins in it that prevents blood from clotting. So what do mosquitoes do with their hematophagous arthropod saliva? They inject it into their victim before they start sucking its blood to prevent any clotting while they slurp.

Hope this helps!


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Analysing papers and providing search
Suppose I want to provide "smart" (AI, meaning extraction etc.) search over many published papers (specifically, biological) to simplify researchers' live.
Now, I have access to my university library that contains text of many papers from different sources, including those with payed subscription.
Is it legal to download all papers, analyse them and provide search without disclosing full text of the paper, only small part of text or image and with proper citation?

You need a legal opinion, not one from a biologist. Your question is therefore off-topic and I have voted to close it. However, apart from the obvious step of looking at the conditions associated with download of papers from (?) — probably through — your library, you should consult your University librarian. I seem to have read that many journals do not allow such data mining. You are certainly not the first to think of doing this.

I'm voting to close this question as off-topic because this is a legal question, not one about biology.

Can we talk about this? contact me at http://Keybase.io/gabefair

I don't have enough reputation on biology exchange so I'm unable to close the question myself. If somebody can close it, please do, I'll ask it on Academia stackexchange as @AlwaysConfused suggested

@AlwaysConfused https://law.stackexchange.com/ would be better.


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Antibacterial soap impacts on septic system?
What impacts do antibacterial soaps have on septic systems?
I know that septic systems rely heavily on bacteria (especially regarding the breakdown of wastes by bacteria), so it seems as though antibacterial agents surely could do some harm to septic systems. Is that the case?

One of my students in my Environmental Science class asked me this question, and it seemed very much worthwhile to post the Q&A to Bio.SE!

Fortunately, this is not a real problem, as you do not need antibacterial soap anyway. It has many other downsides, and regular soap washes away bacteria just as well.

@cody, very true. Antibacterial soaps are bad for long-term human health, and no evidence suggests that antibacterial agents improve soap efficacy. The US FDA has a quick article explaining why you should skip antibacterial soap. An article from Harvard in 2017 further explains the negatives, why the FDA has banned common antibacterial agents, and how/why normal soap works just fine!

Wouldn't the antibacterial soap be diluted beyond the point of effectiveness, and then biodegraded?

I have dry skin and eczema, and my UK doctor prescribes an antimicrobial lotion which is also a soap substitute to be used in washing, called Dermol 500. It contains benzalkonium chloride and chlorhexidine dihydrochloride. I am advised to use it instead of soap and as a moisturiser, especially after bathing or showering.

@CodyGray the craziest thing is people asking for antibacterial soap to avoid a coronavirus infection...

You can do a simple test using a bottle and a serynge... Divide your sceptic volume by 1000 or something, use a similar bottle, and take yoru septic mix from your drain... Fill the bottle with pond slurry, potatos, organic matter that you want to measure decomposition of, let the bottle kick off bacterially for a week at room temperature, and then add 1/4 of the bottle little by little in the relative amount soap that you use... My suspicion is that antibacterial soap will de-activate in about 10% of the tank, leaving 90% of it working normally. In some setups, it will have little effect.

The quick answer is: Yes, it can cause harm.
Think about it...The septic system (both the tank and your drain field) rely on bacteria, and antibacterial soap is not designed to kill only specific species of bacteria. In other words, antibacterial soap can kill a whole range of bacteria, and that certainly includes the bacteria needed in your septic system.
According to University of Arizona Cooperative Extension (Farrell-Poe, 2018):

The use of “antibacterial,” “disinfectant,”or “sanitizing” products in the home can and do destroy both good and bad bacteria in septic treatment systems. “Normal usage” (according to directions) of these products will destroy some beneficial bacteria. Fortunately, the normal bacteria population within the septic system is sufficient and adequate to quickly recover. Significant treatment problems, with conservative use, should not occur. Excessive use of these products in the home can cause significant and even total destruction of the bacteria population. Normally, the use of any single product or single application will not cause major problems.
However, the accumulative affect of using too many such products and excessive application may cause serious problems and damage to the septic system.
It appears that some alternative systems may be more affected by “antibacterial” products than other systems. Additional and more conclusive research is needed.

You can find additional info about antibacterial agents in septic tanks as well as discussion about the effects of the common antibacterial agent, triclosan, on septic tanks here: Svenningsen et al. (2011) and Kirjanova et al. (2014).

 Works cited:
Farrell-Poe, K., 2018. Antibacterial Products in Septic Systems. The University of Arizona Cooperative Extension fact sheet
Svenningsen, H., Henriksen, T., Priemé, A. and Johnsen, A.R., 2011. Triclosan affects the microbial community in simulated sewage-drain-field soil and slows down xenobiotic degradation. Environmental pollution, 159(6), pp.1599-1605.
Kirjanova, A., Rimeika, M., Vollertsen, J. and Nielsen, A.H., 2014. Retainment of the antimicrobial agent triclosan in a septic tank. Water science and technology, 70(4), pp.586-592.

This is interesting. Is it really significantly different to the effect any detergent would have on bacteria? I would guess all soaps kill most bacteria simply by disrupting cell membranes. Is that not the case?

@terdon I would expect it's not significantly different. However, based on the limited sources I could find on the topic (and their own consistent reminder that this topic is under - researched), it looks like there is a measurable difference due to antimicrobial agents. I've just reported what evidence I could find. To be honest, I didn't explore the literature for studies looking at detergent impacts, and perhaps doing so could further inform and improve my answer. If you have any suggested starting points, please feel free to pass on the suggestion or update my response accordingly.

I don't have the faintest idea! Your answer just made me wonder, is all. I didn't mean my comment as criticism.

@terdon No worries - I didn't think you meant it as criticism. I was just hoping not to have to start at ground 0 for exploring a topic for which I have limited existing knowledge! :p. I recognize that my post is a superficial scraping of existing literature, so the post can definitely be improved with additional resources and info. And I hope someone can hep with that. This was -- in my mind -- quite an interesting question my student asked me, and I quite honestly wish I had more time to dive deeper into it!

@terdon triclosan et al have more effects than soaps have; but I'd agree that it's true that it's not significantly different to the effect of any detergent... however it's worth noting that this simply means for a bacteria-based single home isolated septic system like in that picture you should also be selective with what detergents you use. Some forms of septic systems are "dead" and do not care about bacteria, but if you choose to rely on bacteria (which allows for designs with smaller tanks and less draining), then you need to properly select all chemicals that go into your wastewater.

@Peteris if you can find some reputable sources to support the various claims you make, this comment could be converted into an informative 2nd answer :) .

Can the bacteria mutate to a form that is not killed by the antibacterial agent?

@CJ please ask your question in a new post. Comments are not for questions. See the [help] section for more info

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Why do blood vessels in the eye not obstruct vision?
As light enters the eye, it reaches the photoreceptors at the "base" of the retina, which then pass that signal to the bipolar and ganglionic neurons -- the latter of which send the signal outside of the eye via their axons (collectively forming the optic nerve).

The exit point of the optic nerve is sometimes referred to as the "blind spot" because there are no photoreceptors present there and therefore no sensory information is gathered.

Now, I know photoreceptors exist everywhere else along the retina, so it's not surprising that we perceive vision from the otherwise broadly distributed photoreceptors.
However, my question: why do the blood vessels associated with the superficial vascular plexus (which exist between incoming light and the rest of the retina) not obstruct our vision?

More broadly, I guess of interest is: why none of the vascular plexuses (or cell structures of the bipolar and ganglionic neurons for that matter) obstruct our vision despite existing between the photoreceptors and incoming light?

 Sources: LEFT: Figure 1 from Zhongjie et al (2020) ; RIGHT: Figure 5 from Selvam et al (2018)

 Fu, Z., Sun, Y., Cakir, B., Tomita, Y., Huang, S., Wang, Z., Liu, C.H., S Cho, S., Britton, W., S Kern, T. and Antonetti, D.A., 2020. Targeting neurovascular interaction in retinal disorders. International journal of molecular sciences, 21(4), p1503
 Selvam, S., Kumar, T. and Fruttiger, M., 2018. Retinal vasculature development in health and disease. Progress in retinal and eye research, 63, pp.1-19.

To follow-up for clarity: I understand the brain is essentially integrating the overlapping visual fields from both eyes to allow us not to regularly perceive the blind spot. However, it seems these cellular structures (i.e., vessels and nerve cells) must be so prevalent that I'm wondering by what mechanism (perhaps similar) that this more [structurally-]complex process is accomplished.

Fun fact that many probably already know: Cephalopod eyes don't have a blind spot, having the retina in front of the blood vessels and optic nerve.  When Bryan's answer mentions an "inverted" eye, it's as opposed to the "better engineered" cephalopod eye.

I think there are experiments like this to make the blood vessels visible to you: https://www.aao.org/museum-education-healthy-vision/experiment-see-blood-vessels-in-your-eye

https://youtu.be/oAaG34WfsC0?t=9254 has an interesting anecdote about this. This is from an interview of a neuroscientist/Stanford prof/skateboarder, who explains, among others, why we don't see those spiderweb shadows.

Avoid the fovea
Figure 2 from the same paper shows the distribution relative to the fovea:
As you can see, it's pretty much devoid of this superficial vasculature, so anything you are directly focusing on, say, text you read on a computer screen (or even a book!) is not impacted.

Receptive fields might be bigger than you think
Receptive field sizes for retinal ganglion cells in the primate retina are about 50-300 um, depending on eccentricity (distance from the fovea). Capillaries are going to be around the size of a red blood cell in diameter, so about 10 um; it seems like by the time you get to the far periphery, these vessels are mostly going to be quite small relative to receptive field size, and they are even a bit small in the vicinity of the fovea.
Tissue isn't that opaque
I'm mostly focusing on the RBC size themselves, because RBCs have a bit of pigment in them, but otherwise, tissue is overall quite transparent. If you've ever looked at an unstained tissue section less than 100 microns thick, you know that it doesn't look like much at all. If you've lost track of one in any volume of water, good luck finding it. For the same reason that RGCs being on the "wrong side" of the inverted vertebrate eye, this thickness of tissue just doesn't seem to be that big of a problem, and it doesn't seem that any affordances for this issue have evolved outside of the fovea in primates (whereas you can see in the figure above that there is a clear exclusion of these vessels from the fovea).
We perceive with our brain, not our eyes
The general idea of predictive coding models of the brain is that you have some generative model of the world that is constantly making predictions, and sensory organs merely provide evidence to update those models which is propagated as an error signal with respect to the original model; if everything is static and as predicted, nothing needs to be propagated in the brain to alter the perception. Much of what you think you are "seeing" at a given moment you aren't seeing at that moment at all, but merely "remembering" what you saw previously, and having not seen any evidence to the contrary, continue to "see" it there. When a person looks at an object, they do not typically look at one spot, but quickly saccade around to scan different parts of it and form a complete model of the object. It will escape attention until it moves or changes in some way.
These blood vessels are going to be quite static, and not provide much of a changing visual image, so there's nothing there for the brain to be interested in.

+1 for everything, but especially the "it's all in your mind" paragraph!

"Tissue isn't that opaque" — but we do easily see the vessels in fundus photos, so they aren't that transparent either. And they are very noticeable in the Purkinje tree effect.

@Ruslan Those are much larger vessels than the bulk of them that are capillary-sized.

Thanks @Bryan! +1.  3 comments: (1) could you cite/link something about the primate fovea evolution you allude to [very interesting, by the way!]. (2) I've experienced thin cultures before and so can appreciate your comments about their near translucence. However, capillaries  would still have continuous RBCs -- which are more red than completely transparent -- so I'd guess these would stand out slightly more than thin epithelia. (3) final paragraph about predictive coding is informative and interesting -- some of it was familiar, but it's been a long time since studying this stuff. Thanks :)

@theforestecologist 1) I'm really just commenting on the structure visible in figure 2: it's clear that something particular has evolved around the fovea in primates to keep that area clear of vessels, and not elsewhere. I could perhaps comment on the evolutionary history of the fovea but it's a bit of a long story of convergent evolution. 2) Agreed, RBCs may stand out, I mostly meant this to defend my use of a RBC width as a reference point for the size relative to receptive fields, rather than using the vessel diameter. 3) Although I put this point last, it's probably most important.

 You CAN see your blood vessels!
Following-up from Bryan Krause's answer:
Bryan mentioned that the blood vessels are typically not visible partially because they are unchanging (i.e., static). In support of that, one could imagine that if you somehow make these structures appear more dynamic, then one might be able to visualize them.
The American Academy of Ophthalmology actually recommends trying an experiment to do just that: to "see" your retinal blood vessels!
https://www.aao.org/museum-education-healthy-vision/experiment-see-blood-vessels-in-your-eye
Paraphrasing their experiment:

Darken a room.

Hold black sheet of paper in front of face so that the paper fills your field of view.

Hold a small flashlight 1.5 cm in front of one eye so it's aiming just below the center of the pupil.

Move the lit flashlight slowly from side to side a short distance (~0.4cm) without letting your eye follow the motion of the light. Continue moving for ~20 seconds.

A tree-like pattern of blood vessels will become visible.
Why this works:

You can use a dim point of light to cast a shadow of the blood supply of your retina. This will allow you to see the blood supply of your retina, and even your blind spot...
Your light is causing a shadow from the blood supply layer to the other layers underneath. As you move the point of light, the shadow moves, making it visible to you. Normally, there would be no shadow and your brain would ignore seeing the blood supply.

One of my friends experimented with this using a computer program: stare at one point, and the program flashes dim dots elsewhere. Press button when you see the dot. Very slow but the mapping he got corresponds very well with a retinal photo from opthomologist.

Try looking at the blue sky or a white computer screen and focusing very carefully on what you see.  I usually can make out faint pulsing streaks of white/black (like phase contrast - different from floaters) if I really pay close attention.  These aren't continuous like vessels and they aren't even as frequent nor as regular as a heartbeat, so I'm not sure what they really represent (perhaps some type of smooth muscle contraction or leukocyte passing through?), but their repeated motion in one particular direction at any given location suggests some type of blood vessel should be involved.

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Cutting off circulation
How much force is required to cut off the blood circulation of, lets say the average human arm? I'm asking because i'm bored and want to try it on myself. I know that in just a couple of seconds with lack of blood flow you will lose complete use of your arm. I'm only going to do this for a second or two with people watching so please do not worry about safety!

If you are losing use of an arm within a couple of seconds that is because you are compressing a nerve and blocking transmission of motor signals, not because of cutting off blood circulation.

The pressure you need to apply is equal to your systolic blood pressure, about 120 mmHg. This is about 163 g/cm^2.

Thank you for the information boreora I wish you good fortune

Can you add resources to these numbers?

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


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How to contract sternocleidomastoid muscle by thought?
If I do not turn my head, how can I contract ( or tighten) the sternocleidomastoid muscle ( like we can intensely tighten muscle in limbs)?


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Is there any technique can quickly expand one set of cell chromosomes?
Assume a cell type is very scarce while isolated out and hard to expand in vitro, and I wanna have more of its chromosomes, is there any technique , in vivo or in vitro or ex vitro, any would count, that allows me to quickly expand the amount of those chromosomes?
I know it sounds weird but just some curiosity~
Thanks


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Will a sandwich assay work with a GST 26 antibody/protein?
I have a GST 26 kda antibody, and want to use it in a sandwich lateral flow assay. Are there enough epitope regions for both antibodies to bind to the protein?

This is completely dependent on the type of antibody you are using and the epitope specificity of that antibody (or antibodies). Because you haven't given any more detail, it's very hard to give you a definitive answer.
GST is known to dimerise, so even a monoclonal antibody might work in your sandwich assay, as long as the (identical) epitopes are far enough apart in the dimeric structure to allow two antibodies to bind.
If you're dealing with a polyclonal antibody mixture, then your chances are better. But even still, you won't know until you try it.


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Will a polyclonal antibody attach to proteins of different kDA?
If I have a GST 26kDa polyclonal antibody, will it bind to the GST 28kDa protein as well?

If the sequence of the 26 kDa form is included within the sequence of the 28 kDa form then the answer is 'probably yes'.
However if the N- or C-terminus of the short form is an important/dominant epitope and it is masked in the long form (by being extended) then the activity of the serum against the long form could be significantly reduced.

As Alan said, it depends but I'd guess that, yes, it probably does.
Given that you are using polyclonal antibodies against a not so dramatic extension, I'd say it's even more likely that you'll see signal. The various antibodies within the polyclonal mixture will bind different parts of the smaller protein, so unless the additional segment causes a dramatic change in shape or somehow blocks most of the binding sites, you should see binding.
I don't think you can directly compare binding signals between the different protein forms, but it should work for simple detection or purification


text:
How can antibodies in rapid antibody tests be kept at room temperature without denaturing?
The normal temperature for long term antibody storage is around -20 degrees Celsius. However, when developed into rapid antibody tests, they can be kept at room temperature for prolonged periods. How is that possible?

Antibodies have no problem with room temperature. Naturally, antibodies expect to survive for many days or weeks at body temperature, which is much higher than room temperature (at least, mine is).
-20°C is recommended for very long-term storage (many months or years) of antibodies, but they are typically very stable proteins and don't denature very readily at all. Storing them at room temperature can be done for a long time -- certainly weeks, in my experience, with the only real concern being the possibility of bacterial or fungal growth if the antibodies aren't sterile.


text:
If a hand was suddenly chopped off while holding something, would the severed hand still hold a grip?
This question was inspired by Star Wars Episode V: The Empire Strikes Back. In it, Luke Skywalker is battling Darth Vader in a lightsaber duel. Vader manages to win out and chops off Luke's hand, which is holding the lightsaber.

My question is: would his severed hand still hold a grip on the lightsaber? Or would it fall slack and lose grip, likely separating as it falls into the pit?
While this question is from a sci-fi series with a fantasy means of dismemberment, it might apply to other real-world situations (for instance, an industrial worker holding a tool while a piece of machinery accidentally severs his hand).

It seems unlikely, since most of the muscles that provide the gripping force are in the forearm.  Try gripping something forcefully* and notice which muscles tense up.  (*Of course anyone who's done much fencing knows that you don't grip with too much force.)

@jamesqf I'm not real fond of this type of question, but it seems like you could make a simple answer out of that comment.

(Disclaimer: I have no personal or medical experience of cutting off hands, or any other body parts, so this is purely theoretical.)
It seems unlikely, since most of the muscles that provide the gripping force are in the forearm and are transmitted via tendons in the wrists. Try gripping something forcefully* and notice which muscles tense up, and how the tendons on the inside of the wrist transmit the force.  Cutting the tendons would eliminate the force.
Of course anyone who's done much fencing knows that you don't grip with too much force, because that interferes with the fine control provided by the fingers.


text:
How to interpret this PubChem record of L-Alanine
Using the PUG service from NCBI, I am retrieving 3d structure data for a molecule.
Raw data here.
I am trying to understand this record, specifically for the purpose of rendering in a 3D coordinate system using threejs.
Could anyone please assist in understanding this information.
Due to the large size of the json response and as I am using javascript, I have constructed some Typescript types that describe the shape of the data to assist the discussion. I have specific questions, which are stated below.
//// Root Object
interface JSON_Response {
    PC_Compounds: PC_Compound[];
}

//// Compound Object
// must stand for PubChem Compound
interface PC_Compound {
    id: ID;
    atoms: {
        aid: number[];
        element: number[];
    };
    bonds: {
        aid1: number[];
        aid2: number[];
        order: number[];
    };
    stereo: Stereo[];
    coords: Coords[];
    props: Data[];
    count: Count;
}

//////// Sub-types described below

Atoms
The atoms object has two arrays; 'aid' and 'element'.In the above JSON response, these arrays are both of length 13. The data for L-Alanine shows it has 13 atoms. I am correct in saying that the numbers in the 'element' array are corresponding to Atomic Numbers? And these atomic numbers are assigned to ids from the corresponding indexes in the 'id' array?
Bonds
What are aid1, aid2, and order? These arrays are 12 entries each so each must represent 1 bond between two atoms. But what do the number values correspond to? How should they be interpretted?
Coords
In the coordinates object,
interface Coords {
    type: number[];
    aid: number[];
    conformers: [
        {
        x: number[];
        y: number[];
        z: number[];
        data: Data[];
        }
    ];
    data: Data[];
}

The x, y, & z arrays are of length 13. Am I correct in saying that these represent the x, y, and z coordinates of atoms in the corresponding index of the above elements array?
Data
Data Object seems to be part of a esoteric system for attaching arbitrary data to the object. If anyone has any pointer on this it would be greatly appreciated.
interface Data {
    urn: {
        label: string;
        name: string;
        datatype: number;
        release: string;
        version?: string;
        software?: string;
        source?: string;
        parameters?: string;
    };
    value: {
        sval?: string;
        fval?: number;
        slist?: string[];
        fvec?: number[];
        ivec?: number[];
    };
}

stereo
seems to describe planes of rotation
//// Compound sub-types
interface Stereo {
    tetrahedral: {
        center: number;
        above: number;
        top: number;
        bottom: number;
        below: number;
        parity: number;
        type: number;
    };
}

interface ID {
    id: {
        cid: number;
    };
}

miscellaneous chemical information
interface Count {
    heavy_atom: number;
    atom_chiral: number;
    atom_chiral_def: number;
    atom_chiral_undef: number;
    bond_chiral: number;
    bond_chiral_def: number;
    bond_chiral_undef: number;
    isotope_atom: number;
    covalent_unit: number;
    tautomers: number;
}

In addition, if anyone has any techniques or advice on how to extract meaning from the response data from PubChem, if they could please post below it could come in handy for me or some other person working on this.

The PubChem format description is not that easy to find:
https://www.ncbi.nlm.nih.gov/IEB/ToolBox/CPP_DOC/asn_spec/pcsubstance.asn.html
And the ASN file linked here:
https://pubchemdocs.ncbi.nlm.nih.gov/data-specification

I am correct in saying that the numbers in the 'element' array are corresponding to Atomic Numbers?

Yes, 1 is hydrogen, 6 is carbon, 8 is oxygen, etc.

And these atomic numbers are assigned to ids from the corresponding indexes in the 'id' array?

in your example, "atoms": {"aid": [1, 2, 3,  ...,  13], "element": [8, 8, 7, ..., 1]},, the the ID of the first atom would be 1 and element 8 (oxygen), the third atom: ID 3 and element 7 (nitrogen).

Am I correct in saying that these represent the x, y, and z coordinates of atoms in the corresponding index of the above elements array?

Yes

What are aid1, aid2, and order?

aid1 and aid2 are the atom identifiers. order is the bond type.

These arrays are 12 entries each so each must represent 1 bond between two atoms. But what do the number values correspond to? How should they be interpretted?

For example aid1 = [1, 2], aid2 = [3, 4], order = [1, 2] would mean a single bond between atom 1 and atom 3 and a double bond between atom 2 and atom 4.
Good examples of implementations:

PubChemPy
pubchem_2d_structure_json_to_svg.py


text:
Can bacteria grow in rough, deteriorated indoor plastic chairs left in months of rain? (i.e. not made of resin plastic)
I have a problem with indoor plastic chairs (like classroom chairs with metal frames) left outside in the rain for months at my units.  They are not made of resin plastic and the surface is noticeably rougher & more deteriorated.  I think that they can harbour bacteria much like neglected plastic food containers.  There is a possible unfresh smell, and some decomposed plastic seemed to end up on my hands when I moved one.

Plastic does not decompose in nature. Decomposition as per my understanding is a phenomenon wherein an object is broken down into simpler constituents. Plastic just breaks down into smaller pieces of plastic. What you are seeing is most probably erosion of the surface due to rain.

I think that they can harbour bacteria much like neglected plastic food containers.

Nothing to be worried about. That chair was most certainly covered with microbes even before you put it out in the rain. Your body itself harbors about as many bacteria as it does its constituent cells.
What it may harbor in addition though are fungi, which now have a great substrate to hold onto.

There is a possible unfresh smell, and some decomposed plastic seemed to end up on my hands when I moved one.

I don't know what you mean by unfresh smell. If you mean moldy, that can be expected because you have moisture, and a nicely eroded thingy which can act as substrate for stability.
You can very well use the chair. There's nothing wrong with it. Spray it with a shower and keep it out in the sun for a day or two, that should take care of the mold.

There have been some bacteria discovered that can decompose some plastics.

Yes there are. But it would take too long for wild-type strains to decompose a chair in the wild. Therefore, the effects produced by aforementioned bacteria are negligible and are superseded by other effects. For example, erosion due to rain.

I’m not saying they ate the chair, only that plastic can be decomposed.

Erosion from rain is unlikely, but deterioration from the UV in sunlight is fairly likely.


text:
How are chromosomes counted at the end of mitosis in a plant cell?
Page 89 of the Study Guide for Campbell Biology, 11th Edition has the following question:

A plant cell has 12 chromosomes at the end of mitosis. How many chromosomes would it have in the G2 phase of its next cell cycle?
a. 6
b. 12
c. 24
d. 48

Page 449 states that the answer is b.
As far as I understand, the number of chromosomes a cell has in G2 phase is double the number of chromosomes as it has after mitosis (which would imply the answer is c).
For (b) to be true, the plant cell must have had 6 chromosomes at the end of mitosis, but the question states it had 12. The only way I can imagine this to be true is that the question assumes that "a plant cell [...] at the end of mitosis" represents both daughter plant cells before the cell plate & cell wall has fully split the two daughter cells up, but doesn't "the end of mitosis" imply that the cell wall has completely formed and there are two cells (each with 12 chromosomes)?

I think I know what is confusing you.
A chromosome can have one or two chromatids. If you have two chromatids, you don't necessarily have two chromosomes. This is what happens during S-phase, during replication. Before the S-phase each chromosome had one chromatid, after the replication, it has two. So the number of chromosomes stays the same.
In the karyogram (the picture with all chromosomes), each object is one chromosome. Usually those will be double-chromatid chromosomes, and you will see a nick (like here). After these chromosomes divide, you get two separate objects → two identical chromosomes.


text:
When in the cell cycle is the number of chromosomes normally reduced?
Page 96 of the Study Guide for Campbell Biology, 11th Edition has the following question:

A reduction in the number of chromosomes per cell occurs
a. During meiosis I
b. During meiosis II
c. During mitosis
d. During the S phase of interphase

Page 451 states that the answer is a.
I thought that the number of chromosomes at the end of meiosis I per cell equals the number of chromosomes in the parent cell (although sister chromatids remain attached), whereas the number of chromosomes at the end of meiosis II per cell equals half the number of chromosomes of the parent cell. If so, isn't the answer b?

It is the other way around. Meiosis I (or reductional division) splits chromosome pairs so each cell gets half of the chromosomes of the parent. Meiosis II (or equational division) splits double-chromatid chromosomes (making two single-chromatid chromosomes), so cells retain the number of chromosomes, like in mitosis.

If more clarification needed:

before the S phase: 23 pairs of chromosomes, 46 single-chromatid
chromosomes
before the meiosis I: 23 pairs of chromosomes, 46
double-chromatid chromosomes
before the meiosis II: 23
double-chromatid chromosomes without their homologous other
after the
meiosis II: 23 single-chromatid chromosomes without their homologous
other
after fertilization = before the S phase

(I'm talking about humans here.)

You could use C and .5C or something like that for the chromosomes and put the human values in parentheses.


text:
How exactly is casein digested?
I mean it seems first step is rennin or pepsin digestion in stomach - then what happens with remaining peptides?
I am interested in the whole process from casein to amino acids.
Is there brush border enzymes involved in the small intestine or all process is in the stomach?

Casein proteins are soluble in milk but form insoluble curds once they reach the stomach, making it hard for digestive enzymes to break them apart. Slower digestion also is associated with delayed release of the protein's amino acids into the bloodstream.

milkgenomics.org/article/dairy-protein-digestion-life-slow-lane/
These properties of milk caseins may have evolved to benefit mammalian infants, but slowed digestion offers the benefit of increased satiety to milk drinkers of all ages. Eating foods, like milk, that take the slow lane may mean eating less food overall.
Casein proteins in milk form small spheres, called micelles, with the hydrophilic (water-loving) portions of the protein on the outside of the sphere and the hydrophobic (water-fearing) portions on the inside. With hydrophilic structures on the outside, the micelles are soluble in water (or milk, which is mostly water) [1,2].
But when the micelles reach the stomach, “one of the most ingenious events in nature takes place” [2]. The digestive enzyme chymosin snips one of the bonds on the exterior protein (known as the kappa subunit), leaving only the hydrophobic subunits inside [1]. Without their protective layer, the now insoluble proteins form a curd.

It looks like various proteolytic enzymes digest the casein 'curds' in the stomach and intestine.  "Human proteolytic enzymes were obtained in the
activated state by collecting human gastric (HGJ) and
duodenal juice (HDJ)" This is the article: In vitro digestion of bovine and caprine milk by human gastric and duodenal enzymes
Dipeptidyl Peptidase IV's  (DPP IV), a type of protease, has been shown to break down the proteins in gluten and casein. https://www.livestrong.com › Diseases and Conditions

It's in our intestine: https://www.ncbi.nlm.nih.gov/pubmed/7522442

Brush Border Enzymes & casein [that one gives me your stackexchange question!]
This article: "Effect of diet on enzymes of the brush border of the small intestine and kidney of rats" says: "Diets with low starch and high casein contents resulted in higher specific activity of leucineaminopeptidase in the small intestine than diets with high starch and low casein contents."
You can find out a bit more about that enzyme by reading the abstract of the article.
'Digestion of peptides in small intestine' in Google gives this: "The brush border of the small intestine is equipped with a family of peptidases. ... They function to further the hydrolysis of lumenal peptides, converting them to free amino acids and very small peptides. These endproducts of digestion, formed on the surface of the enterocyte, are ready for absorption."

www.vivo.colostate.edu/hbooks/pathphys/digestion/smallgut/absorb_aacids.html
[Hint - it's google searches all the way, with an occasional scholar.google search.  ... Maybe I should get back to my own work and let you all do the searches!]

Thanks for the answer! The problem is that after a lot of hours of reading i was convinced that i will be able to digest very aged cheeses like parmesan because they are predigested by bacteria - the casein should be degraded to free amino acids - i tried 22 month old parmesan - the result was disaster. Also i eat the cheese with ginger enzymes that should work as DPP 4 enzyme - it just did not worked. So after reading your answer it seems there are a lot of things that can go wrong with casein digestion especialy from concentrated foods like cheese.

pH was a variable in a lot of the research, but I didn't talk about that.  I'm sorry about your cheese 'research' - I think I have a slight increase in mucous with dairy products, so I don't tend to eat cheese at home.  But it's only a little problem.


text:
Are VCF headers supposed to change over time?
VCF headers describing the content of the INFO field are supposed to give additional information about a variant.
Example. A VCF file can be annotated against genomic variant databases such as dbSNP or ClinVar. The annotations such databases add to the file are described in the headers.
For instance, the CLNSIG field (taken from ClinVar) describes the clinical significance of a variant. Such field description is contained in the following header:
##INFO=<ID=CLNSIG,Number=.,Type=String,Description="Variant Clinical Significance, 0 - Uncertain significance, 1 - not provided, 2 - Benign, 3 - Likely benign, 4 - Likely pathogenic, 5 - Pathogenic, 6 - drug response, 7 - histocompatibility, 255 - other">

As reported in the field definition, the set of values it can take changes over time:

Other non-standard terms are also used to meet submitter needs. ClinVar plans to add standard terms for other scenarios (e.g. somatic, pharmacogenomic, and mitochondrial variants) when they are available.

Do you know if this is a standard condition? Are headers supposed to change a lot over time? Is this condition valid only for clinical annotations (such as the ones provided by ClinVar), or something that is supposed to be considered for every annotation?
Thank you for your help.

As always with annotations, the annotation of a .vcf-file reflects the current knowledge. If that knowledge changes, the header of a file can be updated. Usually, this is not something you do by yourself but the providers of the file release new versions. However, I have no experience with clinical data and my statement is purely based on personal experience and common sense.


text:
Why does frost increase soil fertility?
I was reading this paper: https://link.springer.com/article/10.1023/A:1011398431524, which makes claims based on the the idea that frost can increase soil fertility. How/Why will frost increase the fertility of the soil? I was always under the assumption that frost was bad for soil and plants in general.

I found this article on why frost increase soil fertility - specifically nutrient density in the soil.  101 years old!
The Occurrence of Bacteria in Frozen Soil
E. C. Harder  Botanical Gazette  Vol. 61, No. 6 (Jun., 1916), pp. 507-517
https://www.jstor.org/stable/2469064?seq=3#fndtn-page_scan_tab_contents
Relevant text pasted below.  In short: it is bacterial action and nitrogen fixation which contributes to soil fertility.  Freezing increases bacterial population and these metabolic activites.  The theory is that freezing kills bacterial predators on higher trophic levels (protozoans) but the bacteria live and thrive in the absence of predators.

An analogous hypothesis proposed by RUSSEL3 for increases in the number of bacteria after partial sterilization by heat, frost, or other means is that by such partial sterilization the protozoa are killed, thus permitting the unhindered development of bacteria which under normal conditions is held in check by protozoa.
BROWN and SMITH (loc. cit.) in their investigations dealt mainly with the physiological activities of bacteria under conditions of low temperature and frost, although they also made some determinations of the number of bacteria in frozen soil. Their principal conclusions regarding the ammonifying, nitrifying, denitrifying, and nitrogen fixing powers of frozen soils are as follows: (1) that "frozen soils possess a much greater ammonifying power than unfrozen soils"; (2) that "during the fall season, the ammonifying power of the soil increases until the temperature of the soil almost reaches zero, when a decrease occurs, and this is followed by a gradual increase and the ammonifying power of the soil reaches a maximum at the end of the frozen period"; (3) that "the nitrifying power of frozen soils is weak and shows no tendency to increase with extension of the frozen period"; (4) that "frozen soils possess a decided denitrifying power which seems to diminish with the continuance of the frozen period"; (5) that "during the fall season, the denitrifying power of the soil increases until the soil freezes, after which a decrease occurs"; (6) that "frozen soils possess a nitrogen fixing power which increases with the continuance of the frozen period, being independent of moderate changes in the moisture conditions, but restricted by large decreases in moisture"; and (7) that "in the fall, the nitrogen fixing power of the soil increases until the soil becomes frozen, which in almost ceases, after which a smaller nitrogen fixing power is established."

hmm how interesting, I never would of thought of that

It is interesting, and I was glad your question provoked me to read up.

@Willk  - Probably better to use newer references. A lot changes in 101 years. (Also, a lot stays the same, so...)

From the introduction (bottom of page 167 and top of page 168) of the paper you linked (Masters and McMillan 2001)

We use newly available worldwide climate data to quantify the prevalence of seasonal frosts, hypothesizing that what the tropics have in common is an absence of winter frost, "the great executioner of nature" (Kamarck, 1976, p.17). A hard frost that kills exposed organisms in nature could have a major influence on the productivity of human investment in agriculture and health, by reducing competition from pests, pathogens and parasites.

But what does that have to do with the soil?

Frost kills pathogens in the soil, making the soil more fertile for crops (it is their hypothesis). Is it unclear?

then why are there no plants in the north pole?

I am not making any claim myself. It is their hypothesis. You're going to have to read the paper to learn more about whether they found support for their hypothesis. Note that your north pole argument is extremely poor because 1) there is no land in the north pole, only ice (unlike in antartica) 2) there is no seasonal frost int he north pole (they are specifically talking about seasonal frost).

oh␣␣␣␣␣␣␣␣␣␣␣␣␣␣␣␣␣␣␣␣␣␣

A lack of plant pathogens is great but that is not the same thing as increased soil fertility.  Fertility and pathogens are completely different things.

@Will sure but it is really not the point to discuss whether their hypothesis is true or not. The question was about understanding in which way could the hypothesis make any sense. If you would like to investigate more about their finding, just have a look at the paper.

@Remi.b - Yeah, I don't see this as answering the question directly either.


text:
Use of pipe character in VCF info field
While annotating my VCF file with ClinVar, I noted the following value for the CLNSIG field (i.e., clinical significance):
CLNSIG=2|2|2|2|2|2|2

This is actually reported in this example, so I think the usage of the pipe is quite common for genomic annotations of this kind.
Which is the use of the pipe (|) character? I looked for it in the VCF file format specification; however, only the meaning of the comma (,) is specified (i.e., presence of multiple alternate value for that field). I am wondering, instead, what the pipe represents.
Thank you.

There's some documentation on the GO annotation (GAF) format which goes on to define the pipe to mean 'OR'. I think this is somewhat supported by the NCBI gene annotation format for gene names e.g. BRCAI | BRCC1 | BROVCA1 | FANCS | IRIS | PNCA4 | PPP1R53 | PSCP | RNF53. But it may still be specific for VCF, so I will dig a little more but if nothing else this is my understanding.

This was my suspect, actually. I think that, e.g., an annotation string such as GENEINFO=BRCA1|BRCC1,BRCA1|FANCS could mean that the GENEINFO annotation can take two possible values, each one suggested by a different annotation source: 1) BRCA1|BRCC1: the first annotation source suggests that the variant is located either on BRCA1 or on BRCC1; 2) BRCA1|FANCS: the second annotation source suggests that the variant is located either on BRCA1 or on FANCS. I cannot find any documentation, though, so I am not sure this is the right interpretation.

Yet another question that could have fit in a bioinformatics stackexchange...

@bli I completely agree with you. Unfortunately, Biology Stackexchange mixes biology and bioinformatics, and there is not a way of separating the two aspects. However, I agree that bioinformatics should have its own identity.

@bli https://www.biostars.org/ is so established at this point it diminishes the need for a bioinformatics SE other than having that integration with the other communities here (which would be nice, honestly).


text:
Why do we have bacteria in our alimentary canal?
Our alimentary canal contains lots of bacteria. Most of these are found in the small intestine and large intestine.
Can you a give a few reasons why is it a good thing to have bacteria in our digestive system.
Thank you.

Is this a homework question? If yes - homework questions are warmly welcomed, barred OP shows prior efforts to answer them. Have a look at our homework policy in the help center. If not, we generally still expect users to give a question at least a shot on their own. For example, What are your thoughts on the subject? Which reasons can you think of?


text:
Plant Nutrition
Alfie has two plants, A and B. He used some Vaseline to coat the top of the leaves on plant A and the underside of the leaves on plant B. He left the plants on the windowsill for a week and watered them regularly.
a) What do you expect happened to each plant?
Plant A: __________________________________
Plant B: __________________________________
b) Explain the result you have predicted for plant B

I think plant A would use a moderate amount of water and would use the least amount of water. I think plant B would use the least amounts because coating the lower surface causes the water loss similar to coating both surfaces (upper and lower).
What are your thoughts on this?

Is the plant a dicot or monocot?

I would try to think about the vaseline layer as a huge cuticle that our man "Alfie" just applied to the plants.
I think you have the right answer here. Just note that there is a typo in the first sentence of your thoughts. You missed a "B" in front of "plant". Took me a bit to understand.


text:
RNA isolation problem
I have isolated RNA from cell culture (T25 flask, mouse cells) with trizol. I've measured the sample on Nanodrop, and this is what I've got:
A260 (10mm): 16.408
A260/A280: 1.98
656.3 ng/ul
How is this possible? What could go wrong here?
Thank you!

What is your problem? The A260/280 ratio? The yield? I don't understand (actually see) the question.

The absorbance A260: 16.408

The absorbance is directly proportional to the amount of nucleic acids (and proteins). Can you show the absorbance curve of your measurement?

no :( this is all i've got

Without any further data, we cannot give you any advice. But the A260 is not wrong, it shows that you have some RNA here. It is most likely still contaminated with Phenol though, this is what the high A260/280 ratio says.

Do you think RNeasy mini kit would help? Thank you very much for your help :)

I can't give you any advice as long as you are not sharing your protocol etc. Trizol in my experience gives fine RNA.

The 260/280 is almost 2, isn't that technically pure RNA? If the A260 readout alone is bothering you, read this article under Quantification of DNA

i used this protocol (RNA isolation procedure for cells) http://www.abcam.com/protocols/rna-isolation-protocol-cells-in-culture except I added 200uL chloroform, 500uL isopropanol and on the end I added 15uL DEPC treated water (because the last time there was small amount of cells).


text:
Is perception contrast based?
If I understand it correctly, humans can discriminate shades and colours based on their inherent contrast, as in we can see colors because there are different colors. Same for shades and for acoustic phenomens, because to differentiate two sounds they have to differ in some quality of sound: pitch, loudness, duration.
So the question is whether all perception is contrast based. One I would presume not to be contrast based is spatial perception, because it simply is there and always works in a standard manner.

I think contrast is incredibly important to perception to the extent that I would answer "Yes" or at least "Mostly yes", but I also think a proper answer to this question would be just far too in depth, which makes the question rather too broad. Note that spatial perception is also based on contrasts, but on contrasts in space rather than other stimulus features. That said, there are some examples of absolute perception, "perfect pitch" is one, and some types of perception are probably more akin to threshold phenomena.

Sure.

I think this question is fundamentally really good. However, as othwe users indicate, it is too broad. Limiting it to a single fundamental concept in one modality would greatly increase the potential of this post, e.g., is intensity perception (luminance perception) in the visual system relative or absolute?


text:
What insect is this
Saw many of these on my broccoli plant. Never saw them in the garden before today

I guess you live in North America?
Your broccoli is infested with the harlequin cabbage bug (Murgantia histrionica)
You took a picture of one of the nymphs.
Link to Wikipedia: Harlequin cabbage bug
To get rid of them, according to Wikipedia:
Handpick every bug and nymph off your plants.
Search carefully for eggs, which are black and white striped and come in packets of a dozen

Some excellent photographs! Garden pest or not, it's a delightful-looking creature.


text:
Complete metabolic map of humans
Do we have the complete metabolic map for humans? Do we know from the genome what enzimes are expressed and what each enzime does?

Simple rule of thumb: If your question is about biology and contains the word "complete", the answer is "no".

As Armatus notes, we don't know ALL human metabolites and the enzymes + metabolic reactions that produce them. Identifying small molecules is hard and metabolism is dynamic, it depends on what is being fed into the system.
The virtual metabolic human (VMH) is an attempt at compiling the information that we do know. You can read their paper here. The human build currently includes (and links together);

13 543 metabolic reactions
4138 metabolites
3695 genes (enzymes)

It also attempts to compile all known metabolic reactions that result from the gut microbiome, nutritional metabolic pathways and genetic diseases that alter metabolism. Everything is linked via stable identifiers which is a real challenge.
The human metabolic database (HMDB) is also very good. It contains more metabolites than the VMH as it includes many partially or poorly characterised metabolites. The HMDB is really useful if you are working to identify metabolites while the VMH focuses on how they connect to one another.

Roche has a pretty amazing map of metabolic pathways in the cell. You can find it here. During my Bachelor degree I contacted Roche and the mailed one to me for free (in a large poster format).

Amazing — Yes. Useful, other than wall decoration? The problem with such composite maps is that they don't distinguish between species — never mind tissues. And they mislead students into thinking that there is a mythical "cell" in which all the pathways are present.

The answer is not yet.  The sequencing of the human genome, considering its size (@ 3.2 bbp), and contrary to what's been hyped in media, is not the end of the quest for understanding the human body.  On the contrary, it is only the first and the simplest step in the elucidation of the intricate workings of the human body.  Even though a lot has been accomplished already, all of those tons of accomplishments still barely scratches the surface.
I can safely estimate that human genome sequencing represents less than 1% of the work that lies ahead, enormous work required to make sense of the whole base pair sequence.  Each succeeding step multiplies the complexity exponentially, and so, even considering the exponential advancement in technology, it is again safe to say that at the rate things are going, the complete elucidation of the human metabolome and metabolic pathways cannot be accomplished within the next 50 years.
To get an idea of the complexities involved, one only has to consider the next step after genome sequencing; the next step is to identify all the human genes making up the coding sections of the genome, which account for less than about 2% of the human genome.  Most genes do not transcribe into RNA in a straightforward manner; introns (which separate the exons that hold the coding sections), have to be spliced out; then the exons making up the code for the protein must be joined together.  All of that accountws for less than 2 % of the human genome.  The rest is non-coding DNA, the function of most of which hasn't yet been figured out.

You don't appear to mention metabolism in your answer. I thought that was what the question was about.

I did mention it, albeit indirectly; i used the words 'metabolome' and 'metabolic pathways' instead, because that was the post was asking for, to wit: "Do we have the complete metabolic map for humans?".
Oftentimes, an entire metabolic pathway has to be determined before the function of a  single enzyme can be known with reasonable certainty.


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Is this an ectopic beat?
First of all, I am unclear as to whether the answer to this question is a matter of fact or of opinion.
Nevertheless, I hope to find the answer.
In the image below, is the green beat considered ectopic?

What do you think, and why?

For reference: a normal P QRS from an EKG

from https://www.healio.com/cardiology/learn-the-heart/ecg-review/ecg-interpretation-tutorial/qrs-complex
The question and the different looking beat: one cannot say it is ectopic because the strip represents some sort of atrial arrhythmia.  Atrial fibrillation is the most common of these.  The beats are not regularly spaced and there is no sign of a P wave (the one produced by the atrium).
From link

Atrial Fibrillation occurs when multiple electrical impulses occur
  within within the atria. This chaotic electrical activity results in a
  chaotic wave form between the QRS complexes. P waves are absent. They
  are replaced by lower case "f" waves. No P waves means there is no PR
  interval measurement. This rapid electrical activity overwhelms the AV
  node causing impulses to enter the ventricular conduction system at
  irregular points. This results in irregular R to R intervals.

"Ectopic" beat suggests there is a regular beat going on and some rogue beat elbows its way in.  In A fib they are all rogue beats - "multiple electrical impulses".  The one you see is not in structure different from the rest - there is a T for every QRS and so they are all coming from the atrium.  It is just that with that beat the S wave is deeper.  Maybe because it is so close to the T?   I bet if you ran that strip a while you would see others comparably deep.
I am betting this is homework.  What exactly is the question?

Thanks for your assistance Will.  I had the assumption that even in atrial fibrillation, there is some ventricular rhythm to be studied, given by the RR intervals of suitably "normal" beats.  Essentially I was wondering whether the size of the beat would qualify it as "not-normal," meaning not part of the intrinsic ventricular rhythm, if any.

And you are right in predicting that there are more beats with the same S-depth as the green one, though they are fairly sparse.

this isn't biology, this is medicine. go to the medicine stack exchange

Beats coming from within the ventricle look different - wide weird QRS.  Google up PVC or premature ventricular contraction to see a common type.

Just to be clear, this is not AFib. March it out. (That's one of the first things to learn when studying EKG's: "march it out". It's tedious but instructive.) You'll see a pattern impossible with AFib. It's a crappy EKG tracing, but information is there. There is, however, an atrial problem.

@Will - Also, "ectopic beat" does not equal "PVC".


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What of Gould's contributions to evolutionary biology are still accepted in the mainstream?
I have been reading Daniel Dennett's Darwin's Dangerous Idea, in which he picks apart many of Stephen Jay Gould's criticisms of neo-Darwinism, particularly in the chapter 'Bully for Brontosaurus'. Turns out Gould wrote a lengthy refutation back, and they ended up throwing slurs at each other for a few years afterwards.
I am interested to know what the current state of mainstream opinion is on Gould's interpretations, particularly on panadaptationism and gradualism. Has the field yet come to any firm conclusions on who was right after all?

His main contribution was making biologist consider that population size affects how fast selection changes a population, but he tended to imply this was some form of categorical difference and not a spectrum. But this was greatly overblown my media into some sort of insistence that they could not be the same. large population slow change and small population fast change are both points on the same spectrum. Nobody was right becasue both sides were not really saying the other could not occur they just emphasised their own area. Gould main problem was the idea of stasis in punctuated equilibrium that large populations somehow did not keep evolving this was a point he contested without ever really being able to provide evidence for. His own evidence often fit both interpretations. Since then it has been pretty thoroughly refuted by genetic studies, better resolution*, and modeling of stabilizing selection, all populations change, large ones just change slower, often with less direction. Gould himself later accepted this, but insisted on keeping the terms punctuated equilibrium and more oddly "stasis" for these periods of reduced change, this led to more misunderstanding especially with the public and media. Many scientist felt it was a sign of being unwilling to truly accept the evidence.
He also contributed a lot to our understanding of evolutionary development and how evolutionary baggage effects future adaptations. We often forget this but without his constant pushed of the importance of constraints and development both would probably be much more poorly understood. Panadaptationism was probably given more service by than many ever though it deserved, but Gould was right that that are far more aspects to selection than many considered. It just was not as popular an idea as his attention implied, but that is part of science harping on bad ideas is not really bad in science, it just starts to get old when the idea never had a lot of traction. It is however understandable considering Gould's own focus.
He has a serious problem(probably not unfounded) with sociobiology but probably pushed too far by implying searching evolutionary history for influence of our behavior was pointless. As much good as he did for understanding physical adaptations he seemed to have a blind spot when it came to behavioral adaptations. He mellowed about this in later years but still seemed to resist it. Sociobiology tended to be over applied, often without evidence, it was easily the worst offender with panadaptationism. Gould was right to push back against speculation but he often treated all behavioral science the same regardless of rigor.
Dennit who primarily researched evolutionary aspects of human behavior and publicly speculated a lot, of course ended up as a stanch opponent. But then as the more rigorous evolutionary psychology arose from sociobiology Gould seemed unable to see the difference which quickly led other to stand against him and probably did more than anything to produce his negative image. I know it is the thing that put me off his writing.
The other issue that I, as well as many other paleontologists, had with him was his resistance to the application cladistics and other computer based analysis. Both extremely important tools in understanding evolution, especially once to could be applied to genetic material. He always seemed to treat it as not real science, which always struck me as weird considering how much he emphasised rigorous investigation. He struck me a brilliant mind falling behind the technological curve and becoming disapproving of it. To myself as a young scientist he seemed to resist anything new regardless of rigor despite his own emphasis on rigor.
In short he was hard working scientist. He improved our knowledge in some areas while being unhelpful in others. He was a scientist who got a huge amount of media attention, which few scientist can do without sooner or later showing normal human flaws. Now take all this with a grain of salt, this is all my own personal impressions from observation of his work in paleontology along with reading his (and just about every other) book about evolution. I have not read many of his paper outside of paleontology. I say this becasue speculating on the beliefs and motivations of the dead has always struck me as dishonest especially without laying your cards on the table.

I wanted to give special mention to resolution and darwin finches, darwin finches undergo different selection every year depending on rainfall, large and small (specialized) beaks during wet years and medium (generalist) beaks during dry years, this changes every breading season with the amount of rainfall on any large scale this would appear to be no change as they tend ot average out, but with better resolution we can see many many small directional selection pressures adding up to no net change on a large scale.


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Can Phosphogycolate buildup in a plant kill it?
I'm trying to think of some things for the science fair, for part of my experiment I need to know if Phosphogycolate build up in a plant can kill it. Also, are there any chemicals that may disrupt the enzymes which break down phosphogycolate. Thanks!

Too late to tell you, but phosphogycolate doesn’t exist.

Phosphogycolate can break down enzymes needed in the Calvin Cycle along with other enzymes in a plant so that is a yes.l.


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Are the fossil sites in Hadar geographically separated?
The Hadar fossil record is made up of, from oldest to youngest, the Basal Member, Sidi Hakoma Member, Denen Dora Member, and Kada Hadar Member.
Are these regions geographically distinct, or, are they layers on top of another on the same geographical region?

Here is a map of the region where they found the Lucy skeleton.

The researchers speak of the Hadar formation at Dikika, so they are giving it an expanse of 10-15 kilometers at least.
it's quite flat as well.
Why do you want to know?


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Why don’t humans have eyes at the back of their heads?
How does evolution rule out the possibility of humans or others fragile herbivores from having 2 pairs of eyes, one at the front and the other at the back of their heads? Why didn’t that ever happen?

I’m sorry but I’m not a biology student; currently pursuing mechanical engineering. So, I don’t have any knowledgeable viewpoint over the same. The idea was that you people could hopefully provide some intellectual insight.

“Given limited resources” - what does that mean ?

On top of the question marked as duplicate, you might want to have a look at Why don't mammals have more than 4 limbs?.

First, humans aren't fragile herbivores, they're omnivores, and quite successful hunters even pre-technology :-)  Now that that's out of the way, the basic vertebrate body plan - four limbs, two eyes, &c - was fixed hundreds of millions of year.  Herbivores, such as horses, have the eyes located at the sides of their head, and have nearly a 360 degree visual field.  Predators tend to have front-facing eyes, the better to focus on potential prey.

Vertebrates have ears which sense 360 degrees for a range of many meters, and they have social eyes, where they group many eyes and ears into one social group, it's easier to listen and live in groups, than grow eyes in the back of the head.
2 eyes exists in nearly all bilateral animals, arthropods, flatworms, sea-slugs, crabs, crickets, squids, flies. Arthropods have compound eyes and it would be easier for them to have 4 eyes, and only spiders and horseshoe crabs have more than 2.
It would be easier for a vertebrates to develop 4 nostrils and ears than 4 eyes because they are simpler than the orbs of the eye.
Same reason as 5 fingers has been the optimal numbers for all vertebrates since early lizards. in short, it's very easy to lose extra organs and to modify old ones, but it's very difficult to evolve new organs, and to relocate ones around the nerves and veins... centrally connected organs travel around the body and the circulation moves in front of them, i.e. if you did get 4 eyes and two of them moved to the back and sides, the nerves for your face expressions that are next to your ear would have to go in front, around, and through the moving eye pathways.

To simplify, we stopped evolving our symmetrical archetypes when we were related to starfish, ammonites and ediacaran fauna, and the fastest most versatile animals all had 2 sided symmetries, with entirely symmetrical nervous systems, and forwards moving at that point in time, using binocular compound vision, which did have 180, and that binocular compound vision afterwards became our 2 eyes. We share the kingdom Animalia with starfish, our common ancestor experimented with shape during the Ediacaran era.
To understand the difficulty of adding new eyes later, you should learn why nearly all vertebrates have 5 fingers, except some frogs which have 4. it
google: why do animals all have two eyes?

The mysterious downvoter is back I guess.

I should post more to compensate then.

2 eyes and 5 fingers has been the optimal numbers for all vertebrates this is fantastically wrong (might want to have a look at Why don't mammals have more than 4 limbs?). we stopped evolving our symmetrical radiation is wrong. when we were starfish sounds like you mean that the common starfish is our ancestor which is wrong. You seem to equate symmetry with binocular vision which is also wrong. Your only two links are google search!

We share the kingdom Animalia with starfish, our common ancestors experimented with symmetries during the Ediacaran era resulting in worms, corals, urchins, bivalves. Terrestrial vertebrates have 5 fingers.... you send me to a page called "mammals have 4 limbs" I send you to 4 pages called "why nearly all vertebrates have 5 fingers" .... bi-focal vision is a common theme in planar symmetry or in radial? PLANAR symmetry.

"Optimal number" is wrong.  It's much more of an accidental number: the long-ago last common ancestor just happened to have 4 limbs, 5 digits per limb, 2 eyes (and ears &c), and those are buried so deep in the genes that any changes make the organism non-viable.  See e.g. Hox genes.

Quadruped 5 digit number = "The number chosen by natural selection of fitness" was "optimal" because there were 7, then 6, then 5 digits on Both limbs of archetype quadrupeds. Neither 7 nor 6 digits could have been optimal, because they were both lost by selection against ray fin derived Hox Genes for 6/7/4 digits. Eyes: Planar symmetry arthropods can all develop multiple eyes, and they dont. Even all Flatworms and seaslugs have two eyes, which is certainly the chosen number of eyes for planar symmetries, for the same reason that we have 2 ears, it's genetically efficient.

I downvoted too.  This is the very worst kind of answer for StackExchange; it's superficially plausible and written with great confidence and authority, so a naive reader will probably think that the author is deeply knowledgeable; yet the answer is simply bluster, mistaken stereotypes, and sweeping claims based on ignorance. If you don't actually understand the field, you shouldn't answer questions. The fact that you think you understand this is simply Dunning-Kruger in action.

@comprehensible Even the expression natural selection of fitness is non-sense.

You don't know the difference between a limb and a digit, Remi.B. Also, learn to speak english. natural selectrion of fitness for purpose. https://www.google.fr/search?q=%22natural+selection+of+fitness%22&oq=%22natural+selection+of+fitness%22&aqs=chrome..69i57j0l5.6993j0j7&sourceid=chrome&ie=UTF-8 <--- check that, selection according to fitness of a phenotype and morphology... iaYork you yourself are like tim-nice-but-dim. WHY? hyper beginner question = beginner answer, at least i bothered. It just shows that you don't have basic knowledge of evolution, you reply without facts/content, vaguely

Remi.b, you must feel like an idiot telling me "that doesnt even exist' and then reading it www.genetics.org Ph.D texts ... and confusing 5 digits (polydactylism) with 4 legs? you are truly the one talking nonsense.

@comprehensible: Then by your argument, 5 digits aren't optimal either, since many vertebrate lineages are evolving away from that.  E.g. snakes with no digits (or limbs), dogs with four (plus a largely vestigal dewclaw), cows and such with two, horses with one...

That's a fair comment, snakes are not quadrupeds, there are 4 species of dogs (40 species of cats) and 350 species of primates including humans, 5000 lizard, 200 species of squirrels, 5000 frogs, all 5 digits, a dog and a horse can never evolve back into a forest environment. losing all grabbing ability is not an optimal design unless it gets wings/trunk/aquatic. all land vertebrates that survived after the dinosaurs had 5 digits except snakes? all non grasping species didn't survive, and ungulates would all vanish when there is another apocalyptic winter.

@comprehensible: If you think that having single-digit hooves means the critter loses all grabbing ability, I can deduce that you've never spent much time around horses.  And hooves seem to work pretty well if your niche in life is as a grazing herbivore :-)

ok, so the dominant big species of african ecosysters have soft pads and hooves. That knocks over my theory. perhaps hooves are not digits, so when 1 finger vanishes the limb ceases to have a hand a very fast becomes a clawed pad and a hoof. no rodents, marsupials, lizards and salamanders have 4 finger hands, and pandas, koalas, opossums and some frogs have opposable thumbs. It's a theory I read on a Polydactyly biology page, I only copied it.


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Why is E.coli used as a model?
Is there a reason for the choice of E.coli as a model for many bacterial systems? Other bacteria such as B.subtilis are also used, but why is E. coli preferred?

Short answer. It was discovered pretty early (late 1800's). It is easy to get (you probably know where it comes from), purify, grow and is not virulent. E.coli spreads very rapidly (30 minutes division rate).
Why this one in particular and not another similar bacteria? Well you have to choose something at some stage and usually the more an organism is used the most valuable it becomes which means that more and more scientists will start to use it creating a loop which favors certain organisms, like it happened with E.coli.
E.coli started to be studied because Theodor Escherich wanted to prove the "germ theory of disease" which led him and later other scientists to work with E.coli and everybody uses it today.
By the way, the mouse model is actually quite interesting. Started by breeding huge amount of mice for selling them as pets.

Not virulent? It's a pretty nasty bug

@AliceD The E.coli strain used routinely in laboratories is part of the group A and is a non virulent one.

That's interesting. +1


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Two heterozygote mice for skin color are reproduced. Find the probability that in 3 children 2 will be dark and one white
Two heterozygote mice for skin color are reproduced. Black is dominant to white color. Find the probability that in 3 children 2 will be dark and one white. How did you do the ordering. Well I found it that in F1: 1/4 are AA, 1/2 Aa, 1/4 aa or 3/4 black and 1/4 white.Now nI think I should multiply the chances: 3/4*1/4*3/4, but it would be according to an order. What should I do? Is my answer correct?

You are on the right track, but you have to keep in mind there are multiple ways to have two dark and one child in a group of three. You have to add the probabilities of each unique outcome that results in two dark and one light child. So, the probability is (1/4) x (3/4) x (3/4) PLUS (3/4) x (1/4) x (3/4) PLUS (3/4) x (3/4) x (1/4)

Alternatively, multiply one outcome by 3P1.


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Why do plants produce so many hybrids as a kingdom?
Why do plants produce so many hybrids? I have read that they are the largest kingdom of organisms to do so. Does this have something to do with polyploidy events?

Might be a bit related

Yes, it has very much to do with the poliploidy events. Specifically if you look at the grasses, most grasses that are diploid (eg., AA, BB), cannot hybridize, but in some rare events when they form polyploid (AAAA, BBBB), they can readily hybridize to form fertile progenies (AABB).

Do you have a citation for this claim?

I don't have the citation, but I recently attended a talk by Dr. Kellogg, who talked about this. I think her paper talks about it briefly.

I found no evidence to your claims in the paper you linked. thus -1, I'll revoke if you can point me to it.


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Effects of HRT on transgender(M to F) physiology and athleticism.
I often heard of athletes in the Olympics who would be accussed of having an advantage because they were intersexed.
Now I know transgenderism and being intersexed are not the same thing, but they can both involve Hormone replacement therapy.
Therefore would a transgender women (ie: a person assigned male at birth, who transitioned to female) have advantage over cisgendered(not transgender or intersexed) women in sporting events due to anatomy or physiology from previously having a male form?
To add detail, I guess it would depend on the state of their transition, so one could use MMA competator Fallon Fox, as an example, or any other transgender women.
My thoughts on the effects of HRT on athleticism for transgender people is that if they were more advantageous, then they should be dominating their respective fields.
As for the biology, I know that bone growth stops at around 20, but how would the HRT affect their muscles, and would muscles even matter without the corresponding frame?
.

The only advantage that I could see is if they stopped taking HRT female hormones and allow their male hormones to build back up in their system, though I think that people probably made the choice to undergo reassignment for reasons other than gaining competitive advantage in sports.

@AMR            I totally sympathize with trans people and their desire or need to transition, but as to your point, why would a build up of male hormones give them an advantage?

Why do athletes inject themselves with testosterone? It is needed to increase muscle mass. Male hormones lead to bigger muscles, so if the person was originally XY, then they will begin to produce more testosterone if they come off of the HRT. If they had reassignment surgery, then it will obviously be less than an XY person with testicles, but there will be a higher level of testosterone and other androgens that will cause the body to begin to masculinize again. I am not going to say that there are women who cannot outperform men, but all things being equal, that may lead to an advantage.

One thing I think I left out, is that I believe that Male to Female transgender individuals also take androgen blockers to bring them down to similar levels as XX females. Females also produce androgens, but in much lower concentrations or they make fewer androgen receptors in their cells than males.

@fredsbend.       But fallon fox is on hrt according to this article, http://www.mmaweekly.com/transgender-fighter-fallon-fox-says-she-is-actually-at-a-disadvantage-to-her-opponents.       .        and she is an active combatant.

We have two groups of people or better to say scientists and specialists that have their own ideas and theories and approvements.

People that are relay on genetic related ideas that mostly consider rule of Y chromosome on men and how some genes' rules will not be diminished only by hormone therapy or non genetically engineering methods.

Case example:

Chloie Jonsson, 34, who transitioned more than eight years ago, is legally recognized as female in the state of California. Despite the medical community's consensus that transgender women do not have a competitive advantage over cisgender (nontrans) women, Jonsson's application to participate in CrossFit's women's division was rejected with a bizarre letter claiming she and her supporters do not understand "the human genome" and "fundamental biology." In response, Jonsson filed suit against the fitness giant.
The letter from CrossFit general counsel Dale Saran reads:
"We have simply ruled that based upon [Chloie] being born as a male, she will need to compete in the Men's Division. The fundamental, ineluctable fact is that a male competitor who has a sex reassignment procedure still has a genetic makeup that confers a physical and physiological advantage over women. ... Our decision has nothing to do with 'ignorance' or being bigots — it has to do with a very real understanding of the human genome, of fundamental biology, that you are either intentionally ignoring or missed in high school."
  Later, Saran disputes the statement made by Jonsson's attorney that "by all accounts, both physically and legally, Chloie Jonsson is a female."
"This is simply wrong as a matter of human biology and if you can't see that, there really isn't much to talk about," writes Saran, citing Encyclopedia Britannica. "Chloie was born, genetically — as a matter of fact — with an X and a Y chromosome and all of the anatomy of the human race. Today, notwithstanding any hormone therapy or surgeries, Chloie still has an X and a Y chromosome."

To add some details to group one's idea, if you think of some genes and their rules in men that makes them more accurate and more muscular than women in the field of physical activities, you'll get to the point of how to control or change behaviour of these genes in the body of a man to make him woman, both muscularly and neurologically which is not possible for now because we need some very detailed and powerful calculations to know the exact equilibrium of a man genome as if he was a woman.
To change the complicated mechanism of Y chromosome on Biochemistry and behaviour of other chromosomes we have so much to learn and we need very fast computers to simulate the behaviour of molecules and new formation of mass body.

And we have other ideas by people who insist on level of hormones that has a great effect on mass of bone and muscles in men and women regardless of how their sex and genome is.

Case example:

Eric Vilain, Director of the Center for Gender-Based Biology and Chief Medical Genetics Department of Pediatrics at UCLA, says of any perceived advantage a transgender woman may have, “Research suggests that androgen deprivation and cross-sex hormone treatment in male-to-female transsexuals reduces muscle mass; accordingly, one year of hormone therapy is an appropriate transitional time before a male-to-female student athlete competes on a women’s team."

A great article and detailed explanation by an example that helps to answer your question is here.


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Do dogs and cats know the names of other people / pets in the house?
I have a dog named Penny and a cat named Milo. I always wonder if Milo knows Penny's name, and vice versa. So if I call Penny, does Milo know that I just called her? Similarly for humans, if someone is over the house that they're familiar with, do they know that person's name? If someone calls me by name, do my pets know that I've been called?
What about other interactions - not just calling someone (scolding, feeding, asking to do a trick, etc).
I'm looking for a more scientific answer if possible - meaning studies and facts. I've had dogs all my life, and cats for the past 10+ years, so I know they're very smart. But I want more than just "I know my dog knows my cat's name, because she's just so smart". I'm wondering if anyone has ever studied this and proven it one way or the other.

reason for downvote?

Not my downvote, but I would assume because simple observation would provide an answer.  For instance, I can tell my dog and a friend's dogs that he frequently associates with to go to a particular person, or do something with a particular other dog.

I specifically said that I'm not looking for simple observation, I'm looking for scientific proof. That's different. Also, what about cats?


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can dissolving be endothermic process
can dissolving be endothermic process. I have a container with glucose(solid state) and added water and found the container getting colder. was wondering there is no reaction(just a physical process) and why would it absorb heat.

Yes, it can. This a question for [chemistry.se].

The answer to your question in general is yes.
There are many salts and compounds that are endothermic - they cool the solution when they dissolve.  It also turns out that glucose is endothermic when it dissolves if this sheet i found is to be believed.  Its not a strong effect but you made an accurate observation!
Endothermic salts can be quite cold.  This is how home ice cream makers often work in fact - rock salt dissolves into the ice and makes it even colder than it started out to be. I believe that is how ice cream was made before refrigeration and ice storage arrived in the 19th century.

Welcome back! How have you been? How's the company going?

thanks Alice!  very well - raising funds for a new startup...


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What is the scientific name of this flying insect?
It looks like some relative of dragon fly.

To give an idea about its size I picked it by its wings

It had quite a flexible abdomen

I set it free after clicking the pics. I live in central India (If that matters)

It seems that you were careful, but generally speaking try not to pick up insects by their wings, they are often the most fragile part and are one of the most essential for the insect's survival in many cases.

@ttbek OK I'll remember that!

@ttbek - that sounds nice in theory, but what else can you actually grab? Sure, for a hard beetle you can just grab damn thing by the body, but nearly everything else is too squishy for that.

@ttbek In general you are right, however dragonflies are about the only insects were it can't hurt to hold them by there wings (if done carefully off course).

Davor: I was wondering that I bit myself.... , but more in the sense of potential wing damage if one tries to hold on to somewhere else as they try to fly away.  The bodies are often not quite as squishy as you may imagine due the their exoskeletons, at least relative to the thin membrane that the wings often consist of.  Coyote Peterson often uses a special set of forceps for handling insects, and does grip them by the body this way, not a perfect reference but just from the top of my head for now.
RHA:  Yeah, dragonflies are pretty badass like that.