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How to add oxygen to indoor air without opening windows?
I'm not a biologist. I have read that low oxygen levels in the home can have a negative effect on health. I am interested in increasing the amount of oxygen in the air in my home.
To open the windows would be the most effective way but the air outside is cold and measurably polluted (PM2.5 usually greater than 30µg/m3) so I would like to find other ways.
I know that plants add oxygen to the air but I have read that an unrealistically large amount of plants would be needed to make a meaningful difference to the oxygen levels.
I am wondering what other methods I can use and also whether what I have written above is correct.
Please forgive me for my ignorance. If this is the wrong place to ask this question then please help me to find the right place. Also sorry for not knowing what tags to use.

You should not keep so many plants inside a closed room. In addition to the above answers, there is another thing to consider. If you don't open the window there will be no air circulation. In absence of fresh air germs can grow inside the room, which may cause health issues. The indoor air can become more polluted than the out side air. If you really can't open the windows, I would suggest you to install a good quality air purification system, which don’t produce ozone by-product. Even though the air purifier cleans the air, you still need to keep the windows open

You should also have in mind that, meanwhile plants produce oxygen through photosynthesis, they also carry out aerobic respiration. In short, this process requires oxygen which is normally not a problem during daytime as photosynthesis covers the oxygen needed. Nonetheless, during nightime, plants remove oxygen from the atmosphere and do not replenish it. This is why nurses normally remove plants from hospital rooms at night. So if you want to put plants in your room, have in mind that is best to take it outside during the night.
Refer to this link for more information: http://www.saps.org.uk/saps-associates/browse-q-and-a/453-do-house-plants-remove-oxygen

When plants photosynthesize they take carbon dioxide from the air and water from their soil, and using energy from sunlight combine these into sugar. In the process, oxygen gas is released as a waste product
This is pretty much the reverse of what you are doing. You take in oxygen from the air and you use this to break apart fuel, releasing energy and breathing out carbon dioxide and water as waste
Plant
[carbon dioxide + water + sunlihgt -> sugar and oxygen]
You
[sugar + oxygen -> carbon dioxide + water + energy]
Therefore, to add more oxygen you want a photosynthetic plant. this website lists the best ones for adding oxygen and also for cleaning the air. when plants pull gases out of the air, they filter and kill bacteria and spores out of the air too using their leaves.
https://www.bhg.com.au/best-air-cleaning-plants
You want leafy green, fast growing for the best effect.


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Calculating fraction of protein unfolded from spectroscopy data

This is a question from a homework pset of previous year. We are given the absorbance at 222nm of both a wild type and mutant protein at different temperatures. We are then asked to calculate various thermodynamic quantities from these data. The first thing it asked for is the Tm of both wt and mutant. To get the Tm, I need the fraction of protein unfolded, since Tm is defined as the temperature at which fraction unfolded is 0.5. However, I am confused as to how to calculate fraction unfolded. In the answer key, the professor used a equation, f=2*(A222-0.5), without any explanation. Can anyone explain to me where does this equation come from?
Edit: Sorry, I forgot to tell you that f stands for fraction unfolded.
Thank you very much
Zeyuan

I've plotted the data for ease of answering, though it is not necessary if you know what to look for in the data.

As expected, the melting curves are sigmoidal with horizontal asymptotes at approximately 0.5 and 1. You should be able to see this in the raw data as well: the absorbances hover around 0.5 before rising rapidly and then plateauing around 1.
You want the fraction of unfolded protein as a function of absorbance, so you need to normalize this data to the range of [0,1]. There's a straightforward formula for this which, put into the terms of your question, would be:
$f = \frac{A_{222} - min(A_{222})}{max(A_{222}) - min(A_{222})}$
$f = \frac{A_{222} - 0.5}{1 - 0.5}$
$f = \frac{A_{222} - 0.5}{0.5} = 2(A_{222} - 0.5)$
Intuitively, you might think about it as follows: at low temperatures, when the protein is folded, absorbance is 0.5. Consider this a blank or baseline measurement which gives the absorbance of the solution when no protein is unfolded. Since you are only interested in the signal from unfolded protein, you can subtract this value (0.5) from the rest of the data.

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About. Autosomal recessive diseases in genetics
What happens if homozygous dominant  alleles are present in an individual for an autosomal recessive disease will he be affected ?

What are your thoughts? Knowing your thoughts on the subject would help us understanding what could be unclear to you

You are talking about an extremely simple system of inheritence that is a single bi-allelic locus with simple dominance relationships. You are talking about a autosomal recessive disease. In other words, let a and A be the two alleles, where A is dominant of a. By definition of your model, the individual expressing the disease is the individual carrying both a alleles (a aa individual). Anyone carrying the dominant allele would not express the disease (by definition of the term dominance and because you define a model where a and not A is causing the disease).
In short aa express the disease, while aA, Aa and AA individuals don't express the disease. aA and Aa are carrying the allele causing the disease though and might have kids expressing the disease if they mate with an individual that carries at least one allele a.

No. Because you said it's homozygous, meaning that two alleles are identical, both dominant in this case. Hence, there's no recessive allele at this locus so he won't be affected.

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Trouble amplifying microsatellites using a 3 primer protocol, positives in negative controls
I'm trying to collect microsatellite data using primers developed on a related species but instead of having primers with fluorescent dye already on them, I'm trying to attach an M13-dye to the forward primer which also has an M13 tag on its 5' end. I am having some difficulties though because my negative control bands look identical to the positive bands, regardless of annealing temperature and MgCl2 concentration, and the bands seem too large for it to be primer-dimers, it seems like genomic DNA.. it's about 100-150bp.. so I'm not sure what is going on.
Before somebody suggests that it is contamination - I started over at a whole different lab bench, different pipettes, pipette tips, reagents, ordered new primers, thermocycler, everything, but the problem did not go away. Since I'm still optimizing the microsatellite primers I also ran a test using some invertebrate COI which I have positive results from in the past, and included a little bit of each reagent into each reaction instead of DNA, and I got a very strong band at the M13-dye. This was brand new, reordered after the last batch had this problem, suspended with TE and diluted with nuclease-free water. I am wondering if it has to do with the gel sybr-safe filter? Or the UV illumination for visualizing the gel? I am grasping at straws, please help or let me know if you have the same problem. The dye is just M13 labeled 6FAM: 5'-/56-FAM/TGTAAAACGACGGCCAGT-3' from IDT

I have no experience with this, but what is your negative control?

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Eukaryotic equivalent of bacterial tmRNA
According to this Wikipedia article,
tmRNA is only found in bacteria, with its purpose being to “rescue stalled ribosomes”.
This brings me to the question of is there a eukaryotic equivalent of this RNA? If not, how do eukaryotic cells (or any other type of cell) prevent or stop stalled ribosomes?
Every time I search for “eukaryotic rescuing stalled ribosomes”, I am constantly only  presented with references to tmRNA in E. Coli.

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5311927/

Googling works fine with a slight amount of persistence: the 6th result for stalled eukaryotic ribosomes is this overview paper.

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

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What are the causes of abortive initiation?
I was reading more about DNA transcription, and it mentioned abortive initiation. The article gave no explanation as to why the phenomenon occurs.
The only explanation I can think of is that it is an error in the "machinery" of the RNA polymerase.
Is there any scientific research as to why abortive initiation occurs?

What article did you read? Did you read wiki > abortive initiation also?

@Remi.b The Wikipedia article is one of the articles I read. I also read https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2563432/


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What is the distinction between deoxyribonucleases and restriction enzymes?
Both deoxyribonucleases (DNases) and restriction enzymes are endonucleases (some DNases can be exonucleases).
They both break the bonds between nucleotides. Therefore, what is the difference between the two?
My original thought was that restriction enzymes, unlike DNases, cut at specific sequences of DNA. Then this raises the question of whether restriction enzymes are just a category of DNases, but I have found no sources to back that up. Also, according to this Wikipedia article:

There are more than 900 restriction enzymes, some sequence specific and some not...

This further erodes the distinction I had created between the two types of nucleases.

You already mentioned that all restriction enzymes are endonucleases but DNases may be endonuclease or exonuclease

...so could u be a bit more specific.


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Is there a hypernym for enzymes that "cut" other molecules?
I have searched on Google for a hypernym/umbrella term that encompasses all enzymes whose function is to cut other molecules, but I have yet to find such a term. The term I am looking for would encompass enzymes groups such as proteases, nucleases, and lipases.
Is there such a term in molecular biology?

Aren't all enzymes named with the suffix "-ase"?

Oh yeah d'oh. Don't know why I forgot that. Ignore me!

Hydrolases can "cut" other molecules using hydrolysis (see proteases), and Lyases can catalyze "cutting" with other reactions (see aldolases). These are umbrella terms for families of enzymes classified by function.
I think this is a fair open-access review of enzyme classification.

Please provide links to the EC classification or the like to support your assertion. You may be right, but how is anyone to know?

The term you want is "scission enzyme".  Scission is from Latin scissio, the same root as for scissors.  This is a broad umbrella term which does not speak to mechanism of cutting.

Never heard this used. Please support your suggestion by citations and links, otherwise they are likely to be flagged as low quality.

Also never heard this. Strongly doubt it is a common term.

I appreciate you 2 asking for clarification rather than just down voting.  Here is a google search with 632 uses of the term. It is such a broad category that the term is not that useful, which may be why you two are unfamiliar with it.


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Tight Junctions in Cell Types
I took a quiz today on cell structure basics, which included cell junction types. I disagree with the "correct answer" according to the teacher.
Here is the question:
Which cell type would have the most tight junctions?

a) Pancrease cells
b) Ovarian cells
c) Epithelial cells (in the intestine)
d) Muscle cells (skeletal)

According to my teacher, muscle cells is the correct answer.
I argued that the answer should be epithelial cells, as muscles cells (according to the text) primarily use desmosomes for cell-to-cell adhesion, while epithelial cells rely on tight junctions primarily.
I searched it up quickly on Google, and from what I have found, epithelial cells is the correct answer.
Is my teacher incorrect?

Tight junctions are very specifically a structure found in epithelial cells, so your teacher is incorrect. Tight junctions are what allow epithelial cells to form a selective barrier between compartments. Fibroblasts can be induced to form tight junctions under certain experimental conditions, but I'm not aware of any case where a skeletal muscle cell expresses a tight junction. Regardless, it would not be normal physiology.
You can read more about tight junctions here, in the online Albert's Molecular Biology of the Cell. This figure from that Chapter illustrates the barrier function.

If you want to get into more of the details re: what we know about the various proteins involved in creating and regulating tight junctions, this is a good review.
One small correction to your reasoning, though, I wouldn't say the primary purpose of tight junctions is cell-to-cell adhesion, per se, it's selective permeability. These junctions may help the cells to hold together, but the tissues can resist shear stress in knock-out models. A knockout model without a necessary tight junction protein, however, will not maintain selective permeability.


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Functional Difference between the Distal Promoter and Enhancer Region
According to the Wikipedia article on eukaryotic promoter regions, the distal promoter is:

Anything further upstream (but not an enhancer or other regulatory region whose influence is positional/orientation independent)

What is the difference between the regulatory region and the distal promoter? Does the distal promoter region have a greater effect on the rate of transcription?
If so, is the determination for what has a big enough effect to be a distal promoter subjective?


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The difference between Mast Cells and Basophils
While reading the Wikipedia article on Mast cells, I came across something that confused me. What is the major difference between a Mast Cell and Basophil?
They both seem to do the same exact function: triggering the inflammatory response. The only difference I can pick out is that Mast Cells are kept resident in a tissue while basophils move around.
Is this the only major difference?

There are differences. This article is a little old, so advances may have been made, but try reading through it. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2847274/


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Oculus rift (or, what do other eye placements see?)
I could be WAY out of line in the placement of this question, but here goes:
Everyone I'm sure has heard of the Oculus Rift or any of the several other VR headsets making their way around.
It reminded me of a friend who, when in art school, said, "Dali's eyes were crooked [whatever the opposite of crossed is], and it may have helped him develop a different sense of perspective, and we have been taught to practice letting our eyes go relaxed to recreate similar effects."
I don't know if he did it, and I never saw a representation. But now I am interested...
If an Oculus used a model with eyes pointing different directions...or on the "sides of the head" with a wider field of view like many non-predatory animals...
What would we see?
(And maybe if it's an interesting answer... a VR Dali or VR cow simulator might be in order...)

Your question is not very clear. What exactly are you asking? Are you asking how our brains would process split imagery (i.e., VR with vision for one eye pointing one way and the image for the other eye pointing another way)??

I think the question is whether we can simulate for humans what we would see if our eyes were on the sides of our heads, as is found in many animals.

Yes to canadianer. A creature's sense of the world is certainly informed by the way it senses the world. Predators have eyes similar to ours, forward facing, focused, sharp. Many prey animals have eyes with wide fields of view, ostensibly for defensive purposes, sensing the most of what is around, if not in the tight focus of a predator. So, what might that look like for them, and us if simulated. It is one of those things that is hard to imagine because we have simply never experienced it. We focus tightly, not a wide field like a sentry. Like Dali, how would that affect perspective?

I might have to try this, since I have one and can program for it. Will report back if I get around to it.

It would probably be quite disorienting, maybe even make you sick.
There is a much more limited fun classroom demo that my institution uses with kids, where they wear goggles that shift their view a couple degrees to the left (this demo is quite common, you can find many examples on YouTube as well). They stand a couple meters from a wall and throw a ball at a target: inevitably, they miss wide right for the first few throws, but eventually they adapt and hit the target no problem; then when they remove the goggles, they miss again to the left.
So, your visual system can adapt to some shifts in visual field. However, if the view was very skewed, oriented for example like the eyes of cattle, on the sides of the head, it would be much more difficult to adapt to where it feels natural. I would expect the strategy people would use would be to attend to only one visual field or the other, since there is no longer any binocular area of vision, sort of like if you would look as far to the right as you possibly can you see a lot of visual space with only one eye.
An important element to immersive VR is that you feel like you are actually having the experience - in VR when you have some sort of joystick or controller to manipulate, for example, it is really helpful to orient people by allowing them to see the controller in virtual space. Providing the eyes with very unusual inputs is going to make it much harder to maintain the illusion.

Interesting... I wonder how this 'prism adaptation' (correct term?), would work if, instead of off a couple of degrees, each eye is straight ahead, instead of toward a focal point? That would approximate the 'Dali' example I mentioned. Or... if there was even a wider disparity so a view of, say, a cube, was rather cubist...like almost seeing the same face from two different perspectives?

@Mark The straight ahead situation you describe would be pretty hard to create, because the eyes themselves move. I suppose you could, with sufficiently responsive electronics, position the screen image such that the independent movements of the eyes are discarded. For the wider disparity, I am having a bit of trouble wrapping my head around that one but I suspect you would simply perceive things as being smaller and closer to you: disparity cues are one of the depth cues. There might be some confusion because other cues would be violated (like the expectations of particular object sizes).

@Mark For example consider the Wikipedia article on Binocular Disparity to think about what I said about disparity.

interesting. Thank you. Yeah, "having trouble wrapping [one's] head around" is exactly why I am curious. I wonder if, as a 'game' perhaps, one emulated a bovine perspective...if appropriate goals or feedback would increase immersion/minimize disorientation? Say, 'sensing'/detecting movement (of a predator), and responding or 'locating'? Or something similar that might function like holding a controller and having it on screen to orient oneself, something that pushes one to make 'functional' sense of the perspective...  Thanks!


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Relation between bases while changing into a SNP
Is there any relation or influence among the bases (A, C, G, T) while they are converted into a snp? Such as, is A converted into T, similar to converted into C or G? Or is this all random and no way to evaluate?

Interesting question. You can start here: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1790724/ and here: http://www.nature.com/nature/journal/v505/n7485/full/nature12861.html I may convert this into answer later, time allowing.


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Which plant's part is this?

I found this plant in Rajasthan, India.
This sample is 4-5 cm long.
This is an ornamental plant. It was a potted plant.
I put my fingertip in the photo to give an idea of size of the specimen.
I can't figure out which plant this part belongs to.
Please give the species name if you can.
I would be very thankful to anyone out there who will help me.

This is a bit hard to say exactly, since there is a number of possibilities. We can be pretty sure that these sample is from a Cypress, belonging to the family of Cupressaceae, but which subfamily or species this is exactly, can't be identified here. Therefore a wider image would be necessary, but since this is a potted plant, even this might not be enough, as a lot of these plants are used in gardening.

Can u explain how one can figure out that this sample belongs to a cypress?

@Anonymous Members of the Cupressaceae family are the predominant group with scale (or scale-like) leaves. See here & Schulz, Knopf, and Stützel (2005) for more info.

Those scale-like green structures are likely to be the foliages of Platyclaudus species, they are attached densely on the branches of the plant. Hence the whole thing in your picture shall be the branch with the leaf from some kind of gynosperm tree.
It's common in Gynospermum the foliage is highly abbreviated and deformed(comparing to Angiosperm).

Welcome to Biology.SE! It isn't clear that this adds anything to the existing answer. In addition, answers are much more likely to receive a favorable response if you include supporting references (primary literature is best). Without that support, your answer is indistinguishable from opinion. ——— Please take the [tour] and then consult the help pages for additional advice on [Answer] effectively on this site and then [edit] your answer accordingly. Thanks!


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Do unique communities of bacteria form inside water storage in plants?
I assume that plants, like animals, have an ability to fight off bacteria that invade their cells (support: here and here.
However, water often harbors quite a bit of bacteria in even unsuspecting locations (e.g., see here).
Moreover, plants store a lot of water in their vacuoles.
I was wondering, whether the water stored in plant cells tends to harbor bacteria...
If so, are the bacterial communities in such water-storage organelles unique to plant vacuoles or do bacteria get transferred with the water as it moves through the plant?

As stated in Plant Signal Behav. 2010 Dec; 5(12): 1568–1570:

Phytopathogenic bacteria do not enter plant host cells, but proliferate in the intracellular space.

But as they can reach the apoplast, pathogenic bacteria can take advantage of environmental humidity levels and manipulate water content inside plant leaves to reproduce and spread infection as shown in
Nature volume539, pages524–529
So yes, bacteria can infect water inside plants but usually not inside the plant cells themselves. As they infect the intracellular space, they can spread in the water and infect the whole plant. It is also to mention that we are not speaking about the same bacteria as in standing water or something else. Viruses on the other hand can infect the plant cells themselves.


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How do booklice avoid dessication?
I often find booklice (aka psocids) in old paper notes I have in semi-storage. These pages of paper are intentionally left in dry conditions on my desk to avoid damage. However, if the psocids live and feed totally within these pages, how are they getting any water? How do the booklice avoid drying out and dying?


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How can a child be blood type AB, if both of the parents are blood type A?
Basically, both of my parents are blood type A (both are confirmed and it's also certain both of them are my biological parents). I recently found out my blood type is AB. How is this possible? I tried reading about different mutations in blood type, but I couldn't find anything that was similar to my case.

Blood type A has a variety of subtypes, which have different features in terms of their antigens. This leads to people with different A subtypes having somewhat different kinds of antibodies in their blood (for a technical article, see here). I don't know the population prevalences well, but I read somewhere (can't find it now) that as many as 20% of blood type A people actually have one of the subtypes. And these are themselves going through their own mutations. It is possible that you have an A subtype of some kind.
Testing blood types usually consists of testing which antigens and antibodies are present in your blood (see e.g. here). So if you have some kind of A subtype that didn't fit well into the blood test's expectations, you might have shown up as AB. I'm not a hematologist or physician, so I'm not sure how plausible that is.
But if you are really interested, you might consider getting a DNA test that will identify which type/sub-type you have, as this will add a different source of information on top of the standard blood test. In the jargon, the standard blood test is for "phenotype" (what are your blood cells actually doing), whereas DNA tests are for "genotype" (what is your DNA sequence). Often genotype and phenotype have less to do with each other than you might expect, or they don't fit in all that well with the cut-and-dried tests. In particular, a lot of medically underserved populations have variation that isn't really accounted for by standard medical typology.
Hope that helps.

Of course this, while possible, overlooks the most obvious cause.  As Homer put it '“My mother,” answered Telemachus, "tells me I am son to Ulysses, but it is a wise child that knows his own father."'

@jamesqf : Well, we have to trust OP: "Basically, both of my parents are blood type A (both are confirmed and it's also certain both of them are my biological parents)". (my emphasis).


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If coelocanths are more related to humans than groupers -does a Coelocanth's DNA literally have more sequences in common with a human than a grouper?
Would a coelocanth and a human still have more sequences in common than a coelocanth and a grouper? Would the coelocanth and human dna basically "look" more similar than either would to a ray-finned fish based on sequences?

This question is unclear.  Are you asking about comparing the coelacanth-to-human distance to the coelacanth-to-grouper distance, or are you comparing the coelacanth-to-human distance to the grouper-to-human distance?

Yes, in virtually every way. In terms of pairwise distances, measured in percentages, humans and coelacanth are closer to one-another than coelacanth would be to any ray-finned fish. In terms of individual genes, there would be genes that humans and coelacanth share with their common ancestor, but are not found in any ray-finned fish. Remember, humans are bipedal terrestrial fish.

Thank you, it just seems so odd to me because groupers and coelocanths have such a similar morphology and lifestyle. Is this true of pretty much any more closely related taxa compared a less closely related outgroup? i.e. are the sequences always closer among more recently diverged groups compared to groups that diverged farther back?

@KarlKjer Good answer. Would be great to have the statistics for the # of pairwise differences between Coelacanth and a ray-finned fish species and between coelacanth and humans.


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Are there any known plesiomorphies of all living mammals relative to a newer trait state in all living reptiles?
If I understand how a "trait" is defined, a turtle's shell is a synapomorphy relative to mammals and the common ancestor of living amniotes. The same would go for a snake's limblessness, etc. But are there any synapomorphies all living reptiles have in common relative to an older trait state found in most or all modern mammals? Traits modern mammals share with the common ancestor of living amniotes which reptiles do not also possess?

What do you mean by reptiles? Do you mean "Reptilia" or do you mean " turtles, crocodilians, snakes, amphisbaenians, lizards, tuatara". See this post and that post.

"living reptiles" so what you listed plus birds.

So not reptilia, that would be Sauropsida or possibly diapsids, in which case the answer is no, since mammals fall outside the clade.

What your asking is really unclear, especially when you use terms like "relative" Are you asking for a plesiomorphy uniting mammals and early amniotes but excluding Sauropsids? You may want to read this so you can use the right terminology. https://upload.wikimedia.org/wikipedia/commons/thumb/b/bb/Reptilia-Sauropsida.jpg/800px-Reptilia-Sauropsida.jpg

Yes, that is my question. I don't see how my terminology is incorrect. Is "living reptiles" not a correct description of a subgroup of sauropsids? Do "living reptiles" not constitute a monophyletic clade in contrast to things like reptillomorphs that gave rise to mammals and modern reptiles? Is the term "reptile" just not used at all anymore despite common usage?   That was my question, traits that unite mammals with the reptillomorph common ancestor of living amniotes, in relation to a synapomorphic trait in living sauropsids.

No living reptiles do not constitute a monophyletic clade, neither does reptile by itself.

Early mammals and early reptiles are both anapsides but modern mammals are synapsids while modern reptiles are diapsids (or at least ancestorally diapsids in the case of turtles).

Modern reptiles aren't monophyletic if you include birds?

modern reptiles is monophyletic if you include birds, but it does not include the ancestors of mammals nor the common ancestor of amniotes.

The following article lists some distinctive skeletal differences in synapsids and sauropsids, and reptilia and non-reptilian amniotes:

Sauropsida is defined as "reptiles plus all other amniotes more closely related to them than they are to mammals" (Gauthier, 1994). The characters supporting Sauropsida include the following:

Presence of a single coronoid. Synapsids and the diadectomorph Limnoscelis have two coronoid elements. The coronoids are bones on the dorsomedial surface of the lower jaw.
Supinator process parallel to humeral shaft and separated from it by a groove. In synapsids and diadectomorphs, the supinator process is strongly angled relative to the shaft.
Presence of a single pedal centrale. Two centralia were present in the tarsus (ankle) of synapsids and diadectomorphs.

Reptilia is defined as "the most recent common ancestor of extant turtles and saurians, and all of its descendants" (Gauthier et al., 1988). Characters supporting Reptilia include:

Tabular small. The tabular (a bone on the posterolateral corner of the skull table) of early synapsids and diadectomorphs is large, but reptiles have only a small tabular, when it is present.
Suborbital foramen present (Fig. 1B-D). The suborbital foramen is a small hole near the lateral edge of the palate, between the pterygoid, palatine, and ectopterygoid (or jugal, when the ectopterygoid is absent). This structure was not found in early synapsids and diadectomorphs (Fig. 1A).
Supraoccipital anterior crista present. The supraoccipital of mesosaurs, synapsids, and diadectomoprhs lacks anterior parasagittal flanges. The supraoccipital of reptiles has a paired anterior parasagittal flange called an anterior crista.
Supraoccipital plate narrow. The supraoccipital is a bone in the back of the braincase. The supraoccipital plate of mesosaurs, synapsids, and diadectomorphs is broad and extends farther laterally than the postparietal.

Phylogeny and Classification of Amniotes, Michel Laurin and Jacques A. Gauthier


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Is Urea excretion a shared ancestral trait of amphibians and mammals relative to synapomorphic Uric Acid excretion in living reptiles?
Is the ancestral condition of prehistoric amphibians and early amniotes urea excretion? Would it follow then that the lineage leading to living reptiles went on to evolve uric acid excretion as a derived trait? Therefore urea excretion is a shared plesiomorphy of living amphibians and living mammals relative to a synapopmorphy of uric excretion in living reptiles?

There are reptiles that also use urea, and mammals that excrete uric acid.  it is likely that urea is the ancestral condition (compared to uric acid) as it occurs in adult amphibians and some fish. But ammonia is even more ancestral than that, occurring in young amphibians and most fish. It is likely uric acid developed alongside terrestrial eggs, as every egg laying amniote (including monotremes) uses uric acid at least during the embryonic stages. Uric acid is more metabolically costly so there is some incentive to switch to urea if you can, although there is a counter factor as urea requires significantly more water. so it comes down to which a group can afford more water or calories. It is notable that the few reptile to witch use urea only switch during their adult stage. It is possible to do both a few desert mammals produce uric acid and urea at the same time, producing more uric acid when water stressed.


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Does focusing on a certain part of the body increase electrical activity in that region?
I am batting around ideas for master's thesis topics and was wondering whether or not just focusing on an area of the body would cause of boost of  neuronic activity? Not sure whether this would fall under the rubric of a self-fulfilling prophecy of the mind, or some other secondary body function. I though it might be interesting to examine the relative differences between varying parts of the body and their respective degrees of responsiveness to intentional cortical activity, as directed by a person. If anyone has an answer please respond soon as I can't quite nail down how to search for a question like this online (finding specific phrases, etc.) Also, feel free top point me to any readings related to this (would-be) phenom.
Thanks!

Gut reaction, I don't think this is a solid thesis idea. If you attach an EMG to my finger, and then I concentrate on my finger, and then my finger moves (due to stray thoughts), there will of course be a whole bunch of action potentials firing. However, that's kind of trivial and not really that interesting.
If your theme is "weird EM effects in the human body", one possible decent idea (and one that's gotten some quantity of buzz in the recent past) would be to focus on the role of electric fields in wound healing. You could even add in an intentionality/focus angle, if you really wanted to.


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What is the best food to eat at this type of day since it is so vey very late?
Best food to eat? In this time of the day because it's late very soon to be

Welcome to Biology. It's 20:15 in my time zone, and in the West Coast in the US it's still morning. So be specific. Further, this question may be opinion based and even if it's not, it's better suited for Health. SE. Could you improve your question such that it is clear what you define as 'late' and consider the fact that the question should be answered in a scientific fashion without a medical advice component?

Following AliceD, it is currently 1:35pm where I live. Also, note that The dose makes the poison and therefore nothing is fundamentally healthy, everything is toxic, it just depends upon your needs (and therefore a lot on a standard diet). Also, "Best" is very subjective. What are you trying to achieve?

If this question relates to evolution then everything on this website really does.

@Remi.b - If by evolution, you mean the physiology all biological organisms evolved, their genetic and environmentally adapted behaviors, etc,. then yes, it probably all does.


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Would canines that consume the stomach of ruminant prey animals benefit from any of the bacteria and enzymes present in the rumen?
This question is inspired by the growth in popularity of raw diets for pet dogs. Green tripe is a common addition to these diets, with many claims of probiotic benefits.
Here's an example from a site that sells ground, frozen green tripe for pet dogs: http://greentripe.com/
Another article with some of the claimed benefits (I already know there is some misinformation in this article - it claims that dogs don't naturally produce the enzyme amylase, but that is false) http://ivcjournal.com/raw-green-tripe/
Do these claims make sense? I know most of the bacteria in the rumen would die after being exposed to oxygen, but would the rest of the bacteria, fungi, and enzymes present in the rumen be of any benefit to a canine when consumed?
What about after the tripe has been ground, frozen, etc?


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Is Fluoride really that good for tooth enamel?
Recently, I started to pay more attention to my teeth because of the high number of tooth decays, and I'm trying to understand different concepts and biological functions of the teeth and bone. By searching around, I have found that enamel is the strongest bio-material in our body and that it is the main player in tooth decay. So I started searching for methods to restore the enamel, and I can see that most of the dentists recommend using Fluoride-based toothpaste. At the same time, the literature tells us that Fluoride is quite toxic. So I looked for healthy options available for end-users, and the organic toothpaste that I found are all without Flouride.
Now my questions are:

Should I go for an organic Toothpaste without Flouride or a non-organic with Flouride for restoring the enamel?
Is Flouride really the only enamel restorer?
Can it be replaced with something else for the restoration?

I'm a mechanical engineer and I can understand technical language, therefore any type of technical explanation would be great (even with chemical reactions)

"At the same time, the literature tells us that Fluoride is quite toxic." Does it tell you the doses it's toxic at ? How much toothpaste are you planning on eating ?

Here is a reference where you might find some information. And here another one dealing with an in vitro comparison of the effect of organic and inorganic fluoride on enamel.

this paper answers your second and third question :http://www.jisppd.com/article.asp?issn=0970-4388;year=2012;volume=30;issue=1;spage=2;epage=6;aulast=Goswami

Getting fluoride in drinking water is more effective, since its concentration in water depends on the temperature , it may lead to overdose and may cause mottled teeth.

Thank you guys for the links! I will start reading it. Not sure how to interpret your last comment JM97. Edit: I'm not trying to kill myself :-) At least not yet.

This question appears to be framed in more of a "personal health question" vs asking strictly about the biology/biochemistry involved in the fluoride-enamel "strengthening"  process. As a result, I think this question will be voted to be closed as being off topic. However, even with additional edits, I'd say you'd find your answer through a quick google search.


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Cat's tail movement as an indicative of tension
It appears to me that tail's twitching in the cats indicates how much tension the individual is under. During a hunt, when a cat tries to stay invisible, while approaching a target it is almost immovable, yet the tip of the tail keeps on moving restlessly.
Is there an explanation for such a behavior? How does it help?

No idea of the biological explanation but as someone who 'knows' / grew up with cats yes, it seems exactly like that
Tail lashing is a sign of stress, mild beating is mild irritation and so on
Often a growl will be followed by beating the tail
Anyone can guess at the reasoning but I' say it's not unlike a person tapping or drumming their fingers or hands - depending on the strength it can mean different levels of annoyance and different 'messages' but I assume they're satisfying the same urge that makes people pace or drum their fingers while waiting / annoyed


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What would be a reason for a tree to have flowers of different colors?
The spring is here and the cherry trees along my street are blooming again!  Some trees have white flowers, some dark pink. But then... there're these trees which are all white yet just a few flowers are pink, just like that:

Is there a layman explanation for this phenomenon?

This is probably an example of Co-Dominance
As you may have learned according to mendelian inheritance
there exists dominant and recessive allels. However in reality there also exist phenomena like incomplete dominance and co-dominance where no specific allels are said to be dominant over the other.

There are a couple of possibilities for what's going on here:

The most likely explanation is Position Effect Variegation (PEV). Genes are, at the most basic level, organized linearly on chromosomes (very long strings of DNA). Some parts of chromosomes contain stretches of genes that are actively silenced, or turned off, by cells (large silenced regions like this are called heterochromatin). The boundaries of where this silencing starts and ends are sometimes fuzzy. If a gene necessary to produce pigment happens to be next to a silenced region, the silencing can randomly creep in and shut off that gene as well, or creep back to its normal boundary. (This is why it's called 'position' effect variegation: it depends on the physical position of a gene, in this case the pigment gene, on the chromosome, and how close it happens to be to a normally 'silenced' region.) This process is (probably) effectively random, so it won't happen in every cell, which means some cells will produce pigment whereas others won't. A famous example of this happens in fly eyes, as in the image on the left. Importantly, the difference here isn't 'genetic' (the actual content of the DNA), but 'epigenetic' - essentially, the way cells modify and read their own DNA.
Another possibility is an active jumping gene, or transposon: unlike most genes, transposons can move around in the DNA, and can sometimes carry with them a piece of DNA that tells nearby genes to be turned on or off (or are simply silenced by the cell, like in the PEV case above). If a transposon sits right near a pigment gene, it can cause that gene to be silenced. However, if the transposon up and jumps somewhere else at a random time (which active transposons do!), the gene nearby is no longer silenced, and can now cause pigment to be produced again. There's an example of this happening in snapdragons (see middle image). In this case, there is an actual genetic difference between the pink and white cells: one group has a jumping gene sitting next to the pigment gene, and the other doesn't.

Importantly, PEV silencing--like the transposon jumping--is inherited when cells divide, so if a stem cell that eventually makes a whole flower silences the pigment gene (or transposon jumps out), the whole flower will be white. If the silencing happens later in development, maybe when the early divisions forming the flower have happened, then a single petal, or just a sector of a petal, could be white, and the rest pink. Such sectoring is a telltale sign of PEV or transposon-related effects.
In your photo and description, the tree is mostly white, and individual sectors are pink, not vice versa. If the cause of the color switch is PEV, then the pigment gene's 'default' in this tree being silenced, with the silencing randomly moving away from the pigment gene in some cells. Or there could be a particularly active transposon that tends to bring gene silencing along with it at play here.


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Is there a glossary about which infrared (IR) colors which body parts reflect?
I am doing medical research and I'm trying to find parts of the body that look about the same to the human eye, but reflect different "colors" in IR, so that using a light source and a camera of that frequency helps to distinguish between them. Thus I was wondering if there is a glossary out there that lists all the colors (visible or invisible to the human eye) for all body parts (cells, bacteria, organs etc.) that get reflected.
I'd also be interested in literature on that topic, but it's sort of difficult to feed the right words into search engines without getting tons of unrelated results.

Are you referring to dead bodies? Because living human tissue emits a lot of IR radiation but in comparison hardly reflects any. There are actually not many natural materials that reflect IR well.

I refer mainly to living human bodies, but some test runs will include dead animal meat as well, and whether IR light is emitted or reflected is actually not that important to me, so I'm basically interested in both. But thanks for the info that not many natural materials reflect IR well.

Whether you want to detect reflected or emitted light should be incredibly important to you. Those are very different approaches that require different equipment. I think you should talk to someone from the department of physics.


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What is a sequencing artifact?
I'm rather new to bioinformatics, so this might be a rather basic question, but what are sequencing artifacts, in the context of variant calling?

Artifacts are variations introduced by non-biological processes. Sequencing involves a lot of chemical reactions, and changes in nucleotides that can seem like mutations are really introduced somewhere in the processing of the sample. That's what we call "sequencing artifacts". Proper experiment design, with careful replication, should help you clarify which changes in nucleotides are biologically significant.

Some specific artefacts are:
apparent insertions or deletions in the sequence, which are really just skipped base or duplicated base errors during the sequencing
apparent variants which do not exist in the sample but are introduced in the data because of miscalling at individual bases
differences in abundance of variants between the output and the sample due to biases in PCR amplification, or biases in the ability of the sequencer to sequence each variant, or due to stochasticity in abundance of molecules in the sample

I believe an artifact is something that appears in the first analysis but is not actually present in the sample. You would want to sort out all of the artifacts so that your final analysis is accurate.


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The detail about the exact time of heart attack
Storage of cholesterol in coronary artery tends to heart attack. But in which phase heart attack occurs? Why only a definite time is called heart attack? Why this is the extreme point of coronary block?

Acute myocardial infarction (MI) usually happens when a coronary artery is abruptly occluded, typically by a blood clot. The clot can be an embolus that forms elsewhere (such as in the heart itself) and then happens to flow into a coronary artery, or more often it occurs when an atherosclerotic plaque (containing cholesterol) ruptures. Because a ruptured plaque looks a lot like tissues outside the blood vessels, the clotting machinery in the blood responds like it would to stop bleeding from a wound.
MI can also occur in other situations where blood flow is reduced to a level insufficient to supply the cardiac muscle with oxygen, without complete blockage, either from vasospasm or when increased activity (such as exercise) demands more flow than can be delivered through a narrowed atherosclerotic coronary artery.


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Understanding the derivation of the Nernst equation
I am trying to understand how the Nernst equation can be derived and am mostly referring to the explanation given in the book Theoretical Neuroscience by Dayan and Abbott.
Given we have a concentration gradient and consider only Potassium, the overall approach to derive the Nernst equation is to find the equilibrium state where the flow of ions out of the cell and the flow of ions into the cell due to diffusion are the same. For the flow of ions we find the following two expressions:
$$
F_{out \rightarrow in} = \gamma [K^+]_{out} \\
F_{in \rightarrow out} = \gamma [K^+]_{in} \cdot exp({\frac{q V}{k_b T}})
$$
In these two formulas $\gamma$ is some complex factor that we don't know that e.g. encodes the number of channels but it does not matter since it will disappear when we equate both equations. $[K^+]_{out}$ is the concentration of potassium ions outside the cell and $[K^+]_{in}$ is the potassium concentration inside the cell. $V$ is the difference in electrical potential between the inside and the outside and $T$ is the temperature.
The reasoning given by Abbott and Dayan is that the flow of ions from inside the cell to the outside needs to overcome the energy barrier of the electrical gradient. Only ions that have sufficient thermal energy can do so, this is why the Boltzmann factor appears. The flow of ions from the outside to the inside does not need to overcome such a gradient. It is therefore proportional to the concentration of the outside.
The last part is where I struggle. Don't we need to account for the fact that positively charged ions are pulled into the cell due to the potential difference. Am I wrong in claiming that there is an electrical field that will increase the number of ions traveling into the cell?

This is not how I would approach thinking about the Nernst equation; check the derivation on Wikipedia I find it very straightforward: https://en.wikipedia.org/wiki/Nernst_equation

Unfortunately, I am not really familiar with electrochemistry and cannot follow the employed formalism on Wikipedia. Do you think the more physical approach presented in the question is not rigorous?

I think it's probably perfectly rigorous (though I suspect there is a hidden simplification in there), just not a direction I've approached it from before and I don't have Dayan and Abbott in front of me, though I trust them and typically recommend their book as a starting point for those interested in theoretical neuroscience. See also http://www.columbia.edu/cu/biology/courses/w3004/Nernstequationderiv.pdf or https://onlinelibrary.wiley.com/doi/pdf/10.1002/9781118687864.app1


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How thick is the neural tube at Stage 10 in a chick embryo?
As the question states - I am really struggling to find ANY website/paper/article which states this. I want to know if the neural tube is still one cell thick and stage 10 of development. Any evidence that can be supplied to show this would be useful.
Thanks


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What do I need to do to make a Reverse colorblind image?
As a 15 year suffering from moderate Protan colorblindness, I've wanted to find any advantages of colorblindness. I discovered there are Reverse colorblind tests, which only colorblind people are able to see the objects. This has fascinated me, and I want to make one of my own. How can I do this? Since I cannot tell the difference between the colors only visible to colorblind people an their normal vision counterparts, how could I do this without buying a pair of Enchroma colorblind glasses so that I may see it with both visions?


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What are some potential consequences for attempting to cure Type one Diabetes?
Type one diabetes has been in my family for a few generations. As a carrier and having a mother with the disorder, I've done a lot of research on it. As I am completing my High school Biology course, I've gotte a better understanding of how the disorder may be treated. (Stem cell therapy, gene replacement, etc). Here's a hypothetical scenario: Scientists develop a modified virus that contains a normal person's beta cell genetic makeup, injects it into the pancreas, and reproduces. The virus and beta cells reproduce, and the body detects the virus, but not the beta cells. (or neither, and the virus is not harmful). The beta cells create insulin, and the Diabetes is cured. Would this work, and would this hurt the immune system? Would it be possible for the scientists to blunder and either create too potent a virus or too much of the virus?

A virus is much smaller than a cell. It cannot carry a cell into the pancreas. Just infecting the pancreas with a virus carrying a gene or two (DNA) for islet cells wouldn't do anything worthwhile, and might damage the pancreas. That's why stem cells (whole cells) hold potential.

High school biology apparently failed to teach you that many conditions, like type I diabetes are not classically Mendelian. The term "carrier" does not apply to you...you are just someone with a predilection who hasn't developed the condition (but who might...I have heard of someone developing type I diabetes in college)

Scientists develop a modified virus that contains a normal person's
  beta cell genetic makeup,

How much DNA do you think you can cram into a virus?  Not having the right beta cell DNA is almost certainly not the cause of type I diabetes, anyway.

The virus and beta cells reproduce, and the body detects the virus,
  but not the beta cells.

How do you think the immune system responds when it detects a virus?  Hint, it kills the hosting cell.
A virus that induced a small percentage of pancreatic alpha cells to undifferentiate and redifferentiate beta cells might work...but you would still have the same immune system that went agro on your beta cells the first time.  They might do the same when exposed to new beta cells.  And there is a fine line between undiffernetiated cells and cancerous cells.

This might strike some as ironic, but -1 for the hostility. If you think a question is stupid, bypass it, or DV/VTC it, or comment, but an answer like this one ("High school biology apparently failed to teach you ...", "How much DNA do you think...", "How do you think the immune system responds...", "Hint..." is pretty rude. I sure hope you don't teach students anywhere.

When someone says "Well, I've done lots of research and I don't understand why scientists who are supposed to be experts haven't tried this obvious thing that my research told me should work".  That's a little hostile to the intelligence and integrity of people who do work on researching diabetes for a living.

That's nonsense. With that attitude, as a scientist and a physician, I would be continually insulted by people who don't have my experience. People have ideas and opinions that are ill informed. We are all confident idiots. You can go through life offended or just accept it as a reality.


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Genetic Inheritance
With suppression in mind consider the following in a system that requires two genes (and their products) to produce a function or phenotype:
The products of the two genes are both necessary and sufficient to produce the phenotype (fluorescent flowers). Call the genes A and B and the mutant forms a and b. What would be the ratio of phenotypes of the progeny if a heterozygous plant AaBb were allowed to self pollinate? The genes are not linked.
Now you take a plant that is aaBb and you mutate it, then allow it to self pollinate and find that one of the progeny has the fluorescent flowers. When you allow this progeny plant to self pollinate you get a ratio of 3 progeny with fluorescent flowers and 1 without. That is not the expected ratio for a reversion of the "a" gene.
When you cross this plant with the original AaBb plant you get a ratio of 3:1 also.
Propose an explanation.

Explanation? You are trying to cheat on your homework. Do it yourself!


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What is the conversion between r and FST?
From Schonman (2013):

...allele A can only invade under Hamilton’s condition  R=$F_{ST}$ > C/B.

From Harpending (2002):

The best general definition of the coefficient of relation $R_{XY}$ between individuals X and Y is (Bulmer, 1994) $R_{XY}$ = $F_{XY}$/$F_{XX}$, where $F_{XY}$ is the kinship between X and Y and $F_{XX}$ is the kinship of X with himself [..]
[..] $F_{ST}$ is just the coefficient of kinship between members of the same deme [..]
[..] $F_{Self} = \frac{(1 + F_{ST})}{2}$  [..]

This means, unless I am mistaken, that if I take Harpending's equation and substitute $F_{ST}$ for $F_{XY}$ and substitute 1/2(1+$F_{ST}$) for $F_{XX}$, I can calculate within-deme relatedness: 2*$F_{ST}$/(1+$F_{ST}$).
Yet Schonman says R=$F_{ST}$?
What am I doing wrong here?

The low attention your post received is likely related to its format. I've improved the format for the quotation and  the references. You probably want to improve the format for the equations. For example, "Fst" should be "$F_{ST}$" (by typing $F_{ST}$). Here is a tutorial for formatting math equations.

@Remi.b Is this question too difficult or too trivial?  Do you know the answer?

It is not an easy question. My first thoughts were that $F_{ST}$ depends upon the genetic diversity while $r$ (or $R$ as it is apparently called here) is not. So equating the two sounds hard. You first quote comes from the social evolution literature and Nash's work into the discussion just makes things unnecessarily complicated.

Sentences like FST is just the coefficient of kinship between members of the same deme sounds wrong to me because $F_{ST}$ depends upon the genetic diversity in the total population but it might be hard to give an opinion on an out-of-context quotation (I have not read the paper). Also, I am not used to work with he coefficient of relatedness (or of kinship; to me these two concepts are the same but I might be mistaken) and might gets a bit lost here.

@Remi.b What do you mean by Nash's work?  You're not used to using coefficient of relatedness (r)?  Isn't that measure very commonly used?  Could you read the paper?  It is rather short and I think you would be able to understand it because you are familiar with math formulations in evolutionary biology.

I was referring to John Nash who's work underlies Hamilton's work. I just meant social evolution stuff.

I could maybe work out from Bulmer's definition that $R_{XY} = F_{XY}/F_{XX}$. However, this definition does not specify whether Y is drawn from the population or not. $F_{ST}$ only makes sense in structured populations. I suppose Y would mean an individual drawn at random from the total population, what do you think?

I am not sure I understand the concept of kinship of X with himself too.  How can this value differ from 1? (I might be too used to think in terms of probability of identity by descent to think this problem correctly)

According to the paper, kinship with himself is 0.5 in a sexual population.

I am very unsure but here are my thoughts...
We can work out from
$$R_{XY} = F_{XY}/F_{XX}$$
I do not really understand the concept of coefficient of kinship and the concept of coefficient of kinship with oneself but you say

According to the paper, kinship with himself is 0.5 in a sexual population

So, let's assume
$$R_{XY} = 2F_{XY}$$
Let's assume that the individual Y is drawn from anywhere in the total population. Again, I don't really understand the concept of coefficient of kinship but let's assume that $F_{XY}$ is the same as the probability of identity by descent between these two individuals, then in Nei (1973) terms, $F_{XY} = J_T = 1 - H_T$. Hence, $R_{XY} = 2\left(1 - H_T\right)$ or $H_T = 1-\frac{R_{XY}}{2}$
Given that
$$F_{ST} = 1 - \frac{H_S}{H_T}$$
it results that
$$H_T = \frac{H_S}{1-F_{ST}}$$
and therefore,
$$1-\frac{R_{XY}}{2} = \frac{H_S}{1-F_{ST}}$$
solving into
$$R_{XY} = \frac{ 1 - \frac{H_S}{1-F_{ST}}  }{2} = \frac{1-F_{ST} - H_T}{2(1-F_{ST})}$$
I would recommend you making some more reading on the coefficient of kinship to ensure that my interpretation here is correct.

Oh Remi, I apologize.  The thing is, in the paper, Harpending says that kinship with oneself is 0.5.  But later on in the paper, Harpending gives a different equation for kinship with oneself in a subdivided population.  That is the one I thought should be used, since $F_{ST}$ implies a subdivided population, right?  So, that is the one I used in phrasing my question above.

Ok.... see new answer then! I am not sure it is of any help though.

I am not very at ease with the concepts of coefficient of kinship but
if $F_{self} = F_{XX}$, then
$$R_{XY} = 2F_{XY}(1 + F_{ST})$$
Assuming that Y is a random individual from the total population and if $F_{XY}$ is the probability of identity by descent of haplotypes X and Y (which I am unsure because I don't really ), then $F_{XY} = H_T$ and hence
$$R_{XY} = 2H_T(1 + F_{ST})$$
But really I am very unsure about all that. Note also that the small calculation is based upon the equation $F_{Self}$ = 1/2(1 + $F_{ST}$, which I don't really understand! I would recommend you making some more reading on the coefficient of kinship to ensure that my interpretation here is correct.

$R_{XY}$=2$F_{XY}$/(1+$F_{ST}$), correct?

Is the original expression $F_{Self} = \frac{1}{2(1 + $F_{ST})}$ or $F_{Self} = \frac{1 + F_{ST}}{2}$? It is unclear from the format you are currently using in the question. I might have assumed the wrong one.

The original is the latter.

I tried to modify the format but I don’t think it worked.  I’m on my phone and won’t have a computer for the rest of the day.

The format is corrected now.


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Thermoregulatory characteristics
I have a question that probably is to obvious, or just bad wording..
The terms endorthermy, ectothermy, and heterothermy, are used to describe:
A) cold and warm individuals
B) the three layers of the skin
C) different types of body cavities
D) the source of an animals heat
E) none of the above
I think it's E) or D). My thinking process is B and C completely irrelevant.  A) i think it is very ambiguous as an answer as those three terms refer to a type of classification rather than the characteristic itself (like if their skin is cold or warm). On the other hand D) the source of an animals heat, doesn't seem very right to me. The 3 terms refer to the source of the heat that predominatly determines the body temperature, meaning that it is not THE SOURCE, but the way they exchange and regulate their temperature... That means that probably it is E?!
Thanks

Related: https://biology.stackexchange.com/questions/61444/are-homeothermic-and-endothermic-synonymous

"The 3 terms refer to the source of the heat that predominatly determines the body temperature, meaning that it is not THE SOURCE, but the way they exchange and regulate their temperature". What do you mean by this? We use heat to change our core body temperature so why does this seem wrong?

@ANNAMARIA I am not sure I understand what kind of semantic issue you are pointing to for answer D. But, in short, I don't think it is such a trick question. The answer is D.


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What is the most durable electronic pipette?
We have a routine task of pipetting substance concentration series in triplicate on cell cultures under a laminar hood. To speed up the process, we use an electronic pipette in the repetitive pipetting mode and an electronic dispenser. The pipettes are several times a day wiped with 70% ethanol for decontamination, as they are moved to and from the hood. Up to date, we used the Eppendorf ones, but they fail after roughly a year of use. The failing parts are usually piston position sensor and pipette tip sensor on electronis dispenser.
Does anybody have an experience with the durability of different brands of electronic pipettes (Socorex Acura electro, Gilson Pipetman M, MT E4, maybe, others), especially under a laminar hood in repetitive pipetting mode?
Thank you in advance!

What type of alcohol do you use? We used to wash plastic cuvettes with cheapest version of denatured alcohol. It had negative effect on properties of the plastic. Then one of our colleagues researched it and found that not the alcohol itself but the denaturing compound was the main culprit for deteriorating the plastic. Since then we switched to ethanol denatured with methanol.

We use 96% ethanol diluted to 70% with distilled water. I am not sure if the source ethanol contains any denaturating agent, but I will find out - thanks for the point @BagiM


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Why do same type of fruits come in different sizes?
Why don't fruits come in exact same size even they're the same type of fruit?
This sounds like an obvious question,
but why are some apples bigger than others?
and why are some bananas larger than other bananas? or some trees grow taller than others?
What affects them to grow in different sizes, although they are from the same type of trees?
Is it because the fruits grew in different conditions?
Are there any articles or research about this?

Phenotypic variance
This variance in the appearance of living things is called phenotypic variance. There are a number of reasons for the existence of such phenotypic variance. In other words there are a number of underlying variances that can explain phenotypic variances.
Primary source of phenotypic variance
The two most obvious source of phenotypic variance are

genetic variance
environmental variance

Genetic variance is caused by individuals having different genetic predisposition in the population. Environmental variance is caused by the fact that different individuals experience different environments (both macro and micro - environmental differences).
Monozygotic twins look alike because, among them, they have no genetic variance. Even if raised in the same home, they still experience slightly different environments. If raised separately (which sometimes happen) then twins will differ a little more as they experience very different environments.
Other source of phenotypic variance
The other sources of phenotypic variances include
- epistatic variance
- developmental noise variance
- all covariances between all of these causal factors.

Are there any articles or research about this?

Well yes! Your question is underlying an entire field of knowledge which is called quantitative genetics.
More information
For more information, I recommend having a look at the post Why is a heritability coefficient not an index of how “genetic” something is?


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BLAST protein sequences from 2 different bacterial species
I am interested in finding a consensus sequence of a protein found in e.coli, in Pseudomonas aeruginosa. I am using pseudomonas.com to BLAST p the amino acid sequence of the protein that i have found with help of PDB. However i have seen that people do the BLAST N first and then BLAST P if they are interested to check whether they can find similarity of the protein sequence. Also in PDB the aa sequences are strange since they are not that specific.
Any advise on this issue or reliable links to databases when i can search and align sequences for similarities?
thanks


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How often do retrotransposons jump in human cells?
If I followed the life of a typical cell in my body, how many retrotransposon jumps would I observe per day? I'm only interested in a rough order-of-magnitude estimate: should I think of it as a common event that happens basically all the time in most of my cells, or is it a rare event that happens only occasionally in my body?

For just rough order-of-magnitude, try this reference. Their experimental design seems to maximize transpositions so it should be a reasonable upper bound.
There is a lot of variability, but some retrotransposons jumped in ~1000 cells per million, others only a few per million such that they were difficult to detect, after about 1 month in HeLa cells.
The same reference gives an estimate of 10,000 retrotransposon elements in a mammalian genome, though, again, their transposition frequencies vary considerably.

You should also point out that the HeLa genome is incredibly unstable, which could definitely account for some (a lot?) of the activity seen. I haven't had a chance to read the whole paper in detail, but it very well could be that some of the genetic defects in HeLas related to "protecting" the genome and mutational repair are at play here.

@MattDMo Oh absolutely - I didn't go into specifics but I did mention that their design seems to maximize the transpositions.

true, I did see that. I just didn't want the OP to think that the numbers were in any way applicable to normal cells. Good answer, though, the paper was interesting.


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Can plants be grown using lights in the home?
Plants need sunlight to grow, mainly the blue and red wavelength of the sunlight . The lights used in homes are also white light, it will also have red and blue wavelength of light.
So , can they be grown in such lights perfectly?

Yes, though you may need special full-spectrum lights.  Ask any operator of a marijuana grow house :-)

@Jim Young: People still use incandescents?

It depends on what kind of light you are using. I recently did an experiment on this for my school's science fair and I found that you can use LED lights to grow plants. Nowadays you can actually buy LED lights called "Grow Lights" to grow your plant and the only difference is that Now the current LED lights that are used include four LED lights into groups where each light can produce the correct wavelength that will allow for increased production of growth. For beneficial growth of the cannabis plant for example  you want to use your LED lights directed at 439nm, 469nm, 642nm and 667nm. Link http://easy420grow.com/what-is-the-difference-between-hid-grow-lights-and-led-grow-lamps

Typically, regular incandescent bulbs like the ones you'd use in your house omit orange and yellow light. These wavelengths of light are used in photosynthesis but foliage growth relies more on blue wavelengths of light. Therefore regular lights aren't ideal for the growth of plants. Incandescent bulbs also generate a fair amount of heat which can damage plants when the bulbs are placed too close. Usually supplemental lighting is needed to grow plants with artificial life (eg. fluorescent, grow lights etc).
However, if there is a window in the room, plants generally do well even with just diffused light.


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How does further hybridization affect fertility?
Numeruous scientific sites state that hybrids (like mules) are infertile. On the other hand, ligers are known to mate with both tigers and lions and still have viable offspring.
So my question is: if the hybrid is fertile in the first generation, does further mating with either of the parents' species somehow affect its offsping's fertility?
For example: if liger mates with tiger let the odds to produce viable offsping be 50%. If this offsping further mates with tiger, are odds the same or are they lower / higher?

Some first generation hybrids[f1] are viable and fertile, but when they mate with each other or back to either parental species[P}, the successive generations[f2] are sterile or feeble.  this concept is known as hybrid breakdown.  This is often seen in hybridized forms of domestic crops.  I am aware that some female tiger/lion hybrids are fertile, but I'm unaware of successful breeding of the f2 generations.  It could be a case of hybrid breakdown.
Article about hybrid breakdown in rice
Hybrid breakdown in Cichlid Fish


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How is a specific fragment isolated for PCR amplification?
For background I am interested in studying engineering applications of a specific protein, which is not commercially available. My end goal is to express the gene for the protein in bacterial cells, most likely E. Coli, if that is a feasible procedure. I am mostly familiar the process of forming recombinant DNA, and though our lab does not specialize in Biology, we will be working with another lab in our Biomedical department which can provide necessary equipment and some advise.
The last time I did a lab where we expressed a new gene in E. Coli cells was a biotechnology class in high school, though much of the set up was done for us. I recall that our first step was amplifying the desired DNA fragment through PCR, but what I don't know is how the fragment was initially isolated. I know the primers help by essentially setting the start and end positions for the DNA cloning, but if you were to use an entire chromosome that contains the desired gene, it would seem likely that there would be many possible sites that the primers could attach besides the desired region. So if the DNA sequence for the protein I want is already known, how would I get a fragment that contains the gene I want?
Additionally, how difficult will this process be? Since the end goal is actually to study the protein, I do not want this step to turn into a full thesis on its own. For some specific proteins, the process seems well documented and can be done using relatively common materials and by following simple instructions, but how much should I expect the procedure to diverge for attempting this with gene that has not been specifically done before?

There are a number of primer testing tools that will compare primer sequences against the genome to ensure specificity, or help you design specific primers to amplify a specific region. One place to start is NCBI Primer BLAST; the linked page explains how to use it to generate primers to amplify a specific gene.
Doing PCR on genomic DNA can be a bit tricky, though, since you have to deal with a lot of confounding factors like DNA accessibility, contamination, and PCR inhibitors that get through your purification procedure. In addition, genes often contain huge introns, so you're going to end up doing PCR on an extremely long template (which is very hard or even impossible, depending on the size of the gene) and you'll end up with the whole gene sequence with introns which is not what you need in order to express it as a transgene.
Instead, I'd recommend purchasing a cDNA clone of your gene of interest and amplifying it from that. cDNA is made from the spliced mRNA sequence, so it will be a much more managable length and will prevent problems with alternate splicing.
If you go to the NCBI page for a gene, on the right sidebar under "Related Information" you'll see a link to Order cDNA clone. This will give you a few options to purchase a purified plasmid containing that gene for around \$60 - \$90. It will be much easier to work with this plasmid than genomic DNA and it will definitely save you time and money, especially if you're still inexperienced at molecular cloning.

Of course, it's not 2003 anymore and there's a good argument to be made that the whole idea of doing molecular cloning yourself is a waste of time and money. If your budget allows it, the easiest and fastest way is to pay a company to synthesize your gene for you. Genewiz, for example, offers snythesis for $0.28/bp, but you can probably get a better deal if you shop around.
The advantage of synthesis is that you can get the exact sequence you want cloned into exactly the right vector done perfectly the first time. If you don't have experience with it, trying to clone a gene yourself will take longer and cost more money than you think. It's better to just get it synthesized so you can move onto your real experiment.

I was going to suggest getting a synthetic gene, but now I’ll just second your answer. Some (most?) companies will even correct for codon bias, etc if you so desire.

@canadianer That's a good point. Since the asker mentions "engineering applications", they're probably going to care about getting good levels of expression.

but if you were to use an entire chromosome that contains the desired
  gene, it would seem likely that there would be many possible sites
  that the primers could attach besides the desired region.

No.  The point of the primers is that they should be long enough to bind to one specific locus (or at least, there is only one place where the two primers bind close enough to each other and in the right orientation for PCR to happen)


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When muscles contract is the process similar to how non-newtonian fluids react?
I'm trying to understand how muscles contraction/tension works but getting loss in on the cellular level. From my understanding, when muscle tissue need to contract, the cells are flooded with calcium? Does that mean they get filled up with calcium? If so, are the cells hollow or does the calcium replace the fluid that was originally there? Or does the calcium cause the reaction in the cell for it to firm up?
I'm asking because there's an alien character who's quite thin but is also very strong and I was wondering about the science of that. I know them being alien means that their biology wouldn't necessarily follow earth rules but they could also share similar traits.

Calcium ($\ce{Ca^{2+}}$) is a signalling molecule and it acts like a chemical switch that tells other chemicals in the cell to enact the contraction. It's not accurate to think of the cell "filling up" with $\ce{Ca^{2+}}$ since $\ce{Ca^{2+}}$ wouldn't significantly change the volume of the cell alone *. Also, during contraction, the muscle cells contract in on themselves - they don't swell out.
It's also not accurate to think of the cells as hollow. Other chemicals inside the cell (such as actin and myosin) act like machinery that enact the contraction. Instead of thinking of the cell filling up like a balloon, I think it would be better to think of it containing a chemical winch (as in the figure below) whose pulling force causes the contraction. Similarly, instead of thinking of $\ce{Ca^{2+}}$ as a fluid, think of it as a bunch of particles that cause a chemical reaction to turn on this winch when they're allowed into the cell.

Reference: https://www.ncbi.nlm.nih.gov/books/NBK21670/
* During a $\ce{Ca^{2+}}$ spike, intracellular $\ce{Ca^{2+}}$ rises around 10-100x from 100 nM. Assuming $\ce{Ca^{2+}}$ has a 100 pm ionic radius, the volume of the cell ($x$) is only increased by around $10^{-9}x$ to $10^{-8}x$, which is negligible.


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Why don't primates have galactose-alpha-1,3-galactose (alpha-gal), but other mammals do?
I read in wikipedia that:

Galactose-alpha-1,3-galactose, commonly known as alpha gal, is a carbohydrate found in most mammalian cell membranes. It is not found in primates, including humans.

My question is : Why not?
In the sources for the wikipedia article about alpha gal allergy, I spotted the (pay-walled) article Evolution and pathophysiology of the human natural anti-α-galactosyl IgG (anti-Gal) antibody which has this to say in the abstract :

It is estimated that anti-Gal appeared in ancestral Old World primates less than 28 million years ago, possibly as a result of an evolutionary event which exerted a selective pressure for the suppression of α-galactosyl epitopes expression by inactivation of the gene for the enzyme α1,3 galactosyltransferase.

However this is more than a bit over my head, biology-wise.

That is because of the presence of IgE antibody. IgE response to alpha-gal causes anaphylaxis in humans. If you would like a more biological detailed mechanisms check out this article: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4600073

@m4rio Are you saying that having the IgE antibody causes us to not have alpha-gal ? If that's the case, that's just passing the buck : why do we have the IgE antibody in the first place ?

The general idea is that infectious agents use certain cell-surface proteins to enter the cell, and presumably recognize them by their particular glycoproteins. There are examples (cited in the extract below) of changes in e.g. blood group antigens in populations that are thought to convey (at least temporarily) an advantage against particular pathogens.
In this context, let me cite the rest of the section of the article that you didn’t have access to:

However, after the geographic separation of Africa and South America,
  Old World primates appear to have been subjected to a selective
  pressure for the suppression of autologous α-galactosyl epitope
  synthesis and for the subsequent production of anti-Gal. Possibly, an
  infectious agent endemic to the Old World, which was detrimental to
  primates, and which expressed α-galactosyl, or α-galactosyl like
  epitopes, exerted a selective pressure for the evolution of Old World
  primates able to suppress autologous α-galactosyl epitope expression.
  Thus, immune tolerance toward this epitope was lost and anti-Gal
  antibodies could be produced in these primates as a protective
  response to such putative pathogens.
An alternative scenario for the
  evolutionary suppression of α-galactosyl epitope expression could
  have been one in which ancestral Old World primates suppressed
  expression of these epitopes on their cell surface glycoconjugates as
  a result of exposure to a pathogen which exerted its detrimental
  effect via α-galactosyl epitopes functioning as receptors. A current
  example for such a pathogen is Clostridium difficile. Enterotoxin A
  produced by this pathogen was found to bind to the cells it damages
  through interaction with α-galactosyl epitopes on cell surface
  glycoconjugates [12, 56]. A bacterial toxin with a similar ligand
  specificity and which was detrimental to ancestral Old World primates
  could exert a selective pressure for the evolution of primates which
  suppressed the expression of α-galactosyl epitopes and, thus, lost
  the immune tolerance toward this carbohydrate structure.
[12] Clark GF, Krivan HC, Wilkins TD, Smith DF (1986) Toxin A from Clostridium difficile binds to rabbit erythrocyte glycolipids with terminal  Galα-3Galβ1-4GlcNAc sequences. Arch Biochem Biophys 257:217
  [56] Krivan HC, Clark GF, Smith DF, Wilkins DT (1986) Cell surface binding site for Clostridium difficile enterotoxin: evidence of a glycoconjugate containing the sequence Galα→3Galβ1→4GlcNAc. Infect Immun 53:573

Whatever the reason, the consequence of this was:

This also resulted in the loss of immune tolerance to the α-galactosyl epitope and the production of anti-Gal.

I presume this explains the IgE problem referred to in a comment, and I would consider this as an unfortunate side-effect of the change, and not a reason for it.


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Osmotic Pressure Clarification
My textbook states that the higher concentration of solutes, the greater the osmotic pressure will be and the greater the pull of water in will be. However, osmotic pressure is defined "as the pressure that would have to be applied to a pure solvent to prevent it from passing into a given solution by osmosis." Therefore wouldn't a high osmotic pressure PREVENT water from passing, not pull water in? Can someone please clarify this for me so it makes sense? Thank you!

I think you've got the solutions the wrong way round and that you should be applying the pressure on the non-pure solution, not the pure solution. Pure water is drawn in through the membrane so you have to put pressure on the non-pure solution to keep it out. Which textbook are you using? See the following quote from Voet et al. 5th ed. p. 30 and figure from Lehninger. Principles of Biochemistry p. 57.

The osmotic pressure of a solution is the pressure that must be applied to
  the solution to equalize the flow of water across the membrane in both directions
  (the added pressure forces more water from the solution through the membrane);
  it is proportional to the concentration of the solute.


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How do scientists transfer the specific DNA in Optogenetics?
I'm a bit new to genetic modification and I was wondering in Optogenetics (a field in neuroscience) how the scientists transfered the desired DNA strand from the light-sensitive ion channel opening cell (I forgot the name) to the specific neuron that will grow these cells sensitive to green light and trigger an action potential in the neuron? (open the neuron ion channels)
I don't understand how scientists know exactly which strand of DNA to cut from the source and where to put it in the target. I mean, if scientists can do this, why not cut the legs growing part of my DNA and insert in a butterfly and boom, you have a butterfly with legs, no?

I think your question can be broken down into a few parts:
1. How do scientists know which DNA sequence encodes a specific protein?
It seems that you've asked this question here, which I'll answer separately. So please go read my answer there first :)
2. How do scientists transfer genes between organisms?
@CKM did a great job of explaining how lentiviral transduction works. It is a very common method for introducing genes into organisms. A few steps before that: if you know the sequence of a gene and want to cut it out, you can use restriction enzymes which recognize specific sites in the DNA and only cut there. You can then purify and amplify that DNA sequence by polymerase chain reaction (PCR).
To address one of the subpoints of your question, it is true that a lentivirus will integrate the gene of interest at a random location within the genome. It could be in a non-coding region. It could be in another gene. You would have to do some sequencing to find out.
3. How did scientists do this to invent optogenetics?
In the case of channelrhodopsin, scientists noticed that microalgae were able to detect and swim towards light. They used EST sequencing to find the responsible genes. Once the a photoreceptor gene could be isolated, scientists constructed lentiviruses containing this gene (plus a fluorescent protein gene) and infected neurons with them. The rest is history.
One final tidbit: though you can't exactly give a butterfly the genes for human legs, you can make it grow butterfly legs in weird places, thanks to a family of transcription factors called the Hox genes. People learned about Hox genes in flies by mutating the different genes and observing the wacky stuff that ensued, such as legs growing where antennae should grow. Google Antennapedia to see what I mean.

Well for one, just having a gene doesn't mean you can make it work as intended, and indiscriminately tweaking the genetic material can produce unwanted effects. For example, if I overexpress p53, a common tumor suppressor gene, the cell undergoes apoptosis (1). If I break/delete the same gene, the cell might undergo apoptosis or it might become cancerous. Human development is of course regulated by hundreds of genes at a time, however, so legs on a butterfly is far more complex than just a single gene.
A common approach for inserting genes into a host genome is the lentiviral transfection. Generating a lentiviral vector is detailed here. A similar strategy for transfection using HEK293 for viral production is described in the following paper. I have no knowledge of optogenetics but I tried my best to find a paper in the field that employs the method in practice. In case you have no access to the article,
Viral Production

HEK293T cells (ATCC, UK) were cultured in Iscove’s modified Dulbecco’s medium (Sigma-Aldrich, Germany) supplemented with 10% (v/v) FCS (Sigma-Aldrich) and penicillin–streptomycin–glutamine (Sigma-Aldrich) in 5 × 150 mm dishes. After 80% confluency was reached, cell were transfected in serum-free medium with the helper plasmids pRV1, pH21 and pDFΔ6 and pAAV1/2-hSyn-BLINK-IRES-eGFP or pAAV1/2-hSyn-IRES-eGFP at a molar ratio of 1:1 with CaCl2. On the next day, the medium was replaced with serum-containing medium, and 48 h after transfection cells were harvested, pelleted and resuspended in lysis solution (150 mM NaCl, 20 mM Tris, pH 8).....

Culture & Transfection

Hippocampal neuronal primary cultures were prepared from embryonic day 18–19 (E18– E19) rat hippocampi as previously described43. All the experiments were approved by the Institutional Animal Care and Use Committee of University of Milan and by the Italian Ministry of Health (#326/2015). Neurons were transfected at 7 days in vitro (DIV7) via the calcium-phosphate precipitation method with 4 μg of plasmid DNA for GFP for the experiments assessing the axonal and dendritic distribution of BLINK2 reported in Fig. 2c. Neurons were infected with AAV1/2-hSyn-BLINK2-IRES-eGFP at DIV10 and fixed at DIV12 for the immunocytochemistry assays.

There's more to the method, but in short they transfect the 293 cells with these plasmids that create a functioning virus enclosing their plasmid of interest, and then they harvest the virus and use that to further transfect their neural cells with the gene(s) of interest.

Thank you! This kinda answers my questions, but I'm just 16, I need a simpler approach to the topics :\ I did learn a lot from your answer tho.


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How do scientists know what part of DNA does what?
There are many genetically engineered foods and animals and I was wondering, how do scientists know which part of a DNA to cut in order to produce the desired result. For example I want to make a tomato more durable and to do that I cut the durability part of the DNA of something long lasting and put in the tomato. I'm not sure, but I guess that's not how things work. If I wanted to make a human with tiger arms, I'll just cut the arms DNA part of the tiger and put it in the human DNA, no? I'm sure it's much much more complicated than that.
P.S - I'm just 16 and interested in biology, I do not posses any university/professional academic knowledge.

This is a tough question (scientifically)! Generally speaking, it's impossible to look at a DNA sequence and predict what function it might have. It's easier to go backwards: identify a function/trait of interest, figure out what proteins are necessary for that function, and then deduce the sequence.
I'll describe one strategy to go from protein to gene, and name some techniques which you can read up on if you want to learn more.
To find the amino acid sequence of a protein, you can chop it up using proteolytic enzymes. This gives you fragments of varying lengths, since the enzymes will cut semi-randomly at different sites in the protein. Run these fragments on chromatographic paper. You can deduce the amino acid sequence from the pattern, because larger fragments will move slower. This is the same idea behind Sanger sequencing (aka chain termination sequencing) of DNA, and was invented by the same guy.
If you know what the amino acid sequence is, you now know the mRNA sequence, since protein is translated from mRNA. However, in eukaryotes, you don't know the DNA sequence, since we have introns - i.e. bits of the sequence which get cut out between transcription and translation. We need a way to get from mRNA (protein precursor) to DNA (gene).
To do this, purify mRNA from a cell and generate a library of complementary DNA (cDNA) using reverse transcriptase. Then, sequence the cDNA library to generate expressed sequence tags (ESTs), which are subsets of the full cDNA sequence. Because the ESTs are subsets of the sequence instead of the full transcript, it's possible to "CTRL+F" the organism's genome and find the gene which contains the EST.
Scientists have been doing this for decades, so nowadays you can search a gene/protein database and instantly know which sequence is responsible for, say, a specific channel protein.
To go in the other direction from gene to protein to function/trait, you have to do a fair bit of legwork as well. In very, very simplistic terms, you "cut" some DNA, put it into a package, and deliver the package to your favorite organism. As you said, it's a bit more complicated than that. :)
For complex, polygenic traits, it's harder to (1) identify the genes responsible and (2) successfully engineer an organism to have all of those new genes. You're unlikely to see a human with tiger legs any time soon. It's much easier to give an organism a few genes that confer very specific traits. Look at this list of genetic modifications to crops and click on one of the traits; usually only 1-3 genes have been introduced.

This answer feels incomplete and pretty much skips over the very important work in genetics done in lower organims like yeast to identify the function of genes.

@Cell thank you for pointing this out. I felt this particular user was looking for a simple explanation that they could visualize, so I chose to describe one specific approach. In fact, I started writing this answer in response to a different question that the user asked shortly after this one, but the other question was so broad that my answer was better broken into pieces. I'll edit my response today to give a brief sketch of yeast genetics and am welcome to further suggestions.

I will name one classical methodology to associate genetic variation in population to phenotypic variation.
We can figure out functions of specific sequence thorugh correlation analyses. We sample a number of individuals from the population, sequence them (or genotype them) and measure a phenotype of interest. Then, we screen through their genome and for each locus (locus = position in the genome) we investigate whether there is a correlation between the genetic variation at this locus and the phenotypic variation. It is classic to represent these correlation tests throughout the genome with a Manhattan plot

, where the Y axis is the negative of the log of the P.value and the X axis is the position in the genome. From the above plot, one can tell that several loci at the end of the 19th chromosome are associated with the phenotype of interest. There is therefore likely at least one SNP over there that affects this phenotype.
This type of analysis are called Genome-Wide Association analyseS (GWAS; pronounced G-wass).


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Melting point of animal fat and plant fat
I notice in daily life that animal fat typically has a higher melting point than plant fat does. I wonder the reason why this happens. What exactly contributes to this difference? Is it because of the difference between molecular structure? I understand that substances have different melting point because the intermolecular forces are different. But how does intermolecular force vary between animal fat and plant fat. Is it possible for any animal fat to have lower melting point than plant fat?

Is it possible that "daily life" is imposing a selection bias?  That is, we mostly see plant fats in the form of things like cooking oils (or cocoa butter), which are selected because they have low enough melting points to be liquids.

Plants contains monounsaturated fats while animals contains saturated fats. The high proportions of fatty acids in animal fat means it takes longer to heat it up. I don’t know the melting points of different things off the top of my head, but you can find a meat that is as unsaturated as possible and compare it to the most saturated plant fat to test your last question.


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Is this how female and male gametes look like in plants?
In the red box, the pink one is female sex cell I presume and the blue one is a male sex cell.
http://prntscr.com/dsii2x Am I right? or are these chromosomes.. I'm confused.
This is law of segregation.

Gametes don't look like that. It is a simplified colourful diagram to explain Meiosis. Cells and cell components are not coloured in nature unless they have pigments in them (e.g. Nostoc sp. doesn't need staining it appears green under microscopel).

Then what is that though? And how do gametes look like?

The blue and red colours are to distinguish between the maternal and paternal chromosomes as you have thought. I don't find any other possible reason for colouring them differently.

I just have one more question though.. If these these two are diploid cells, and both of them separate then how is gametes related to this at all? is it because gametes are needed for this to occur in the first place (the occurring diploid cells?)

It's not very clear what you are asking.

@OkamaKsakas Please note that with the icon that looks like a landscape, you can insert an image directly in the post and not just a link to an image stored somewhere on a different site. It makes the post much more pleasant to read.

The comments are very unclear and your interpretation of the figure seems very wrong (no offense). You should have a look at an intro course (such as this one by Khan Academy) as asking such intro questions here will require for one to rewrite an entire course.
The pink and blue thingies on the image are chromosomes, not gametes. A gamete is a haploid cell (we can see 4 of them at the bottom of the figure). One chromosome (say the pink one) has been inherited by the mother of the individual and the other chromosome (say the blue one) has been inherited by the father of the individual.
Let's assume that the segregation we see on the figure happens in a female individual. So, on the figure we see female diploid cells and female haploid cells. The female haploid cells are called ovules (there is a bit of oversimplification here). You can imagine the same process of segregation could occur in a male individual. The male haploid cells are called spermatozoid (there is a bit of oversimplification here). The male and female gametes might fuse to become a zygote which will develop in a new fully grown individual. The colors of the chromosomes in this scenario indicate whether the chromosome originally come from the grandmother or the grandmother of the zygote.

Is there a way I can contact you in PM?

@OkamaKsakas You can find my contact information via my website which you'll find via my profile. Just click on my name and select the tab profile.

I'm not sure how to send you a message via twitter, unfortunately. I sent you a tweet though

Just send an email then. All the info is on my website.